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A 
 
 PRACTICAL TREATISE 
 
 ON 
 
 EENAL DISEASES 
 
 URINARY ANALYSIS 
 
 WILLIAM HENRY PORTER, M.D., 
 
 PROFESSOR OP CLINICAL MEDICINE AND PATHOLOGY IN THE NEW YORK POST-GRADUATE MEDICAL. 
 
 SCHOOL AND HOSPITAL ; CURATOR TO THE PRESBYTERIAN HOSPITAL ; ACTING CURATOR TO 
 
 BELLEVUE HOSPITAL ; MEMBER OF THE NEW YORK PATHOLOGICAL SOCIETY ; OF THE 
 
 CLINICAL SOCIETY OF THE NEW YORK POST-GRADUATE MEDICAL SCHOOL 
 
 AND HOSPITAL, AND OF THE NEW YORK NEUROLOGICAL SOCIETY 
 
 CONTAINING ONE HUNDRED ILLUSTRATIONS 
 
 NEW YORK 
 
 WILLIAM WOOD & COMPANY 
 
 56 & 58 Lafayette Place 
 
 1887 
 
Copyright 
 WILLIAM WOOD & COMPANY 
 
 1887 
 
 PRESS OF 
 
 STETTINER, LAMBERT 4 CO., 
 
 22, 24 & 2« READE ST.* 
 
 NEW TORK. 
 
THE FOLLOWING PAGES 
 
 AEE DEDICATED TO 
 
 MY FATHER, 
 
 FREDERICK EDWARD PORTER, 
 
 AS A TOKEN" OF RESPECT 
 AND AFFECTION. 
 
PREFACE. 
 
 Dukikg the past ten years, the author has had ample opportunity 
 for studying the various lesions of the kidneys, as they are found in 
 human and animal subjects. The essential ideas advanced in this 
 book, if any originality can be claimed, are based upon the statistics 
 gathered from over one thousand post-mortems. 
 
 Attention was devoted specially, during the course of studies in 
 comparative medicine, to the class of lesions commonly known as 
 Bright's disease, and it was from these observations, taken in con- 
 nection with the opportunities that have offered since of watching 
 these conditions from their inception in the human being, through 
 the different phases of the disease, until finally they came to the post- 
 mortem table, that the deductions employed throughout the work 
 were obtained. 
 
 Among the lower animals, the necropsies were made immediately 
 after death, and consequently accurate results were obtained in regard 
 to the morbid changes in the epithelial protoplasm, and the exam- 
 iner was enabled to judge how much of the metamorphotic change 
 was due to the disturbed physiological condition prior to death, and 
 how much was more directly due to the post-mortem alterations. 
 
 Eenal diseases have been studied chiefly from the clinical and. 
 pathological point of view, but we have tried to present them not 
 only from this standard, but also from the physiological standpoint, 
 deducing the methods of treatment not only from the physiological, 
 but from the pathological phenomena. 
 
 Preceding the group of diseases usually classed as Bright's disease, 
 a brief resume of the anatomy and physiology of the kidneys has been 
 inserted, in order that the reader, by refreshing his memory, may be 
 
VI PREFACE. 
 
 enabled to obtain a clear understanding of the various lesions; and in 
 connection with this, the various pathological conditions found are 
 described at some length. 
 
 A chapter is also devoted to the consideration of diabetes. 
 
 The second portion of the book is devoted to a study of urinary- 
 analysis; not simply the chemical or microscopical examination of 
 samples of urine, but also the physiological indications, with their 
 bearings on clinical medicine. A more accurate interpretation of the 
 exact conditions of the diseased organs may be obtained, and a more 
 definite prognosis pronounced, when these considerations receive full 
 weight, than can be the case if only the chemical and microscopical 
 results, as usually noted, are borne in mind. 
 
 An extended bibliography has been omitted purposely, in order 
 that the work might be kept within bounds; but the author takes this 
 opportunity of acknowledging the assistance obtained by a perusal of 
 the chief authorities upon both renal diseases and urinary analysis. 
 
 The original drawings, some fifty in number, have been made by 
 his clinical assistant, Dr. George G. Van Schaick, from sections in the 
 author's possession, and the credit is due him for their accuracy and 
 perfection. 
 
 Through the courtesy of Dr. Francis Delafield and the kind co- 
 operation of the publishers, Messrs. William Wood & Co., a large 
 number of plates have been employed in illustrating different por- 
 tions of the book, that have appeared in other works on this subject. 
 
 It gives me much pleasure, also, to testify to the valuable aid 1 have 
 received from two of my former students, Dr. William C. Carroll and 
 the late Dr. William Hustace Hubbard. 
 
 Before closing, the author wishes to extend his sincere thanks to 
 
 his friend, Dr. Samuel Lloyd, who has rendered most valuable aid in 
 
 the final revision of the manuscript and in the correction of the 
 
 proofs. 
 
 W. II. P. 
 STRATHMORE, 1674 Broadway, cor. 52d st. 
 April 20lh, 1887. 
 
CONTENTS. 
 
 PART I. 
 
 DISEASES OF THE KIDNEYS. 
 
 CHAPTER I. 
 
 PAGE 
 
 Anatomy of the Kidney 1 
 
 CHAPTER II. 
 
 Physiology of the Kidney ; Inflammation and its Bearings on the Pathol- 
 ogy and Treatment of Acute Parenchymatous Metamorphosis of the 
 Kidney , 12 
 
 CHAPTER III. 
 
 Chronic Parenchymatous Metamorphosis of the Kidneys; Parenchymatous 
 Metamorphosis of the Kidneys Associated with Pregnancy; Parenchy- 
 matous Infiltration of the Kidneys associated with Wasting Disease. . 2? 
 
 CHAPTER IV. 
 
 Acute Diffuse Nephritis ; Chronic Diffuse Nephritis, First, Second, and 
 Third Forms. 45 
 
 CHAPTER V. 
 Complications of Renal Lesions ; Treatment of Chronic Diffuse Variety. . . 62 
 
 CHAPTER VI. 
 
 Acute and Chronic Sclerosis of the Kidneys ; Gouty Kidneys ; Hyalin e, 
 
 Albuminoid, or "Waxy Kidneys ; Summary 92 
 
 CHAPTER VII. 
 Renal Hemorrhage ; Hsematoglobinuria ; Anaemia 105 
 
 CHAPTER VIII. 
 Acute Congestion ; Chronic Congestion Ill 
 
vi 11 CONTENTS. 
 
 CHAPTER IX. 
 
 PAGE 
 
 Pyelonephritis ; Pyelitis ; Pyonephrosis 118 
 
 CHAPTER X. 
 Hydronephrosis ; Renal Calculi 127 
 
 CHAPTER XL 
 Acute and Chronic Atrophy of the Kidneys ; Cysts of the Kidneys 132 
 
 CHAPTER XII. 
 Tuberculosis of the Kidneys 136 
 
 CHAPTER XIII. 
 
 Infarction of the Kidneys : Fat Embolisms of the Kidneys ; Pysemic Em- 
 boli of the Kidneys 141 
 
 CHAPTER XIV. 
 
 Tumors of the Kidneys: Sarcoma; Carcinoma; Adenoma; Fibroma; 
 Congenital Rhabdo-Sarcoma ; Angioma ; Lipoma ; Lymphoma ; Os- 
 teoma ; Angioma or Cavernous Neoplasms 146 
 
 CHAPTER XV. 
 
 Parasites : Echinococcus; Bilharzia Hasmatobia ; Strongylus seu Eustron- 
 gylus Gigas; Ascaris Renalis 157 
 
 CHAPTER XVI. 
 
 Glycosuria or Diabetes Mellitus— Its Etiology, Pathology, Clinical History, 
 
 and Treatment 165 
 
 PART II 
 
 UEINAEY ANALYSIS. 
 
 CHAPTER I. 
 Introductory Remarks 195 
 
 CHAPTER II. 
 C inical Examination 202 
 
 CHAPTER III. 
 Albumin ; Tests for Albumin ; Clinical Significance 217 
 
CONTENTS. IX 
 
 CHAPTER IV. 
 
 PAOK 
 
 Glucose or Grape Sugar ; Tests for Glucose 234 
 
 CHAPTER V. 
 Nitrogenous Excretory Substances .... 254 
 
 CHAPTER VI. 
 Urates, Phosphates, and Chlorides 275 
 
 CHAPTER VII. 
 
 Adventitious Coloring Matters ; Bile Pigment ; Fat ; Mucus ; Blood or 
 Haemoglobin 279 
 
 CHAPTER VIII. 
 How to use the Microscope ; Red Blood Corpuscles ; Leucocytes; Mucus.. 285 
 
 CHAPTER IX. 
 Uric Acid ; Oxalates ; Urates ; Phosphates ; Microscopic Pigments 294 
 
 CHAPTER X. 
 Epithelial Cells ; Spermatozoa 802 
 
 OHAPTER XI. 
 Vegetable Organisms ; Fungi 308 
 
 CHAPTER XII. 
 Casts 317 
 
 CHAPTER XIII. 
 
 Sediments of Doubtful Origin : Lime Carbonate ; Fatty Matters ; Choles- 
 
 terin; Cystin ; Leucin ; Tyrosin ; Xanthin ; Foreign Matter 324 
 
 CHAPTER XIV.; 
 
 Animal Organisms : Echinococcus ; Filaria Sanguinis Hominis ; Bilhar- 
 zia Haematobia ; Trachinas Cystica ; Eustrongylus seu Strongylus 
 Gigas ; Tetrastoma Renalis ; Spurious Entozoa ; Pediculus Pubis 332 
 
 CHAPTER XV. 
 Analysis of the Case ; Indications as to Diagnosis and Treatment 338 
 
LIST OF ILLUSTRATIONS. 
 
 FIG. 
 1. 
 2. 
 
 3. 
 4. 
 
 5. 
 6. 
 
 7. 
 
 10. 
 11. 
 
 12. 
 13. 
 14. 
 15. 
 16. 
 
 17. 
 18. 
 19. 
 
 20. 
 21. 
 22. 
 23. 
 24. 
 25. 
 26. 
 27. 
 28. 
 29. 
 30. 
 31. 
 32. 
 33. 
 34. 
 
 Cross section of kidney, ..... 
 
 Markings of the cortex, ..... 
 
 Diagram of uriniferous tubules, .... 
 
 Malpighian tuft, ....•• 
 
 Section from snake's kidney, showing rods of Heidenhain, 
 Looped tube of Henle, ...... 
 
 Prickle cells taken from kidney of dog, . 
 Section showing vascular arrangement of the kidney, 
 Kidney of dog, natural injection of secreting portion, 
 Rods of Heidenhain, ..... 
 
 Acute parenchymatous metamorphosis of the kidney, 
 Chronic parenchymatous metamorphosis of the kidney, 
 Chronic parenchymatous metamorphosis of wasting disease. 
 Acute diffuse nephritis, ..... 
 
 Chronic diffuse nephritis, ..... 
 
 Section from cortical portion showing thickened and expanded 
 
 afferent vessel, .... 
 Chonic diffuse nephritis, atrophied kidney, 
 Miliary aneurism of the brain, 
 Acute parenchymatous metamorphosis of the kidney following a 
 
 surgical operation, ..... 
 
 Acute interstitial nephritis, .... 
 
 Chronic interstitial nephritis, .... 
 Chronic interstitial nephritis with thickened blood-vessels, 
 Section from a typical gouty kidney, 
 Waxy degeneration of blood-vessels of glomerulus, 
 Early stage of waxy metamorphosis of the kidneys, . 
 Acute renal congestion with infarctions, 
 Pyelo-nephritis or surgical kidney, 
 Bacillus tuberculosis, 
 
 Acute congestion of the kidneys, with multiple infarctions, 
 Fat embolism of the kidney, 
 Round-cell sarcoma of the kidney, 
 Medullary carcinoma, 
 Lipoma of kidney, .... 
 Tsenia echinococcus complete, 
 
 PAGE 
 
 3 
 
 4 
 
 6 
 
 7 
 
 8 
 
 9 
 
 9 
 
 10 
 
 14 
 
 15 
 
 19 
 
 30 
 
 42 
 
 46 
 
 53 
 
 56 
 59 
 63 
 
 77 
 
 93 
 
 94 
 
 95 
 
 97 
 
 99 
 
 100 
 
 112 
 
 119 
 
 138 
 
 142 
 
 144 
 
 147 
 
 149 
 
 154 
 
 157 
 
Xll 
 
 LIST oV ILLUSTRATIONS. 
 
 FIG. 
 
 35. Cuticula of echinococcus cyst, 
 
 36. Endocyst of Huxley, 
 
 37. Scolices of Taenia echinococcus, . 
 
 38. Hooklets from scolex of taenia echinococcus, 
 
 39. Bilharzia hannatobia, 
 
 40. Strongylus seu Eustrongylus gigas, 
 
 41. Miliary gumma, .... 
 
 42. Large gumma, .... 
 
 43. Syphilitic pneumonia, 
 
 44. Chronic parenchymatous metamorphosis of the kidney, 
 
 45. Diabetic parenchymatous metamorphosis of the kidneys, medullary 
 
 portion, ..... 
 
 46. Diabetic parenchymatous metamorphosis of the kidneys, cortical 
 
 portion, ..... 
 
 47. Diabetic metamorphosis of the liver, 
 
 48. Glass cylinder graduated, 
 
 49. Conical glass, .... 
 Vogel's test-plate of colors, 
 
 50. Crystals of ammonia magnesium phosphate, 
 
 51. Uric acid crystals, .... 
 
 52. Urinometer, .... 
 
 53. Fermentation saccharometer, 
 
 54. Graduated cylinder, 
 
 55. Urometer of Doremus, . , 
 
 56. Blood-corpuscles as seen with the square ocular micrometer, 
 
 57. Human blood-corpuscles, . 
 
 58. Human red blood-globules, 
 
 59. Human blood-corpuscles crenated, 
 
 60. Pus-corpuscles, .... 
 
 61. Pus in various stages of development, 
 
 62. Highly magnified leucocytes, 
 
 63. Uric acid crystals, .... 
 
 64. Uric acid crystals, .... 
 
 65. Uric acid crystals, .... 
 
 66. Uric acid crystals, .... 
 
 67. Oxalate of lime crystals, ordinary forms, 
 
 68. Oxalate of lime crystals, typical forms, . 
 
 69. Oxalate of lime crystals, rare forms, 
 
 70. Urate of soda, .... 
 
 71. Stellar phosphate of lime, 
 
 72. Epithelial cells found in urine, . 
 
 73. Epithelial cells found in urine, 
 
 74. Epithelial cells found in urine, 
 
 75. Human spermatozoa, 
 
 76. Sphero-bacteria, .... 
 
 77. Micro-bacteria, .... 
 
 78. Leptothrix buccalis, 
 
 79. Bacillus tuberculosis, 
 
LIST OF ILLUSTRATIONS. 
 
 XIII 
 
 80. Desmo-bacteria 
 
 81. Penicillium glaucum, 
 
 82. Yeast and sugar fungi, 
 
 83. Casts, 
 
 84. Casts, 
 
 85. Casts, 
 
 86. Conical glass, 
 
 87. Cystin, 
 
 88. Leucin, 
 
 89. Tyrosin, 
 
 90. Whetstone-shaped crystals of xanthin, . 
 
 91. Hydrochlorate of xanthin, 
 
 92. Foreign matter, .... 
 
 93. Hooklets from scolex of taenia echinococcus, 
 
 94. Scolices of the taenia echinococcus, 
 
 95. Filaria sanguinis hominis, 
 
 96. Filaria in human blood, 
 
 97. Bilharzia haematobia, 
 
 98. Stronyglus seu Eustrongylus gigas, 
 
 99. Pediculus pubis found in urine, . 
 
 PAGE 
 314 
 
 315 
 316 
 318 
 319 
 320 
 323 
 326 
 327 
 328 
 328 
 329 
 330 
 332 
 333 
 334 
 335 
 336 
 336 
 337 
 
RENAL DISEASES. 
 
 PAET I. 
 
 CHAPTER I. 
 
 ANATOMY OF THE KIDNEY. 
 
 The kidneys, the two largest glandular organs in the body, are in- 
 tended for the excretion of urine, and are situated in the lumbar re- 
 gion, on either side of the vertebral column; the left on a level with 
 the last dorsal and two upper lumbar vertebrae, the right lying some- 
 what lower, on account of the large space occupied by the liver. They 
 rest upon the crura of the diaphragm, behind the peritoneum, the 
 upper end approaching nearer the vertebral column than the lower; 
 and they have a quantity of connective tissue and fat called the tunica 
 adiposa surrounding them, which, together with their blood-ves- 
 sels, nerves, lymphatics, and ureters, holds them in proper position, 
 and through which they receive their nutriment and discharge their 
 excretions. They are about four inches (10 centimetres) in length 
 and one inch (2.5 centimetres) in thickness, but these dimension 
 vary in individual cases. The left is usually larger and narrower than 
 the right, and weighs one and a half drachms more. The average 
 weight of the kidney in the adult male is from four and a half to live 
 ounces (125.572-141.747 grams); and in the adult female from four 
 to four and a half ounces (113.398-127.572 grams). The specific 
 gravity of the kidney tissue is about 1.052. 
 
 Regional Relations and Topography. — The anterior surface of the 
 left kidney is in contact with the inferior extremity of the spleen and 
 the tail of the pancreas; covered in by the cardiac extremity of the 
 stomach, and is immediately behind the descending colon. The an- 
 terior surface of the right kidney is in contact with the liver and de- 
 1 
 
'1 ANATOMY OF THE KIDNEY. 
 
 scending portion of the duodenum, and is immediately behind the 
 ascending colon. Both are covered anteriorly by the peritoneum, the 
 tunica adiposa intervening. 
 
 The posterior surface of each kidney rests against the corresponding 
 eras of the diaphragm and the anterior lamella of the transversalis 
 fascia which covers the quadratus lumborum muscle ; the superior 
 extremity is in contact with the corresponding suprarenal capsule. 
 
 Variations. — From the normal standard above described, the kid- 
 neys occasionally vary as regards form, position, size, and number. 
 Sometimes they are long and narrow, sometimes short and broad; one 
 or both may be situated in the pelvic region or any other part of the 
 abdominal cavity; the vessels may^e elongated, the peritoneum form- 
 ing as it were, a mesentery, and thus allowing them to float freely in 
 the peritoneal cavity, giving rise to the condition known as a " floating 
 kidney." which is most frequently met with in women, and usually on 
 the right side. 
 
 One kidney may be large and the other proportionately small; or 
 the two may be united by a band of renal tissue, passing over the 
 vertebra? and connecting their inferior extremities; this condition is 
 known as a "'horse-shoe" kidney; and when it occurs, both glands are 
 usually situated lower than normal. 
 
 One kidney and its ureter may be entirely absent, the opposite 
 organ being normal or increased in size; and in rare instances three 
 have been found in one body, the third occupying a position in front 
 of the vertebral column, or at the side of the normally located 
 glands. There is one case on record in which there were four with 
 their accompanying vessels and ureters; ' all four ureters opening 
 separately into the bladder. The two kidneys have also been found 
 upon the same side, and in such cases they are usually located lower 
 than normal. 
 
 The surface may be traversed by numerous moderately deep fur- 
 rows which give the organ a distinctly lobulated appearance; this 
 condition is always present in the foetal kidney, and may be found in 
 organs removed from the bodies of those who die during the first few 
 years of life; but this is not usually the case in those removed from 
 adults, the external surface being then perfectly smooth. When 
 traces of these furrows and lobules are found in the adult organ, they 
 are called traces of or festal mar kings. This condition is not infre- 
 quently met with, and indicates only a divergence from the general 
 rule, having no pathological significance. 
 
 Macroscopic Appearance. — The kidney is shaped somewhat like a 
 1 Indiana Medical Gazette, Jan., 1874. 
 
ANATOMY OF THE KIDNEY. 
 
 " Haricot " or " Kidneybean." The anterior surface is convex, the 
 posterior nearly flat; the superior extremity is thick and rounded, and 
 is larger than the inferior, which is thinner and more pointed. The ex- 
 ternal border is convex, the internal concave, presenting a deep fissure, 
 about an inch (2.5 centimetres) in length, called the hilum, through 
 which pass the vessels, nerves, and lymphatics, and the excretory duct 
 or ureter. The hilum opens into a cavity in the substance of the 
 gland which is called the sinus renalis. 
 
 The relations of the vessels and ureter to each other in the hilum 
 are as follows: from above downwards, artery, vein, and ureter; from 
 
 Fig. 1.— Cross Section of Kidney. 
 1, Malpighian pyramid; 2, arterio-venous arcade of Flint; 3, striations of the pyramid; 4, 
 base of pyramids of Ferrein; 5, calices; 6, columns of Bertini; 7, pelvis and infundibuli ; 8 
 ureter. (From Sappey's Anatomy.) 
 
 before backward, vein, artery, and ureter; but this arrangement occa- 
 sionally varies. The whole gland is covered by a thin, smooth, 
 fibrillated connective-tissue membrane, called the capsule, which, in 
 the normal state, is not adherent to the underlying surface, and, upon 
 removal, leaves it perfectly smooth, although the foetal markings may 
 occasionally be observed. By making a longitudinal section, the cor- 
 tex, medullary substance, and sinus renalis are exposed. Tlie sinus 
 
* ANATOMY OF THE KIDNEY. 
 
 mialis is the deep fossa in the kidney proper in which the pelvis (the 
 expanded portion of the ureter) joins the renal substance, and through 
 which the vessels pass to reach the nephritic tissue. The hilum is 
 the perceptible notch; the sinus is deep in the gland proper. The 
 medullary substance consists of from eight to eighteen conical masses 
 called the Pyramids of Malph igij their apices being known as papilla, 
 which converge and are invaginated in the ultimate divisions of the 
 pelvis known as the calices. The calices, seven to thirteen in number, 
 converge to form the three primary divisions of the pelvis, which in 
 turn have been termed infundibula; and these join to form the pelvis 
 of the kidney, which is the funnel-shaped extremity of the dilated 
 ureter. The ureter is the excretory duct, and opens into the posterior 
 surface of the bladder. The pyramids are distinctly striated, these 
 
 Fig. 2. — Markings of the Cortex. 
 r, Cortical layer; m, medullary rays or pyramids of Ferrein; c, arterise recta?, with attached 
 Malpighian corpuscles; g, base of Malpigian pyramid; h, bundle of collecting tubes; 6, vascular 
 area between the bundles; p, apex of Malpighian pyramid. 
 
 striations always being straight in the normal kidney, and consisting of 
 diverging blood-vessels and straight or collecting uriniferous tubules, 
 the arrangement of which will be explained hereafter. This striated 
 appearance is prolonged into the cortex, where it is more prominent 
 than in the pyramids. This is accounted for by the greater paleness 
 of the epithelium. The red lines indicate the position of the nutrient 
 vessels; the pale lines indicate the straight tubules prolonged into the 
 cortex, and are known as the Pyramids of Ferrein. These alternating 
 colors are called the markings of the cortex; when straight, they indi- 
 cate a normal kidney, or one in which the lesion is confined to the 
 epithelial cells only; when wavy or tortuous, they indicate a lesion in- 
 
ANATOMY OF THE KIDNEY. 5 
 
 volving the intertubular tissue, which by contraction has caused the 
 vessels to deviate from a straight course. By these striations and 
 their changes, we are enabled, in a measure, to differentiate between 
 a parenchymatous and a diffuse or sclerotic change. This will be 
 fully appreciated later on, when studying the morbid appearances. 
 
 The cortical layer lies immediately beneath the renal capsule; it 
 is about one-quarter of an inch (6.25 mm.) in thickness, and sur- 
 mounts the base of the pyramids, sending prolongations between 
 them as far as the sinus. These interpyramidal portions are known 
 as the " Septa vel Column® Bertini," and mark the original divisions 
 of the kidneys into lobules. That portion of the cortical substance 
 which stretches from one column to another, and which surrounds 
 the base of the pyramids, is called the cortical arch. The columns 
 of Bertini and the cortical arches taken together form the "Laby- 
 rinth of Ludwig." 1 
 
 Microscopic Appearances. — The capsule is composed of fibrous 
 tissue, in which a few elastic fibres are intermingled. 
 
 It is connected with the organ by fine fibrillated connective tissue 
 and minute blood-vessels. An inflammatory thickening and an in- 
 crease in these connecting fibres account for the adhesion of the 
 capsule and the roughening and detachment of small fragments of 
 the renal surface in the intertubular varieties of renal disease. 
 
 The capsule may be divided into two layers : an outer one about 
 y-^-j of an inch (0.143 mm.) in thickness, which becomes continu- 
 ous with the connective tissue surrounding the blood-vessels and 
 the ureter at the hilum ; and an inner, about T oVo" °f an inch (0.025 
 mm.) in thickness, terminating where the papillae join the calices in 
 the sinus renalis. Beneath the latter is a wide-meshed, delicate 
 framework of smooth muscle fibres, some of which traverse the cor- 
 tical substance. 
 
 The uriniferous tubules begin in the cortical substance in small 
 spherical bodies called the Malpighian corpuscles, beyond which they 
 are markedly convoluted, and are known as the convoluted tubes of the 
 first order. 
 
 At the junction of the capsules with the tubes, there is a marked 
 constriction or neck, and beyond this convoluted portion they become 
 straight and pass directly down into or between the pyramids, forming 
 the descending limb, then turning upon themselves they form a loop 
 and pass straight upwards to the cortical arches or substance, thus 
 forming the ascending limb; and these, taken together, form the 
 looped tube of Henle. In the cortical substance, the tubules again be- 
 1 Ludwig : Strieker's Manual, p. 461. 
 
6 
 
 ANATOMY OF T1IK KIDNEY. 
 
 come convoluted ami are called junctional tubes, intercalated tubes, 
 or convoluted tubes of the second order. They now become straight 
 and pass down through the pyramids toward the papilla, being 
 
 Fig. 3.— Diagram of Uriniferous Tubules. 
 
 7?, Cortical Portion. 1, Malpighian tuft; 2, convoluted tube of first order showing neck; 
 3 c, convoluted tube of second order; d, straight portion of tube between convoluted tube of 
 second order and collecting tube; 4, collecting tube near surface of kidney; 4 e. collecting 
 tube entering cortico-medullary portion. Or, Cortieo-Medullary Portion. 3, loop of Henle; 
 (a), descending arm; (b), ascending arm. .1/, Medullary Portion. 4. converging collecting 
 tiilx^; e, collecting tubes; /. intertubular space; g, opening of uriniferous tubule at apex of 
 Malpighian pyramid. 
 
ANATOMY OF THE KIDNEV. I 
 
 called the straight or collecting tubes, and, after uniting at very acute 
 angles, form the excretory tubes or ducts of Bertini. These empty 
 into the calices on the surface of the papillae, sometimes at the 
 bottom of a slight depression, known as the foveola, but more often 
 their open mouths are dotted over the surface. The straight or 
 collecting tubes, just before leaving the cortical substance, are arranged 
 in bundles, the central tubes of which are the longest, while the 
 most external are the shortest; this difference in length gives the 
 bundles a pyramidal appearance, from which they have been called 
 the pyramidal prolongations, medullary rays, or pyramids of Ferrein. 
 They are found only in the cortical arches, and are also known as 
 lobules of the kidney. 
 
 Fig. 4— Malpighian Tuft (Highly Magnified). 
 
 «, Afferent artery; b, efferent vein; c, neck of uriniferous tubule; d, space within the capsule ; 
 f, capillary network; gr, epithelial lining of Bowman's capsule. 
 
 The tubules consist throughout their whole extent of a basement- 
 membrane lined with epithelium. The Malpighian corpuscles are 
 small spherical bodies, regularly arranged in rows in the edges of the 
 pyramids of Ferrein in the cortical arches, but they are also scattered 
 irregularly throughout the columns of Bertini. They vary from 
 tfo ^° Yi-o °f an i ncn (0.25 mm.-0.092 mm.) in diameter, and are 
 composed of an investing or external capsule known as Bowman's, 
 Miiller's, or the Malpighian capsule. 
 
 This capsule is composed of k an investing basement-membrane 
 lined with flat epithelial cells, reflected over the glomerulus, and often 
 
ANATOMY OF THE KIDXI V. 
 
 dipping in between the individual blood-vessels. The glomerulus is 
 formed by a small afferent artery dividing into a number of convo- 
 luted . loops, that unite to form an efferent vessel, which is 
 smaller than the afferent. The two vessels pierce the capsule at 
 points very near each other. Almost directly opposite their point of 
 entrance and exit, the capsule becomes continuous with the convo- 
 luted tube of the first order which has an average diameter of 
 •g-Jir of an inch (0.041 mm.). It is composed of a basement- 
 membrane lined with epithelial cells, which are somewhat triangular 
 
 &CL 
 
 
 Fig. 5. — Section from Snake's Kidney Showing the Rods of Heidenhain. 
 a, Uriniferous tubules with rods; c, tubules without rods; d, intertubular tissue. 
 
 in character, and which project more than half-way across the 
 diameter of the tube. Owing, however, to the fact that the projection 
 on one side is between two projections on the opposite side, the lumen 
 is not closed, but has a spiral character. These epithelial cells have 
 a striated appearance, produced by capillary tubules, one end of 
 which rests against the basement-membrane, while the other projects 
 towards the lumen of the tube. These are called the " Rods of 
 Heidenhain.'* The looped tubules traverse the pyramids for a greater 
 or less distance, and some almost reach the papilla?, while others 
 scarcely enter the medullary substance. The average diameter of the 
 
ANATOMY OK TIIK KIDNKV. 
 
 9 
 
 descending limb is y-^-g- (0.020 mm.), diminishing in some places to 
 
 Wtto °^ an i ncn (0-012 mm.). 
 
 The diameter of the ascending limb is about -g-J-g- of an inch (0.041 
 mm.); the lumen in the latter case, however, is the smaller of the 
 two. The ascending limb is similar in construction to the convoluted 
 tubules of the first order, but it is larger than the descending limb, 
 and ends in the convoluted tube of the second order. 
 
 The epithelial cells lining the descending arm are spheroidal and 
 sparsely set, and the nuclei being large, cause the cells to project 
 into the lumen, giving it a tortuous appearance on longitudinal 
 section. 
 
 The epithelial cells of the ascending limb are cuboidal; those of the 
 intercalated portion are pyramidal, resembling those of the first order. 
 
 Fig. 6. — Looped Tube of Henle. 
 
 B, Descending limb showing the spindle- 
 shaped epithelial cells; A, ascending limb 
 showing cuboidal epithelium with "Rods 
 of Heidenhain." 
 
 Fig. 7.— Prickle Cells taken from Kidney 
 of Dog. 
 
 a, Froni smallest collecting tubes; 6, from 
 larger collecting tubes. X 450 (Satterthwaite''s 
 Histology.) 
 
 In the convoluted portions of both the first and second orders, and in 
 the ascending limb of Henle, the epithelial cells contain the " Eods 
 of Heidenhain." 
 
 The collecting tubules gradually increase in size as they approach 
 the papillae. In the upper part of their course they are about -^ of 
 an inch (0.041 mm.) in diameter, but this increases near the papillae 
 to ilo or ah) °f an i ncn (0.051-0.104 mm.). The epithelial 
 cells lining this part of the tubules are of the columnar variety, the 
 only peculiarity being that their bases are irregular in shape and in- 
 
10 
 
 ANATOMY OF THE KIDNEY. 
 
 terdigitate, the projections of one fitting in the other. They are 
 a form of prickle cell. 
 
 The kidney receives its supply of blood through the renal artery, 
 which, passing through the hilum, between the ureter and vein, 
 enters the sinus renalis and there divides into a number of branches, 
 which spread among the infundibuli and enter the columns of 
 Bertini. Here they subdivide and proceed in straight lines to the 
 cortical substance, where they form arches around the base of the 
 pyramids. These arches are not so complete as those formed by the 
 accompanying veins. The two arches taken together are known as 
 the arterio-venous Arcade of Flint. From the arches small branches 
 are given off, called the intertubular arteries, which pass outward 
 between the double rows of Malpighian corpuscles, intervening be- 
 
 Fig. 8.— Section Showing Vascular Arrangement of the Kidney. 
 b, Zone of arteriae rectae and Malpighian corpuscles; »i, zone containing the pyramids of 
 Ferrein and the intertubular plexus; vi, venae rectae; a<", arteriae rectae; va, afferent artery; 
 gl, glomerulus; re, efferent vein; v, vein from intertubular plexus; z, entrance of vein into 
 venae rectae. 
 
 tween the pyramids of Ferrein, to which they give off branches, viz., 
 the afferent arteries of the Malpighian bodies. The renal arteries also 
 give off branches to the capsule, which anastomose freely with 
 branches from the lumbar arteries. From the lowermost of the 
 Malpighian tufts, and also from branches of the renal artery, straight 
 vessels pass downward toward the apex of each pyramid and break up 
 into cajnllaries, which surround the collecting tubules; these are 
 known as arteries recta). The blood in returning flows through a cor- 
 responding set of veins and finally empties into the intertubular veins. 
 From the Malpighian corpuscle the efferent vessel divides into a net- 
 
ANATOMY OF THE KIDNEY. 11 
 
 work of capillaries, which surround the tubules of the cortical sub- 
 stance and form the inter tubular plexuses, which, as they approach the 
 cortex, form small veins. The small radicles anastomose with one 
 another near the surface of the gland, and from their peculiar star- 
 shaped arrangement are called the stellated veins or " Stars of 
 Verheyen." 
 
 This stellated appearance is more a pathological than a histological 
 condition, for it is not always present; and. when it is distinct, the ves- 
 sels of the kidneys are usually in a state of dilatation, which has resul ted 
 from obstructive congestion. They, however, have been commonly 
 described under the normal histological appearances. These stellar 
 veins are the primary origin of the intertubular or interlobular veins, 
 which pass downward and accompany the intertubular arteries to the 
 venous side of the arterio-venous arcade. From the arcade the venous 
 trunks proceed in company with the arteries in the pyramids of 
 Bertini to the sinus of the kidney, where they ultimately join to form 
 the renal vein. 
 
 The nerves that have been traced into the kidney are small and 
 derived from the solar plexus; some coming directly from the renal 
 plexus, and some from the smaller splanchnic nerve. There are also 
 some filaments derived from the cerebro-spinal system. They follow 
 the course of the arteries and have been traced for some distance, but 
 their manner of termination is uncertain. 
 
 The lymphatics are numerous, and arranged in two sets; one a 
 superficial plexus in the fibrous capsule, the other a deep or internal 
 plexus which emerges from the sinus in company with the blood- 
 vessels. The internal form a freely communicating plexus of lymph 
 spaces, most marked around the tubules of the cortex. This central 
 plexus communicates with the lymphatics of the capsule and those 
 issuing from the sinus. 
 
 The stroma of the kidney is made up of a variety of connective - 
 tissue elements. The fibres are most numerous in the vicinity of the 
 blood-vessels and around the Malpighian corpuscles; they are more 
 marked in the cortical than in the medullary portion, but become 
 abundant near the apices of the papilla?. The stroma is abundant in 
 the kidneys of infants, but is difficult to demonstrate in the adult 
 organ. This latter fact has led some to deny the existence of any 
 stroma whatever. This, however, is not generally recognized to be 
 true, and most, if not all histologists, believe in its presence. 
 
CHAPTER II. 
 
 PHYSIOLOGY OF THE KIDNEY; INFLAMMATION AND ITS BEAR- 
 INGS ON THE PATHOLOGY AND TREATMENT OF ACUTE 
 PARENCHYMATOUS METAMORPHOSIS OF THE KIDNEY. 
 
 During the past few years, many advances have been made, by care- 
 fully conducted physiological experiments, in our knowledge of the 
 excretory function of the kidney and its histological and pathological 
 anatomy, so that we are now in a position to understand better than 
 ever many of the topics of Bright's disease (so-called) that have 
 been unsatisfactory and obscure. 
 
 If, then, we keep these newly acquired physiological data in 
 mind, and study the pathological changes, it will be easy to see that 
 the common term, Bright's disease, covers a number of renal lesions. 
 These naturally fall into groups that are quite distinctive, and, in 
 nearly every instance, have such peculiar clinical characteristics that 
 they can be recognized nearly as well at the bedside as on the post- 
 mortem table. 
 
 In the present chapter it is proposed to take up one form of a 
 single group, in which the morbid changes affect the epithelial 
 elements, and it may be here stated that the data employed were 
 obtained by a study of cases which were followed from the ward to 
 the post-mortem table. It is hoped that the views here advanced 
 will contribute, not only to our knowledge of the disease from the 
 purely pathological standpoint, but will serve to show the relation 
 of the changes to the general condition of the patient, so that our 
 treatment in such cases may be better directed. 
 
 It must be recognized that there are two subdivisions of the excre- 
 tory apparatus of the kidney — one composed mainly of the coil 
 of blood-vessels in the glomerulus, or Malpighian tuft, the other of 
 the epithelium lining a portion of the tubules. 
 
 The glomeruli are generally believed to filter the water and inor- 
 ganic salts held in solution; it is also thought that sugar, albumin, 
 and peptones pass out through the glomeruli, the epithelium of the 
 
PHYSIOLOGY OF THE KIDNKV. 13 
 
 tubules eliminating the urea and the crystalline nitrogenous sub- 
 stances. 
 
 Now, as the passage of solutions through an animal membrane 
 depends to a great extent upon the pressure exerted, the rapidity 
 with which the urine is excreted and its amount naturally vary with 
 the blood-pressure in the glomeruli, and, consequently, the greater 
 the pressure in the vessels the greater will be the excretion, and 
 vice versa. Accordingly, the pressure in the vessels of the glomeruli 
 may be increased — 
 
 1. By any increase in the force and frequency of the heart's action. 
 
 2. By contraction of the arterioles at large or in areas other than 
 those of the kidney. 
 
 3. By relaxation of the renal arterioles, either alone or with con- 
 traction of other areas. 
 
 Or the pressure may be diminished — 
 
 1. By any diminution in the force and frequency of the heart 
 beats. 
 
 2. By dilating the arterioles at large or in areas other than the 
 kidney. 
 
 3. By contraction of the renal arterioles, either alone or with relaxa- 
 ation of other areas. 
 
 The function of the glomeruli is comparatively simple, being 
 immediately under the control of the vaso-motor system. Physio- 
 logical experiments have shown that a division of the spinal cord 
 below the medulla greatly diminishes the flow of urine. The expla- 
 nation is, that large vascular areas are cut off from their communica- 
 tion with the medullary vaso-motor centre, which, associated with the 
 shock to the spinal cord, produces a great fall in the general blood- 
 pressure. 
 
 With this relaxation of the renal artery an augmented flow of urine 
 would be expected, but the great fall in the general blood-pressure com- 
 pletely overbalances the effect produced upon the renal artery and di- 
 minishes the pressure in the vessels of the glomeruli. Stimulating the 
 spinal cord below the medulla affects the cord in an opposite manner 
 from division, but produces the same effect in reference to the quantity 
 of urine excreted. This is explained by the renal artery becoming so 
 firmly contracted that the general increased blood-pressure is over- 
 balanced, the artery being, as it were, ligated, and the pressure upon 
 the vessels of the glomeruli diminished or removed. Therefore, 
 opposite effects upon the cord produce precisely the same action upon 
 the glomeruli. 
 
 Section of the renal nerve produces relaxation of the renal artery, 
 
14 
 
 PHYSIOLOGY OF THE KIDNKY. 
 
 increased pressure in the capillaries of the glomeruli, and an increased 
 flow of urine. Section of the spinal cord, after division of the renal 
 nerve, arrests the polyuria by increasing the general capillary capa- 
 i ity outside the kidney, thus reducing the general blood-pressure, and 
 in this way again establishing a normal pressure in the glomeruli. 
 Stimulation of the spinal cord, after division of the renal nerve, still 
 further increases the flow of urine by diminishing the general capil- 
 lary capacity outside the kidney, thus increasing the general blood- 
 pressure in the glomeruli. 
 
 Fig. [9.— Kidney of Dog. Natural Injection of Secreting Portion, Artificial Injection 
 of^Artery, Vein, and Capillaries. Transverse Section through Cortical Substance. 
 
 a, Afferent vessel, filled with injected material; b, efferent vessel, also filled with injection; 
 e, glomerulus, injected and lying within its capsule, epithelium of latter distinctly seen; 
 d, capillaries surrounding the convoluted tubules, and distended with the injection, at this 
 point four capillaries are seen to unite and form a vein: c, convoluted tubule, filled with 
 crystals of indigo-carmine ; /, convoluted tubule, in which the nuclei have a dark color. The 
 striations of Heidenhain are beautifully shown in the convoluted tubules. X 200. (Satter- 
 thwaite's Histology.) 
 
 Section of the splanchnic nerve, by which the kidney gets its prin- 
 cipal nerve-supply, increases the flow of urine by relaxing the renal 
 artery, but not to so great a degree as division of the renal nerve. As 
 the splanchnic nerve is distributed to the whole splanchnic arcade, 
 
PHYSIOLOGY OF THE KIDNEY. 
 
 15 
 
 the capillaries of which are dilated, the blood-pressure brought to 
 bear upon the glomeruli does not rise so high. Stimulating the 
 splanchnic nerve contracts the renal artery and arrests the flow of 
 urine. 
 
 From these observations, it is quite clear that the quantity of water 
 discharged from the kidney is governed, to a large extent, by the vaso- 
 motor system. 
 
 The function of the epithelium, on the other hand, is much more 
 complex; but it appears to excrete the effete material of the system, 
 chiefly urea — the product of tissue metamorphosis. 
 
 In the experiments of Heidenhain upon the lower animals, sodium 
 sulphincligotate, known as indigo-carmine, was injected into the blood, 
 
 Fig. 10.— Rods of Heidenhain. 
 
 and, after the expiration of a certain length of time, the animals were 
 killed and their kidneys carefully examined. In these experiments the 
 indigo-carmine was found entering the epithelium through the rods of 
 Heidenhain and passing out of the epithelium into the lumen of the uri- 
 niferous tubules. In other experiments a length of time was permitted 
 to elapse after the first injection, which previous experience had shown 
 was sufficient for the complete elimination of the pigment by the 
 epithelium. Another quantity was then injected into the blood; in 
 this instance the elimination of the second injection of pigment was 
 found to be incomplete, as if the cells, exhausted by their previous 
 efforts, were unable to perform the extra work thrown upon them. 
 Thus, so far as indigo-carmine was concerned, it was proved that, 
 as effete material, it was eliminated by the epithelium. These experi- 
 
16 PHYSIOLOGY OF THE KIDNEY. 
 
 ments were followed by those of Nussbaum on amphibia; the newt 
 was the animal chosen for experiment, the kidney of which has a 
 double vascular system — an arterial, from which the glomeruli 
 receive their blood supply, and a venous, by which its uriniferous 
 tubules are surrounded. These two blood-supplies have no connec- 
 tion, the one coming from the renal artery, the other from the 
 bifurcation of the femoral veins, an arrangement peculiar to these 
 animals. If one of these channels is closed, what is excreted by the 
 other cau be readily ascertained. The amount of certain substances 
 was increased, and others not normal to the urine were brought 
 about by injections into the systemic circulation. The result of 
 these experiments showed that water, peptones, albumin, and sugar 
 were found in the urine previous to the ligation of the renal arteiy, 
 but that they disappeared upon the performance of the operation; 
 urea, however, continued to appear in the urine after the artery had been 
 tied. When indigo-carmine was injected into the circulation after liga- 
 tion of this vessel, no urine was found in the bladder; but the pigment 
 could be traced through the epithelium into the lumen of the uriniferous 
 tubules. It appears that the excretion of water, although almost 
 entirely confined to the glomeruli, was undertaken to a slight extent 
 by the epithelium, probably for the purpose of dissolving the urea and 
 rendering its excretion less difficult than it otherwise would be; but, 
 when the additional stimulus of an increased amount of effete material 
 excited the cells to more than ordinary action, the flow of water from 
 them became more abundant. 
 
 Further than this, experiments have as yet shown nothing; but even 
 these go far to prove that, in the normal state, the glomeruli supply 
 almost if not quite all the water and inorganic salts of the urine, 
 while to the epithelial cells lining the uriniferous tubules is left the 
 task of excreting the products of tissue metamorphosis. By apply- 
 ing these physiological data to our present pathological knowledge, 
 we are enabled to understand many conditions heretofore very 
 obscure. 
 
 We now approach a subject concerning which there has been much 
 uncertainty among pathologists, namely, the relation between paren- 
 chymatous change and inflammation. 
 
 In a general way, the latter may be said to include one or more of 
 a series of changes occurring in living tissues as a result of an irrita- 
 tion or injury, which may be induced either by an external or an 
 internal agency, provided the vitality of the part is not destroyed. 
 
 The exciting injury may be extrinsically direct when produced by 
 chemical or mechanical irritants ; intrinsically indirect when produced 
 
ACUTE PARENCHYMATOUS METAMORPHOSIS. 17 
 
 through the blood or lymph-channels; indirect, as when internal 
 organs become inflamed after exposure to cold. So-called idiopathic 
 diseases, the causes of which are internal or imperceptible, come 
 under the head of indirect, for in all cases the inflammatory process 
 must be produced by some injury. 
 
 The usual order of events when an organ has been attacked is as 
 follows : Acute hyperemia — more accurately speaking, determination 
 of blood to the part— followed by stasis; the escape of the liquor san- 
 guinis; the migration of the white and diapedesis of the red corpuscles. 
 Also an increase in the size and the number of the original elements, 
 a deposit of adventitious material, changing in character the elements 
 attacked, and death, with its necessary loss of substance. 
 
 It occasionally happens that changes in the blood and blood-vessels 
 constitute the only signs of inflammation, as in acute meningitis, 
 where death ensues before the exudation of all the constituents of the 
 blood; but, for a full definition of a typical case of inflammation, all 
 of the foregoing are necessary. 
 
 Considering all these changes essential to our conception of a true 
 inflammatory process, it is difficult to see what relation the change 
 called parenchymatous metamorphosis bears to inflammation. 
 
 What actually happens to the cells is that they are overworked by 
 an attempt on their part to free the kidneys and, secondarily, the sys- 
 tem, of an excessive amount of the incompletely formed products of 
 tissue metamorphosis, or of some extraneous poison. The experiments 
 •of Nussbaum with indigo-carmine go to sustain this explanation. In 
 this metamorphosis, as in his experiments, the epithelial protoplasm 
 undoubtedly loses its power of elimination, becomes altered by the 
 effete material, and undergoes various retrograde changes which are 
 known as cloudy swelling, fine and coarse granular metamorphosis, 
 and fatty transformation. 
 
 With these introductory explanations, we come to our first division 
 of this group of renal lesions, commonly classed under the indefinite 
 title of Bright's disease. 
 
 Acute Parenchymatous Metamorphosis of the Kidney. — 
 This disease, commonly known as acute parenchymatous nephritis, is 
 that lesion of the kidney in which the epithelial cells lining the urini- 
 ferous tubules undergo metamorphotic changes — namely, cloudy 
 swelling and fine and coarse granular and fatty infiltration; in 
 which, however, there is no change in the blood-vessels or interstitial 
 tissue. 
 
 This metamorphosis occurs in connection with, or as a complication 
 
 of scarlet fever, pneumonia, diphtheria, small-pox, typhus fever, 
 
 2 
 
IS ACUTE PARENCHYMATOUS METAMORPHOSIS. 
 
 typhoid fever, yellow fever, cholera, puerperal fever, septicaemia, 
 pyaemia, acute yellow atrophy of the liver, rheumatism, peritonitis, 
 meningitis, tetanus, hydrophobia, during the early stage of cir- 
 rhosis of the liver, with severe cases of jaundice, various pigmen- 
 tary diseases, severe burns and following surgical operations; it may 
 also be the result of poisoning by arsenic, phosphorus, antimony, 
 copper, mercury, and all the potassium salts: and, in some rare cases, 
 is said to develop without known cause. This list comprises those 
 diseases in which the exciting cause is some original and impalpable 
 poison which greatly interferes with the normal nutrition of the 
 body, diminishing the perfection of its products, and increasing the 
 amount and rapidity of their formation. The incomplete change 
 thus produced differs from the normal physiological process in the 
 large amount of effete material generated and the great rapidity with 
 which it appears in the system. Great irritation is necessarily pro- 
 duced in the whole animal economy by the combined action of the 
 original poison and of those incomplete products of tissue metamor- 
 phosis circulating in the blood; and to their combined action the phe- 
 nomenon known as elevation of temperature is due. However this 
 may be, the kidneys, which are the great eliminating organs of this 
 variety of waste products, endeavor to remove from the body, by 
 means of their epithelial cells, the irritating substances which are 
 producing such deleterious effects upon the system. At first they 
 may be successful, but, as the labor thrown upon them is increased, 
 they will become exhausted (as in Heidenhain's second injection of 
 indigo-carmine), and the process of excretion be less complete. 
 Their protoplasm becomes infiltrated with minute particles of irritat- 
 ing substances, such as effete material, pigments, etc., which cause 
 them to swell and to lose their transparency. The weakest of them 
 undergo a progressive change which ultimately results in a complete 
 granular or fatty metamorphosis, and a final destruction of their vital 
 property. This process is certainly not inflammatory, but one of 
 transformation and death, which is caused by an unduly prolonged 
 struggle un the part of the epithelial cells to accomplish a work too 
 great for their capacity. As the disease advances, the cells fall from 
 their jolace on the wall of the uriniferous tubules, and appear in the 
 urine as casts and cast-matter. The tubules, thus deprived of their 
 epithelial cells, have in some places only basement membrane to form 
 their wall; but, as only isolated cells undergo degeneration, the 
 damage done is repaired according to the general law of regeneration 
 and proliferation of the epithelial elements, and the wall of the tube 
 
ACUTE PARENCHYMATOUS METAMORJ'IIOSIS. 
 
 I!) 
 
 is restored to its normal condition after the complete subsidence of 
 the disease, provided the chronic form is not developed. 
 
 Macroscopic Appearances. — A kidney in the condition of acute 
 parenchymatous metamorphosis is usually enlarged, but may be 
 normal in some few cases. The capsule is normal in thickness, 
 does not adhere to the underlying tissue, and leaves the surface of 
 the kidney perfectly smooth upon its removal. The cut surface in 
 the early stage presents no marked change which can be positively 
 recognized by the unaided eye. Later on it is pale, and the pyramids 
 are less distinct than normal, but to the unaided eye they appear 
 
 -cu 
 
 Fig. 11. — Acute Parenchymatous Metamorphosis of the Kidneys. X 350. 
 a, Uriniferous tubules showing granular metamorphosis of the epithelial cells; c, c, desqua- 
 mated epithelial cells lying in intertubular spaces; h, swollen [and cedematous intertubular 
 tissue. 
 
 more distinct on account of the abnormal pallor of the cortical por- 
 tion. 
 
 Microscopic Appearances. — This lesion develops four degrees 
 of change in the renal epithelium: First, Cloudy Swelling. — This 
 condition is one in which the elements are swollen by the imbibition 
 of an albuminous fluid, and in which the protoplasm has become 
 turbid. Second, Finely Granular Metamorphosis. — Here the epithe- 
 
20 ACUTE PARENCHYMATOUS METAMORPHOSIS. 
 
 lium is not only cloudy, but is also infiltrated with fine granular 
 particles, some of which are oil globules of minute size, and others 
 granular detritus from the incomplete products of tissue metamor- 
 phosis which are in part drawn from the blood, and in part from the 
 further destruction of the epithelial protoplasm itself. Third, Coarse 
 Granular Change. — This is simply a more advanced degree of the 
 former, with more abundant and larger fat droplets. Fourth, Fatty 
 Transformation. — The protoplasm is entirely destroyed and replaced 
 by fat globules, causing a destruction of its substance and an abolition 
 of its function. 
 
 It seems quite probable that the cloudy and mucoid change is due 
 to the retention of a small quantity of effete material in the protoplasm 
 which causes this imbibition and transformation. The fine granular, 
 too, is a further change, due to the retention of a quanity of these 
 irritating substances now perceptible in the cell, and a commencing 
 disintegration of the protoplasm with a development of minute fat 
 droplets. The retention of a still larger amount of effete material 
 produces the coarsely granular metamorphosis, or a more advanced 
 disintegration of the protoplasm, and an increase in the size of the 
 fat droplets. In the last {fourth), or fatty change, so large a quan- 
 tity of the products of incomplete tissue metamorphosis, pigments, 
 etc., remains in the cells that their normal outlines are obliterated, and 
 the protoplasm is now destroyed by fatty degeneration. 
 
 Early in the disease, the cells having swollen rapidly, while the 
 kidney capsule remains unstretched, the lumen of the tubules is 
 entirely occluded, and under the microscope they are tortuous instead 
 of straight. This, of course, refers to the straight tubules, and not 
 to those normally convoluted; the latter, however, are considerably 
 distorted. 
 
 In the milder forms, the change in the epithelial cells is confined 
 principally to those of the cortical layer and those lining the glomeruli. 
 
 In more advanced cases, the cells of the pyramidal tubules also be- 
 come involved. The degree of transformation of the epithelium, 
 and the extent of territory implicated, will depend wholly upon the 
 intensity of the cause and its duration. 
 
 After the lesion has lasted for some time, what remains of the lumen 
 of the tubules may be found to contain single, or masses of trans- 
 formed and desquamated epithelial cells, which appear like the 
 materials from which casts are made. 
 
 Various forms of casts may occasionally be found in the lumen of 
 the tubules. 
 
 The stroma is not involved, and the blood-vessels remain unchanged. 
 
ACUTE PARENCHYMATOUS METAMORPHOSIS. 21 
 
 Symptoms. — This lesion occurring, as it does, in connection with 
 severe diseases, or as the result of some of the acute attacks of metallic 
 poisoning, the symptoms referable to the nephritic metamorphosis are 
 not well marked at first. Ordinarily, the symptoms of nephritic dis- 
 ease may be classified under two headings — rational, and urinary. 
 The former are divided into cephalic, respiratory, alimentary, and 
 general. 
 
 The cephalic are occipito-f rontal headache, contraction of the pupils, 
 injected conjunctivae, lesions of the retinae and optic nerves, drowsiness, 
 convulsions, and coma. The neuro-retinal lesions will be considered 
 more minutely in studying those lesions of the kidneys in which they 
 are more frequently met with, for in this form they are rarely seen. 
 
 The respiratory symptoms, which are usually asthmatic in character, 
 are more frequently met with in the chronic forms of the disease than 
 in the acute parenchymatous variety, and will receive more care- 
 ful consideration in connection with the affections with which they 
 are associated. 
 
 The alimentary symptoms are dyspeptic in character; they are 
 nausea, vomiting, loss of appetite, and disgust for food, often asso- 
 ciated with diarrhoea. 
 
 Those classed as general are oedema, commencing first in the sub- 
 cutaneous connective tissue under and around the inferior eyelids, 
 oedema of the inferior extremities, watery effusions into all the serous 
 cavities, oedema of the superior extremities, and general anasarca. 
 (Edema glottidis may occur. If the disease lasts for any length of time, 
 a peculiar waxy, almost translucent, pallor of the skin may be de- 
 veloped. This, however, is seldom seen, except in that form which 
 follows chronic metallic poisoning. 
 
 With this form a large number of the rational symptoms are masked 
 by the severe symptoms of the disease which it complicates; but those 
 that do attract attention are usually oedema of the eyelids and feet, 
 undue severity of the cerebral symptoms of the primary disease, and 
 a diminution in the quantity of urine passed daily. These symptoms 
 are followed speedily by those of a more acute character. The patient 
 complains of a severe headache and drowsiness, rapidly followed by 
 convulsions and coma. There may be associated with these cerebral 
 symptoms, or independently, some nausea and irritability of the 
 stomach, which often usher in severe vomiting and diarrhoea. The 
 oedema may now become very marked and be followed by dropsy of all 
 the large serous cavities. Dimness of vision may also occur in some of 
 these cases, but is due to interference with the optic centres, and not 
 to any lesion of the optic nerves or retinae. As the disease progresses, 
 
32 A.OUTE PARENCHYMATOUS METAMORPHOSIS. 
 
 the symptoms become more urgent, the drowsiness is followed by 
 stupor and delhium, the urine may be entirely suppressed, and the 
 patient lapses into a state of coma, which is usually followed by con- 
 vulsions; and death. 
 
 During the course of the disease, which seldom lasts more than a 
 few days, the cephalic, alimentary, and general symptoms may not be 
 associated as above described. In some cases, especially those which 
 occur complicating scarlet fever, pneumonia, typhoid fever, and other 
 acute febrile diseases, only those symptoms referable to the nervous 
 system appear, and headache, accompanied by dimness of vision, 
 drowsiness, stupor, delirium, and coma follow each other in rapid 
 succession; and. if the disease does not take a more favorable course 
 at this point, convulsions ensue, speedily followed by a fatal result. 
 In other cases, the alimentary symptoms present themselves, and these 
 are most apt to terminate in chronic parenchymatous metamorphosis, 
 resulting, as they do, from the mineral poisons. 
 
 Urinary symptoms are always present in all forms of the disease. 
 The urine is always diminished in quantity, high-colored, and its re- 
 action acid; the specific gravity ranges between 1.020 and 1.030, but 
 when the quantity passed is considered as compared with the normal 
 daily quantity, the specific gravity is found to be below the normal. 
 Albumin is always present, sometimes in great quantities, sometimes 
 only a trace, or to the amount of one or two per cent, by volume; 
 while in the most severe types of the disease it may completely solidify 
 the urine when boiled, so that, if the test-tube is inverted, no water 
 flows away. 
 
 On microscopical examination early in the disease, small hyaline, 
 epithelial, nucleated, and fine granular casts and granular debris are 
 seen, while at a later stage the coarsely granular and fatty casts make 
 their appearance; and as the disease advances, the casts increase in 
 size. 
 
 The diagnosis is readily made by remembering the causes, and 
 by a careful examination for casts. The only disease for which 
 it might be mistaken is acute diffuse nephritis. In the latter 
 we find blood and blood-casts in the urine; but in this lesion they do 
 not occur. 
 
 The prognosis is always grave, and especially so when the lesion 
 exists as a complication of acute disease. In scarlet fever, if convul- 
 sions occur, the patient rarely, if ever, recovers; while in pneumonia, 
 diphtheria, typhoid fever, etc., the first symptom of acute parenchy- 
 matous metamorphosis renders a favorable termination very doubtful, 
 
ACUTE PARENCHYMATOUS MKTAMOItl'HOSIS. 23 
 
 although there are instances in which patients recover even with this 
 severe complication. 
 
 In those cases which result from mineral poisoning, the immediate 
 danger is not so great; but the disease is very apt to lapse into the 
 chronic variety, which may end fatally in the course of a few years. 
 
 In treating this lesion, its method of production should be kept 
 constantly in view. It should be remembered that it is not of 
 an inflammatory nature, but that it results from too much work 
 being thrown upon the kidneys which undergo this metamorphosis 
 through their efforts to relieve the system. With this light upon 
 the subject, the great object in the way of treatment is to prevent an 
 excessive amount of work being forced upon these glands. 
 
 There is no doubt that elevation of temperature or heat, as the 
 damaging element in disease, has been much overestimated, and the 
 cause of the increased heat been too much neglected. The increase 
 of body-heat should only be looked upon as a symptom, produced in 
 part by the irritation of the original poison, and in part by the too 
 abundant and incomplete products of tissue metamorphosis, which 
 are excited by the poison and which circulate throughout the system. 
 
 All we can do in reference to neutralizing the original cause is to 
 make the hygienic surroundings as perfect as possible, and to supply 
 the patient with a large quantity of fresh air. 
 
 The original poison, in a measure, is probably eliminated from the 
 system by the kidneys, and also aids in damaging the epithelial pro- 
 toplasm. 
 
 With such a condition as this, the kidneys make an effort to rid the 
 system of this excessive amount of effete material, while at the same 
 time they receive less nutriment than in health, and, consequently, 
 are very likely to suffer irreparable damage. 
 
 The application of cold to the body in such conditions as these, 
 according to well established physiological laws, still further interferes 
 with tissue metamorphosis and adds new fuel to the fire. Many cases 
 have undoubtedly developed a fatal renal complication in this way. 
 It often happens that, following a cold pack or bath, the cerebral 
 symptoms increase in severity, the temperature rises higher, and 
 albumin presents itself in the urine for the first time; a speedy and 
 fatal termination soon following by an induced renal complication. A 
 striking example of this kind was observed in a case of sunstroke. In 
 this case, at the commencement of the attack there was a trace of 
 albumin in the urine; but, following the repeated application of cold 
 to lower the temperature, the quantity of albumin rose to 50 per cent 
 by volume, and all the urinary symptoms of acute parenchymatous 
 
24- a. l IK PARENCHYMATOUS METAMORPHOSIS. 
 
 metamorphosis presented themselves. Subsequent post-mortem 
 exam ination confirmed the diagnosis in regard to the renal lesion. 
 Remembering these facts, the kidneys should demand our first atten- 
 tion in all these severe diseases and in cases of acute metallic poison- 
 ing. Every effort should be made to aid the kidneys during this 
 severe strain and to guard them against this transformation, not 
 waiting until the metamorphosis has actually developed and then 
 try to cope with so formidable a malady. 
 
 In these cases cur attention should be directed to the other excre- 
 tory channels — namely, the skin and alimentary tract — and every effort 
 should be exerted to cause them to perform the largest possible amount 
 of work. By so doing, we relieve, to a considerable extent, the 
 increased strain upon these organs. 
 
 Cold applications to the skin should be avoided, but it should be 
 kept moist and active by bathing in tepid water, or with tepid water 
 to which a little alcohol has been added. 
 
 In bathing the sick, one rule should be rigidly enforced. After 
 sponging a portion of the body, the nurse should rub the skin of that 
 part perfectly dry with the bare hands before another portion is 
 bathed. There is nothing more uncomfortable than to be left wet 
 and clammy. On the other hand, nothing is more refreshing and 
 soothing to a patient than such a bath, provided the skin is dried 
 in the way here suggested. The skin is also rendered more active — 
 one great object to be attained. 
 
 Diaphoretics may also be used to advantage; jaborandi, or its 
 alkaloids, standing first upon the list for promptness and certainty ; 
 but in these severe forms of disease its use would be contra-indicated, 
 as it is sometimes said to be depressing in its effects. The liquor 
 ammoni acetatis, or spiritus aetheris nitrosi, may be found serviceable 
 in keeping up free activity on the part of the skin. 
 
 Alcohol, which is often called for in these febrile diseases, acts as a 
 diaphoretic and diuretic ; it also retards oxidation, thus being of ser- 
 vice in three ways. 
 
 The bowels should be acted upon as freely as the pre-existing con- 
 dition will admit. In typhoid fever, little can be accomplished in this 
 direction; excepting in this fever, yellow fever, and cholera, they 
 should be moved at least once every day. 
 
 Treatment referable to the kidneys is of the greatest importance. 
 The main object is to increase the watery constituents to the maxi- 
 mum, so that the effete material necessarily passing through the 
 renal protoplasm shall be diluted as much as possible. 
 
 To accomplish this object, large draughts of water, demulcent 
 
ACUTE PARENCHYMATOUS METAMORPHOSIS. 25 
 
 drinks, and various mild mineral waters should be freely adminis- 
 tered. 
 
 As medicinal diuretics, tinctura ferri chloridi, digitalis and its 
 preparations, are the only ones to be used. The tincture of iron is 
 an invaluable remedy, acting as a non-irritating diuretic, and enabling 
 the blood to carry more oxygen, thus aiding in bringing about a more 
 perfect tissue metamorphosis. It is most serviceable as the disease 
 advances, and tends to assume a more persistent form. 
 
 Digitalis and its preparations as diuretics are serviceable remedies 
 during the early stages of this lesion. They are non-irritating, 
 and act principally by contracting the arterioles and increasing the 
 general blood-pressure; in this way increasing the pressure upon the 
 glomeruli. They probably have less effect upon the renal arterioles 
 than on the rest of the circulatory system, otherwise they would 
 diminish instead of increase the flow of urine. Further investigation 
 will probably show that they only act when there is venous congestion 
 of the intertubular plexus of veins. Some have advanced the idea that 
 this drug has a specific, and as yet unexplained, action directly upon 
 the kidneys, especially upon the Malpighian tufts. The condition of 
 the intertubular plexus may be the cause of the so-called specific 
 effect. 
 
 The potassium salts are contra-indicated as diuretics, as they 
 depress the heart's action and relax the arterioles. Their action as 
 diuretics is ascribed to their power to increase oxidation and tissue 
 metamorphosis, and in this way force more work upon the renal 
 epithelial cells. They are therefore injurious for three reasons r 
 First, they weaken the heart ; second, they relax the whole arterial 
 system ; and, third, they increase the effete material to be thrown 
 off by the epithelial protoplasm. 
 
 When opiates are used as nerve-sedatives, in this form of renal 
 lesion, a fatal termination often results, if it is not the rule. In 
 some forms of acute urasmia, morphine, hypodermatically adminis- 
 tered, may be efficacious, but is not considered safe. 
 
 The application of dry cups to the loins, followed by warm poul- 
 tices, will be found very serviceable, especially if the renal symptoms 
 become at all severe. 
 
 The functional derangement of the liver, with its inability to pro- 
 duce a sufficient quantity and quality of bile to prevent the de- 
 composition in the alimentary tract, and assist in perfecting the 
 intestinal and hepatic digestion, requires a word in connection with 
 the treatment. 
 
 Recent experiments go to show that all infectious diseases produce 
 
26 At TTK PARENCHYMATOUS METAMOBPHOSIS. 
 
 as tlieir first effect a disturbance in the bile-producing power of the 
 
 liver. 
 
 With this condition the intestinal and hepatic digestion is very im- 
 perfectly performed and its products are quite incomplete and irritat- 
 ing, which, together with the constantly absorbed decomposing ma- 
 terials from the intestine, are the chief causes of the increased bodily 
 heat, and of the overworking of the kidneys. 
 
 This condition may be overcome in a large measure by using the 
 pure or inspissated ox bile, either alone or in combination, as in the 
 following formula : 
 
 I£ Fellis Bovis Inspissati, . . 3 ss. 3.7 grams. 
 
 Quinina? Sulphatis, ... gr. xv. 0.9 grams. 
 
 Extract] Taraxaci, . . . 3 ss. 3.7 grams. 
 
 M. et fiat massa las in capsulas no. xv. dividenda. 
 
 Sig. One ter in die, or every three hours, as the case may require. 
 
 The ordinary pure ox bile may be given in drachm doses, or the in- 
 spissated in doses of two or three grains. 
 
 By either method, the decomposition going on in the intestinal 
 tract is overcome, and digestion, absorption, and assimilation become 
 more perfect, while the liver is supplied with new bile with which to 
 do its work. 
 
 As a result the temperature falls, the products of tissue metamor- 
 phosis to be eliminated are diminished in quantity and rendered 
 more perfect and less irritating to the excretory organs; consequently 
 the work to be accomplished by the renal epithelium is decreased 
 and it is enabled to maintain its integrity and repair the damage it 
 has received. 
 
CHAPTER III. 
 
 CHRONIC PARENCHYMATOUS METAMORPHOSIS OF THE KIDNEYS. 
 PARENCHYMATOUS METAMORPHOSIS OF THE KIDNEYS ASSOCI- 
 ATED WITH PREGNANCY. PARENCHYMATOUS INFILTRATION 
 OF THE KIDNEYS ASSOCIATED WITH WASTING DISEASE. 
 
 Ohkonic Parenchymatous Metamokphosis of the Kidneys. 
 
 first form of large white kidneys. 
 
 Definition. — Chronic parenchymatous metamorphosis of the kidneys 
 is a transformation in which the irritation of the epithelial cells 
 lining the uriniferous tubules has continued for a considerable 
 length of time, and caused a progressive granular and fatty change. 
 The slight alteration in the intertubular tissue is cedematous in 
 character and not inflammatory. 
 
 Etiology. — A large number of the cases appear to result from 
 a previous acute attack which has passed without being recognized, 
 and it is often associated with cirrhosis of the liver and with all forms 
 of chronic hepatic disease which disturb the functions of the liver 
 so that the transformed proteids are less perfectly formed and pro- 
 duced in abnormally large quantities. As a result of this condition, 
 the kidneys attempt to rid the system of the effete material, and 
 the substances which have now to be eliminated by the special renal 
 epithelial cells are not only more abundant, but unduly irritating. 
 For a time, however, the kidneys may succeed in performing this 
 extra work, much of which should have been accomplished by the 
 liver, without suffering any material change, but, ultimately, the 
 cells give way and the abnormal condition is fully established. 
 
 In connection with acute diseases there is a similar transformation, 
 only of a more acute nature, which results in an arrest of the meta- 
 morphosis, and a restoration of the renal cells to a fairly normal 
 condition upon the removal of the cause, that is to say, upon recovery 
 from the condition which gave rise to the morbid phenomeua. The 
 kidneys, however, remain somewhat damaged and consequently more 
 susceptible to a second attack, or later on in life to a spontaneous de- 
 
28 CHRONIC PARENCHYMATOUS METAMORPHOSIS. 
 
 velopment, as it were, of this metamorphotic change, which then 
 assumes a chronic type. It is in this way that many of the chronic 
 cases have their origin. 
 
 Bepeated attacks of acute diseases, witli their accompanying changes 
 in the overworked renal organs, must in time impair the renal cells 
 to such an extent as to place them beyond hope of repair. These 
 attacks decidedly damage the excretory function of the glands, aud 
 as a person advances in years this form of chronic renal lesion is more 
 likely to be developed. These mild, but many times repeated and 
 often unnoticed attacks of acute metamorphosis are the most potent 
 predisposing causes for all forms of chronic nephritic diseases com- 
 monly classed as Bright's. 
 
 Until this fact is more fully appreciated, and the renal cells more 
 carefully guarded, when subjected to such extra strains, chronic 
 renal lesions will remain common. 
 
 By carefully considering the way in which these lesions originate, 
 most of the so-called idiopathic cases can be traced to some definite 
 origin. Overcrowding patients with food and stimulants beyond 
 the capacity of the liver undoubtedly is a very common cause of this 
 chronic type. In the early stage of either form, if the cause can be 
 removed, it would seem reasonable to suppose that here, as elsewhere 
 in the body, the epithelial cells would proliferate and fill up the 
 gaps left by those that have already fallen from their places. 
 
 In many instances this is the case, especially in the acute variety; 
 but in some, another influence appears in the form of an unob- 
 served irritant, which, by being continually applied to already 
 weakened cells, prevents their complete regeneration and causes a 
 subacute which finally develops into the chronic condition. Be- 
 fore the attack of the originating disease, the epithelial cells 
 of the kidneys have no difficulty in removing from the circulation 
 those effete materials which it is their function to excrete ; but 
 the acute attack of parenchymatous metamorphosis lessens their 
 number and quality to a very great extent, so that even where the 
 general system has returned to its original state, the remaining cells, 
 already in a damaged condition, are called upon to perform the work 
 which was previously accomplished by a much larger number. An 
 important question now arises: will this small number of weak cells 
 be capable of removing the products of normal tissue change which 
 are circulating in the blood, and at the same time regain their own 
 normal condition ? If so, they will proliferate and renew the epithe- 
 lial lining of the tubules, and the kidney will be restored to a perfect 
 physiological state; if not, they will tend to undergo further retrograde 
 
CHRONIC PARENCHYMATOUS METAMORPHOSIS. 29 
 
 chauge, and as healthy tissue cannot be built from unhealthy, no new 
 cells capable of performing the functions of the old will be produced, 
 and the remaining corpuscles will be more and more transformed. 
 These in turn finally degenerate, drop from their places, and leave the 
 kidneys wholly unable to perform their task, even though they are 
 aided in every way possible, by increased action of the skin and bowels. 
 In continued and often repeated exposure to cold, and in fail- 
 ure in the functional activity of the liver, the effete material in 
 the circulation is considerably increased and less completely trans- 
 formed, although not to so great an extent as to produce an acute 
 parenchymatous change in the kidneys, but still sufficient to bring 
 about a subacute condition; and, now, if the over-worked cells are 
 not quickly relieved from this extra strain, they undergo the fur- 
 ther retrograde change, and the patient eventually succumbs. 
 
 Renal lesions dependent upon the excessive use of alcohol as their 
 etiological factor are produced in like manner, instead of depending 
 for their cause upon any direct irritation of the renal tissue per se, 
 and when the trouble dates from the ingestion of a metallic poison, 
 it takes first the acute and subsequently the chronic form. 
 
 Pathological Anatomy. — The kidneys are always enlarged, and their 
 capsules are normal in thickness, and non-adherent to the underlying 
 renal tissue, wh'.ch is usually smooth after enucleation. If the disease 
 has been of considerable duration, there may be some slight adhesion of 
 the capsule to the gland. The cut surface may show the cortex and 
 medullary portion to be paler than normal, but to a trained eye both 
 have a granular and fatty appearance. The cortex is several times 
 thicker than usual, the markings are straight, and the Malpighian 
 pyramids distinct. In the gross anatomy, these markings are very 
 diagnostic points. If they run perfectly straight from the base of the 
 pyramids to the surface of the kidneys, they indicate that whatever 
 change exists is almost exclusively confined to the epithelium; but 
 when they are found to be wavy or tortuous in their course, they indi- 
 cate that there is also an interstitial change. It is the development 
 and irregular contraction of the newly-formed connective tissue 
 that causes this wavy appearance, which is found in the chronic, 
 diffuse, and sclerotic, but not in the parenchymatous forms of kidney 
 lesion. 
 
 Microscopic Examinations. — When thin sections are examined, the 
 epithelial cells are seen to be swollen, and to have undergone an ex- 
 tensive granular and fatty metamorphosis; and in aggravated cases of 
 long duration, there is a slight thickening of the interstitial tissue 
 and of Bowman's capsule, which has the appearance of being oedema- 
 
30 
 
 CHRONIC PARENCHYMATOUS METAMORPHOSIS. 
 
 tous rather than a true inflammatory proliferation. Some sections 
 will show the tubules partly filled with desquamated epithelial cells 
 and easts. Some observers, from the slight adhesion of the capsule 
 and apparent swelling of the intertubular tissue might be inclined to 
 class this as a diffuse nephritis, but as the primary and principal 
 lesion is in the epithelial cells, while the interstitial change is slight, 
 secondary, and not inflammatory, it should be regarded as only a 
 parenchymatous metamorphosis, for the causation, pathological ana- 
 tomy, and symptoms are decidedly different from those of chronic, 
 diffuse, and inflammatory lesions of the kidney. In some, if not 
 
 m 
 
 
 mm sp$& 
 
 life 
 
 Fig. 12.— Chronic Parenchymatous.Metajiorphosis of the Kidney. X350. 
 o, Tubules showing epithelial cell in a state of granular transformation and desquamation; 6, 
 tubule showing less marked change ; d, cedematousjntertubular tissue. 
 
 in all, the epithelial cells lining the uriniferous tubules undergo, 
 so to speak, a peripheral molecular death or solution of continuity, 
 analogous to ulceration in the soft parts. The irritating pigment par- 
 ticles and granules from the degenerating epithelium become attached 
 to or imbedded in the hyaline substance which is poured into the 
 lumen of the tubules, and forms the basis for casts. By the amount 
 and size of the granules, the different grades of casts are formed. 
 The most frequent way in which granular casts are formed is by the 
 degeneration, desquamation, and attachment of such cells to this 
 
CHRONIC PARENCHYMATOUS METAMORPHOSIS. 31 
 
 hyaline plug. A close examination of a hyaline cast which appears a 
 little granular will almost always show upon its surface the faint out- 
 lines of what was once epithelial cells. Some believe that this hya- 
 line substance undergoes disintegration, but, as it is generally re- 
 garded as fibrinous in nature, this seems impossible. In other cases, 
 the epithelial cells desquamate in the various stages, and become ag- 
 glutinated together, thus forming casts without the intervention of 
 the hyaline plug. The majority, however, are produced in the 
 former way. 
 
 Symptoms. — The early clinical manifestations of this disease are 
 not well marked, and the lesion has usually existed for some time be- 
 fore it is discovered. The first symptoms to attract the patient's 
 attention are headache, loss of appetite, nausea, and occasional vomit- 
 ing. These, however, are not persistent, but come and go from time 
 to time. There is a diminution in the quantity of urine passed, which 
 may attract attention. (Edema next appears, and is a very marked 
 and constant symptom, commencing first either in the subcutaneous 
 areolar tissue in and around the inferior eyelids, or about the feet 
 and ankles, but usually in the former situation. The areolar tissue 
 of the limbs, and especially of the legs, is soon filled with serum; the 
 scrotum becomes dropsical, so also the peritoneal and pleural cavities, 
 the face has a pale and puffy look, health and strength rapidly de- 
 cline, and, upon slight exertion, the patients feel completely ex- 
 hausted. 
 
 The blood undergoes a change, becoming thin and watery, which 
 causes the skin to assume a peculiar pale, waxy, translucent hue, 
 characteristic of renal lesions. 
 
 These symptoms continue for several weeks, or even months, and 
 may be continuous or intermittent in character. After a time, the 
 dropsy increases so as to interfere greatly with respiration, the dysp- 
 noea being very marked, on account of the diminished chest space, 
 and the interference with a free expansion of the lung, by the effusion 
 into the pleural cavity, and the crowding up of the diaphragm by 
 the fluid in the peritoneal sac. The dyspnoea may also be due in 
 part to an incomplete oxidation of the blood, owing to its watery 
 condition, and in part to the cerebral irritation brought about 
 by the action of the effete materials retained and circulating in the 
 blood. Occasionally there is dimness of vision, which is generally 
 cerebral in origin, and not due to any lesion of the optic nerves or 
 retinas. This lesion is not a marked or common complication. As 
 the disease proceeds, frequent attacks of nausea and vomiting occur. 
 The cerebral symptoms are not very prominent until towards the last, 
 
22 CHR0NTC PARENCHYMATOUS METAMORPHOSIS. 
 
 when what headache there may have been gives place to drowsi- 
 ness or stupor, partial loss of memory, followed by a low muttering 
 delirium, rise in temperature, dry skin, muscular twitchings, convul- 
 sions, and a urinous odor emitted from the body, followed by con- 
 traction of the pupils, coma, and death from uraemia. 
 
 Other cases seem to die from simple exhaustion without any of the 
 active symptoms of ursemic poisoning. A sudden effusion of serum 
 into the pericardial sac may cause paralysis of the heart, and act as 
 the immediate cause of death. 
 
 Urinary Examination. — In this lesion, the daily quantity of urine 
 passed is diminished, varying from ten to thirty ounces; its color is 
 darker than and its specific gravity above the normal, ranging between 
 1.018 and 1.030, and the quantity of albumin varies, but is usually 
 abundant. 
 
 Jficroscojn'cal Examination. — Casts are very numerous, and of the 
 large hyaline, coarsely granular, and fatty varieties, the two latter 
 predominating. There is a large quantity of debris in the field, 
 which is cast matter, or degenerated and desquamated epithelial cells. 
 A few red blood-corpuscles and leucocytes are usually present, but no 
 blood casts are found. Renal, bladder, and vaginal epithelial cells 
 will be found in some of the specimens. 
 
 Diagnosis. — This is readily made by remembering the cause and the 
 general symptoms, taken together with the urinary analysis. The 
 small quantity of urine passed daily, the high specific gravity, the 
 abundance of albumin, aud the great number of large hyaline, gran- 
 ular and fatty casts and cast debris are diagnostic. It is only by a 
 thorough microscopic analysis of the urine that anything like accu- 
 racy in diagnosis can be attained in this or any other form of renal 
 disease. 
 
 There is no other kidney lesion for which this form could be mis- 
 taken, if the above facts are carefully remembered and applied. A 
 positive diagnosis should never be attempted, however, until several 
 samples of urine have been carefully analyzed. 
 
 This variety, as a separate and distinct lesion, is quite common, but 
 it has been often confounded with the chronic diffuse variety. The 
 fibres of the tissue are swollen, boggy, but not studded with inflamma- 
 tory corpuscles. 
 
 From the method of production, the character of the lesion, and 
 the distinctiveness of the clinical and urinary symptoms, all of which 
 differ from those in chonic diffuse nephritis, it should be regarded as 
 a chronic parenchymatous metamorphosis, and not as a diffuse neph- 
 ritis. 
 
CHRONIC PARENCHYMATOUS METAMORPHOSIS. 66 
 
 Prognosis. — The duration is variable, it may last only a few weeks, 
 or it may exist for several months; possibly for one or two years, but 
 the longer duration is extremely doubtful. If the disease is recog- 
 nized and accurately diagnosticated at first, there may, with proper 
 treatment, be some prospect of a favorable result, but the majority of 
 cases even then will terminate in an early death. It seldom happens 
 that a patient completely recovers; an apparent recovery may result, 
 and all the symptoms disappear for a time, but they are almost certain 
 to return and finally to cause a fatal termination. One attack pre- 
 disposes to another, and if once confined to bed, there need be little 
 thought of recovery. Strictly speaking, this lesion is neither rapid 
 nor slow in its progress, but when we carefully consider its etiology, its 
 fatality is easily undertood. 
 
 Treatment. — This is governed by the same laws as in the acute 
 form. The primary effort should be to remove the cause/ This 
 can be accomplished in a great measure by preventing the develop- 
 ment of the acute form, by a guarded use, or better still, a total ab- 
 stinence from alcoholic beverages, and a scrupulous avoidance of all 
 agents which are damaging to the hepatic function. The only reason 
 why the damage is not developed sooner by alcohol may be explained 
 by the marked diminution in oxidation attributable to the alcohol, 
 and also the large amount of fluid usually taken in conjunction with 
 it, which, being eliminated by the kidneys, relieves to some extent the 
 strain upon these glands. But for these conditions its action would 
 be more damaging. Exposure to sudden changes in temperature 
 should be carefully guarded against. 
 
 Unfortunately, most of the circumstances which tend to produce 
 this lesion are to a considerable extent beyond the control of the phy- 
 sician, who is generally called to deal with the fully established lesion, 
 and about all he can hope to accomplish is to stay the progress of the 
 disease, and to ward off the fatal issue as long as possible. 
 
 All through the course of the disease, the diet should be carefully 
 regulated. 
 
 Believing that this lesion is produced by overwork, possibly asso- 
 ciated, as some have suggested, with a deficient eliminating power 
 on the part of the skin and alimentary tract, the first object should 
 be to see that the food is easily digested, absorbed, and assimilated, 
 and to recommend that which will ultimately give the smallest 
 and most completely formed excretory products. By so doing we re- 
 move the strain upon the renal epithelial cells to a considerable ex- 
 tent. A milk diet, or one limited to skim milk alone, when it can be 
 borne, ranks first upon the dietary list. The only therapeutic value 
 3 
 
34 CHRONIC PARENCHYMATOUS METAMORPHOSIS. 
 
 which can be attributed to milk is its diuretic property. Food of all 
 kinds should be limited to plain nutritious substances, not highly sea- 
 soned. Some advise a diminution in meats or a complete abstinence 
 from them.' 
 
 All kinds of food should be taken with moderation; great care 
 being exercised not to over-eat. Experience teaches that fats and 
 starches are more deleterious than the purely albuminous articles. 
 The system may be sufficiently strong to digest and improve upon a 
 purely nitrogenous diet, but the addition of the non-nitrogenous 
 articles interferes with perfect digestion. The latter being more easily 
 assimilated, tire out the system and render it incapable of digesting 
 the proteids which are to follow, and the usefulness of both is thus 
 impaired. It appears to be in this way that the harm comes from a 
 mixed diet. 
 
 The taking of more food than the system absolutely requires must 
 of necessity act as an irritant, and, in a lesion like this, renders the 
 condition much worse. All forms of rich and greasy food and pastry 
 should be absolutely withheld. 
 
 In regard to the curative efficacy of tonics, there is much diversity 
 of opinion. There can be little doubt, however, that they are of value 
 in so far as they tend to improve the digestive and assimilative pro- 
 cesses, and render the tissue metamorphosis more complete and less 
 irritating. The tincture of the chloride of iron stands first, from 
 its action both as a diuretic; and a carrier of oxygen. An almost 
 innumerable list of drugs and mineral waters have been extolled 
 for their curative properties, but there has been no one remedy 
 or series of remedies discovered as yet, whose curative action can be 
 looked upon with any degree of certainty. It is hardly to be expected 
 that any single remedy will be found that will be capable of removing 
 the causes and at the same time of repairing the damage already done 
 to the tissues. No specific virus can be found that will prove antido- 
 tal to these causes. The great object naturally is to reduce as far as 
 possible the intensity of the irritation which the renal epithelial cells 
 are continually suffering. If the cause cannot be completely over- 
 come, the skin and bowels should be kept active, the liver free from 
 over-pressure, and the nutrition as abundant and as perfect as the 
 demands of the system require. In this way the best conditions for 
 recovery are instituted and sustained, and nature has an opportunity 
 to repair the damage inflicted. 
 
 An exclusively " diaphoretic treatment," as it has been called, or 
 one limited solely to the alimentary tract, should be avoided and con- 
 
CHRONIC PARENCHYMATOUS MKTA MOI; IMIOSIS. ■>'.> 
 
 demned; but by aiding all the excretory organs in every known way, 
 their work will be accomplished in the shortest space of time, and 
 with the least strain. This should be the main object, because it 
 gives the longest interval of repose, and allows more time for re- 
 pair. 
 
 The three things to be guarded against particularly are, the accumu- 
 lation of effete products in the blood, their deleterious effects upon 
 the system, and uraemia. 
 
 Diaphoretics. — These agents are of great service, with jaborandi 
 and its alkaloids standing first. In regard to this medicinal agent, 
 much has been said pro et con., and in lesions of this type it has been 
 used with varying doses, some claiming that it has a depressing, 
 others that it has a stimulating influence upon the heart, but the 
 truth is that in small quantities it appears to depress, and in large 
 doses to stimulate that organ. From observation in many of the 
 cases upon which this chapter is based, only one conclusion can be 
 deduced, namely, that in most instances the quantity administered is 
 too small. The dose, as commonly given in most of the works on 
 therapeutics, is from one-fifth to one-half a grain of pilocarpine. In 
 all the cases from which these conclusions are formulated, the drug 
 was always given by subcutaneous injection, and the smallest amount 
 ever administered was half a grain of the muriate of pilocarpine. 
 This preparation is preferable to the nitrate or sulphate, and with 
 this dose the effects were not very marked; but when the quantity 
 was raised to two-thirds or three-fourths of a grain, the most desirable 
 results were obtained. 
 
 In one case, where the patient was suffering from very severe and 
 rapidly recurring urasmic convulsions, and was almost " water-logged," 
 two grains of the muriate of pilocarpine were hypodermatically injected, 
 followed at a short interval by another grain administered in the same 
 wa} 7 . The result was more than could be expected from any human 
 agency. At the time the urine was nearly suppressed, and for weeks 
 before, there had been a diminished quantity, heavily loaded with 
 albumin and containing large numbers of casts. 
 
 The convulsions and coma gradually wore away, the oedema par- 
 tially disappeared, and consciousness returned, so that for eleven 
 days the patient was fairly comfortable. On the twelfth day she 
 died from exhaustion, ivithout a recurrence of the convulsions. The 
 patient had repeatedly taken three-quarters of a grain without any 
 ill effects. When under the influence of the pilocarpine, both 
 ammonia and alcohol were given freely, as both pleural sacs and the 
 pericardium contained fluid. 
 
3<» CHRONIC PARENCHYMATOUS METAMORPHOSIS. 
 
 A patient who was treated in this way, first at the college clinic, 
 and later at his home, by one of the assistants, after being put under 
 the influence of three-quarters of a grain, exclaimed, " Doctor, 
 this is paradise ! " thus conveying a vivid impression of the relief he 
 had obtained. 
 
 In many instances the pilocarpine is substituted after elaterium, 
 croton oil, etc., have failed and before the system has recovered from 
 their effects. Under such circumstances, when reaction commences, 
 a depressing effect must be expected. 
 
 Continued observation has failed to reveal any case where there was 
 evidence of a depressing effect from the use of this drug, but owing 
 to the fact that the opposite has been reported, it is always well to 
 give some ammonia or alcohol, or both, in advance of the pilocarpine. 
 
 The hot-air bath may be resorted to, but as a rule it is more 
 depressing than pilocarpine. If the patient be able to sit up, a 
 blanket may be thrown around the body and chair in which he is 
 sittiug, and a tripod holding a dish of water, under which a lighted 
 alcohol lamp is placed, may be put under the chair. In case the 
 patient is confined to bed, a frame may be placed over the bod} 7 , and 
 by means of a tin tube, curved so as to project underneath the bed 
 clothing, the space around the body may be heated, by an alcohol 
 lamp placed in the tube, near its lower extremity. The air in this 
 case can be moistened by the use of an evaporating dish. Moist air 
 is less depressing than dry. 
 
 Diuretics. — Here, as in the acute variety, the only safe diu- 
 retics are, the tincture of the chloride of iron, digitalis, and 
 caffeine. The digitalis acts by contracting the arterioles throughout 
 the body, in this way increasing the blood-pressure upon the coil of 
 vessels constituting the glomeruli; it also acts as a powerful diuretic 
 only when there is congestion of the intertubular plexus, obstructing 
 the escajDe of blood from the glomeruli. 
 
 The combined diuretic action of digitalis, caffeine, and strychnine, in 
 pill form, will often be found serviceable; each pill should contain 
 three grains of caffeine, one grain of powdered digitalis leaves, and 
 one-twentieth of a grain of strychnine. The potassium salts should 
 never be used, for the reasons mentioned on page 25, 
 
 The application of dry cups to the loins, followed by warm poul- 
 tices, will be found useful, and often will increase the diuretic effect 
 of the digitalis. 
 
 A free use of mineral waters, by increasing the amount of water to 
 be eliminated, keeps the tubules well washed out and free from casts 
 and debris. 
 
CHRONIC PARENCHYMATOUS METAMORPHOSIS. 37 
 
 Ordinary coffee will also act as a diuretic, both, from the bulk of 
 fluid and the contained caffeine, and it also tends, like caffeine, to 
 lessen tissue waste and to stimulate cardiac contraction. 
 
 Caffeine has been recommended alone, as a diuretic in renal as 
 well as in cardiac dropsy, but from the general impression that it 
 will produce severe cerebral symptoms it has not come into general 
 use. The above pill acts well, and does not produce any undue cere- 
 bral excitement. Caffeine should never be used in conjunction with 
 pilocarpine, as the most alarming, if not fatal, symptoms are likely to 
 occur. 
 
 Cathartics are sometimes called for, especially if there is a tend- 
 ency to ursemic symptoms with excessive and persistent cedema. The 
 most efficacious cathartic is elaterium in small and repeated doses. 
 If the oedema of the lower extremities is excessive and troublesome, 
 and does not yield to ordinary treatment, it may in some cases be de- 
 sirable to incise the integument, and also administer diuretics in mod- 
 eration. Several small incisions, one-half to one inch in length, 
 should be made around each ankle and warm fomentations should then 
 be applied, or the limb soaked in warm water. Some advise numer- 
 ous small punctures instead of the longer incision, but the former is 
 generally considered the better method. The objection to this is that 
 occasionally an erythematous inflammation is developed, which, in 
 some cases, is only an erythema, but occasionally it develops into a 
 true erysipelatous inflammation which often terminates in extensive 
 sloughing or gangrene. After the dropsy has been overcome in this 
 way, it can be easily controlled by well-directed methods. 
 
 Another very reliable method of removing the dropsy of the ex- 
 tremities is by the use of Esmarch'* bandage. If at night the limb 
 be firmly bandaged with the rubber roller, the water will be driven up 
 toward the trunk and the pressure in the abdominal vessels will be 
 greatly increased. Having accomplished this, the oedema can be made 
 to rapidly disappear, by the free use of hydragogue cathartics and diu- 
 retics. By repeating this for several nights, excessive and trou- 
 blesome oedema, which has resisted all other lines of treatment, can. 
 be overcome and held in check for a long time. Ten grains each of 
 calomel and jalap is the best cathartic at this time, or the compound 
 jalap powder. 
 
chronic parenchymatous metamorphosis. 
 
 Parenchymatous Metamorphosis of Pregnancy. 
 - second form of large white kidney. 
 
 Etiology. — During pregnancy, the kidneys are liable to undergo 
 metamorphotic changes. Although histologically this lesion closely 
 resembles the last forms, it is classed as a separate lesion, from the fact 
 that its cause is definite, its treatment special, and that, with the 
 removal of the cause, the natural tendency is towards a spontaneous 
 recovery. At first it is similar to the acute parenchymatous metamor- 
 phosis, but later it becomes chronic. 
 
 It has for its cause the general nervous irritability incidental to the 
 pregnant state, which has a tendency to interrupt the physiological 
 metamorphosis and render its products imperfect and irritating to 
 the system and excretory organs. There is also increased work de- 
 manded of the renal glands, as they have to eliminate the effete products 
 of both mother and foetus. At the same time the nutrition of the renal 
 organs is impaired, first, by the general disturbance to the abdominal 
 circulation, and, later on in gestation, by direct pressure upon the 
 renal vessels. 
 
 Pathological Anatomy. — The kidneys are usually large than nor- 
 mal, never smaller; their capsules are non-adherent to the underlying 
 renal surface which is smooth. 
 
 The external and cut surface is pale, the whiteness of the cortical 
 substance being more marked than that of the pyramids which are 
 quite distinct. 
 
 Upon microscopic examination, the various degrees of retrograde 
 metamorphosis known as cloudy, mucoid, and finely granular or fatty 
 transformation are found, this depending upon the stage of the dis- 
 ease (see Fig. 11, p. 19). But as death occurs most frequently 
 during the latter months of pregnancy or after delivery, the changes 
 most commonly seen are those of the coarsely granular and fatty 
 metamorphosis, chiefly the former (see Fig. 12, page 30). The 
 fibrillated connective tissue and Bo\v;nan's capsule have a swollen and 
 cedematous appearance, which appears to partake more of a passive 
 than of an active or inflammatory nature. 
 
 This lesion is progressive from the acute to the chronic form. 
 
 Symptoms. — The disease may develop at any time during pregnancy, 
 but it usually makes its appearance during the latter months when 
 there is often great difficulty in ascertaining whether some of the symp- 
 toms are due to the pregnant condition, to the parenchymatous me- 
 tamorphosis, or to both. Occipitofrontal headache and oedema of 
 
CHRONIC PARENCHYMATOUS METAMORPHOSIS. 39 
 
 the eyelids may become quite marked, and dimness of vision is also 
 often present. (Edema of the feet, dyspnoea, and derangement of di- 
 gestion are almost always seen daring pregnancy, and, therefore, these 
 symptoms must not be too positively relied upon as symptoms of par- 
 enchymatous metamorphosis, as in other cases they would be. 
 
 As pregnancy and the disease advance, the quantity of urine voided 
 becomes much diminished and pale in color; it may even be suppressed; 
 the dimness of vision increases, and the patient becomes very restless; 
 these symptoms usually occur during the eighth or ninth months, but 
 they may appear earlier. 
 
 If the urine is examined at this time, its specific gravity will be 
 found to be a little above normal, albumin will be abundant, and the 
 color will be slightly deeper. But finally the specific gravity falls, and 
 the color of the urine is abnormally pale, resembling that of the 
 chronic diffuse forms. This is explained by the rapidly progressing 
 hydroaemic condition of the blood associated with pregnancy. 
 
 Upon microscopical examination, casts of all varieties, except bloody 
 are found; the size of the casts varying with the different stages of 
 the disease. A few red blood-corpuscles and leucocytes may be found 
 in some samples, but these usually come from various portions of the 
 genito-urinary tract and do not indicate a renal hemorrhage. The 
 symptoms of urasmic poisoning soon become quite marked, the patient 
 is very nervous and anxious, and may become almost delirious. 
 
 The pulse is rapid, compressible, and very weak. In some cases, 
 these symptoms may not progress further, but in others, if not re- 
 lieved, they are rapidly followed by convulsions and death. The con- 
 vulsions may not appear until excited by the pains of pregnancy, 
 when they make the labor doubly difficult and dangerous. 
 
 Prognosis. — Occurring at such a time, this disease should be 
 anxiously watched by the physician; for it may of itself produce 
 abortion or a premature expulsion of the foetus. If the convulsions 
 occur before or during labor, the patient's life is in great jeopardy 
 and the prognosis is serious, though not necessarily unfavorable. If 
 the convulsions do not come on until after labor has been accomplished, 
 the prognosis is much more favorable, for the cause of the disease has 
 been in a great measure removed; and if the patient can be relieved 
 from the immediate danger, she usually makes a rapid and perfect 
 recovery. When the disease is not so severe, and only some nervous- 
 ness and anxiety are present, together with only a moderate amount 
 of albumin and the urine not much diminished in daily quantity, the 
 prognosis is favorable, but the patient should be carefully watched. 
 
 This variety of renal lesion shows quite conclusively that the epithe- 
 
40 OHBOJMC PABENOHAMATOU8 METAMOBPHOSIS. 
 
 lial colls of the kidneys can and do undergo a marked degree of retro- 
 grade change, afterwhich they may be restored to their normal con- 
 dition. The essential thing, however. Is a Bpeedy removal of the 
 irritating agent. 
 
 Treatment. — Owing to the condition of the patient, the treatment 
 for this disease cannot be so active as in other eases of renal disease. 
 
 As soon as the kidney complication is discovered, mild hydra- 
 gogue cathartics, such as jalap and calomel in doses of ten grains each, 
 must be given as often a.- is necessary to keep the bowels freely 
 open: dry cups, sinapisms, or hot poultices should he applied over 
 the loins, together with the internal administration of the infusion of 
 digitalis 3 ss. (1.85 grams) ter in die. This will often improve 
 the condition of the kidneys by lessening the congestion and by 
 increasing the amount of urine excreted. In using the cathartics, 
 great care should be exercised not to produce uterine irritation and 
 premature delivery. 
 
 The action of the skin may be promoted by the vapor-bath, hot 
 wet packs, and diaphoretic medicines, as jaborandi gr. xx. to xxx. 
 (1.29-1.94 grams) or by the following: 
 
 1$ Liquor. Ammonii Acetatis 3 iss. 
 
 Spiritus J3theris Nitrosi 3 vi. 
 
 Tincturae Fern Chloridi 3 ss. 
 
 Aqua?, ' q. s. ad 3 vi. 
 
 M. Sig. One-half ounce every three hours in a wineglass of water. 
 
 The potassium salts should always be avoided, for the reasons given 
 when speaking of the acute parenchymatous metamorphosis, page ".'■">. 
 
 The food should be carefully regulated, and all indigestible sub- 
 stances stricken from the dietary. 
 
 If the patient be anaemic, iron should be given. In plethoric pa- 
 tients, venesection should be performed, and even in anaemic patients, 
 if the physician thinks convulsions probable, the operation will often 
 be followed by good, and seldom, if ever, by bad results. The amount 
 of blood to be drawn should not be more than sixteen ounces; usually 
 much less, but this depends entirely upon the patient's strength. If 
 none of the above methods be successful, premature delivery should be 
 induced. Should convulsions occur, bleeding is indicated as soon as 
 the fit is over, if it has not already been done. Morphine gr. ss. 
 (0.032 gram) may be injected hypodermatically and is followed by the 
 most pleasing results; chloral hydrate gr. xv. (0.9 gram) or bro- 
 mide of potassium gr. xxx. (1.9 grams), either alone or combined, 
 
CHRONIC PARENCHYMATOUS METAMORPHOSIS. 41 
 
 may be given by the mouth or rectum; the best results will be 
 obtained from their combined action. 
 
 Ether or chloroform may be given to prevent the return of the con- 
 vulsions, but at the same time it should be remembered that chloro- 
 form is not absolutely safe even here. The patient should be deliv- 
 ered immediately. The hot wet pack, even at this time, is of service 
 and does not interfere with delivery. 
 
 As a rule, pilocarpine has not been considered safe in this lesion, 
 but what has already been said on page 24 applies equally in this 
 condition. It will undoubtedly cause a rapid expulsion of the child, 
 which is apt to be still-born, but it will often save the life of the 
 mother. 
 
 The method of production being clearly understood, much can be 
 accomplished in the line of prevention and more active symptoms 
 obviated. The bowels should be kept free and the skin active. 
 Especial attention should be paid to the gastric, intestinal, and 
 hepatic digestion, that their functions may be as nearly normal 
 as possible ; in this way nutrition maybe kept at the highest standard 
 attainable, and the excretory products reduced to the minimum both 
 in quantity and irritability. 
 
 ' By accomplishing all this, the pregnant and puerperal state, which 
 otherwise might terminate in the death of both mother and child or, 
 to say the least, with alarming symptoms in the former and death of 
 the child, may be carried to a successful termination without ursemic 
 symptoms, and with the delivery of a strong and vigorous infant. 
 
 Parenchymatous Infiltration Metamorphosis of the Kidney 
 with Wasting Diseases. 
 
 third fokm of large white kidney. 
 
 Definition. — Chronic parenchymatous infiltration metamorphosis 
 is, more strictly speaking, a passive lesion similar to the fatty liver of 
 phthisis and other wasting diseases. In this form, the epithelial cells 
 become swollen and pale from the continued imbibition of fatty par- 
 ticles, which do not irritate the cell protoplasm sufficiently to prevent 
 the performance of its function. It is only classed among the renal 
 lesions on account of its gross appearances, being so nearly like those 
 of the more active type. 
 
 Etiology. — It occurs in connection with phthisis, carcinoma, and 
 all forms of wasting diseases or long-continued suppurative processes, 
 when one of the more active lesions is not established. But the exact 
 reasons for its development have not been clearly explained. 
 
42 
 
 CHRONIC PARENCHYMATOUS METAMORPHOSIS. 
 
 Pathological Anatomy. — The kidneys are much larger than normal, 
 weighing from five to eight ounces (141.747 to 226.796 grams) or 
 more. Their color is markedly pale, and their capsules are normal 
 and non-adherent to the underlying renal surface, which remains per- 
 fectly smooth after they have been removed. 
 
 The cut surface is fatty and almost white, the pyramids are in- 
 distinct. 
 
 
 
 ■'/ -At 
 
 ;^^^y}\ i \ : 
 
 
 W X 
 
 *mm 
 
 Fig. 13.— Chronic Parenchymatous Metamorphosis of Wasting Disease . X 350. 
 a, Tubules showing fatty infiltration of tha epithelial cells ; b, oedematous intertubular tissue. 
 
 Upon microscopic examination, the epithelial cells are found to be 
 swollen and filled with large fat droplets. The cells are seldom separated 
 from the basement-membrane, and consequently the lumen of the 
 tubule remains open. There is little or no change in Bowman's 
 capsule. 
 
 In chronic cases, there may be a slight increase in the interstitial 
 tissue, but even this is rare. 
 
CHRONIC PARENCHYMATOUS METAMORPHOHIS. 43 
 
 Symptoms. — Occasionally slight oedema of the eyelids and of the 
 extremities may be noticed, which would lead us to suspect the exist- 
 ence of some lesion of the kidneys; but further than this, no symptoms 
 except those referable to the inducing disease make their appearance. 
 
 The urinary analysis is practically negative. 
 
 Prognosis and Treatment. — The renal complication of the original 
 disease gives no trouble to the patient and is not to be feared by the 
 physician. The prognosis is, of course, unfavorable, but does not 
 depend upon the lesion of the kidneys, which would disappear should 
 the patient recover from the chronic and primary disease. 
 
 This lesion so closely resembles in its gross appearance the other 
 parenchymatous changes, and is so often found at the necropsy table, 
 that it has been deemed best to describe it with the other parenchy- 
 matous forms, but it should be remembered that its causation, mi- 
 nute anatomy, and clinical symptoms are absolutely different from 
 the other varieties. 
 
 The three lesions just described resemble each other very closely in 
 their macroscopic appearance, but each one has its special anatomical 
 and clinical feature which renders it quite distinctive and by which it 
 can be diagnosticated. 
 
 The first and second are practically identical both in their macro- 
 scopic and microscopic appearances, but the third differs in its minute 
 changes, and is, more strictly speaking, a functional disease, while 
 the other two are active and destructive lesions. 
 
 By having a clear conception of the pathological changes, and by 
 fully comprehending every step in the causation and method of pro- 
 duction, their treatment must of necessity be more intelligently 
 directed, enabling us often to anticipate, rather than to wait for 
 symptoms before applying our therapeutic agents. 
 
 In their macroscopic anatomy they are almost identical and cannot 
 readily be separated, but the variety associated with wasting diseases is 
 usually the palest of the three and the most fatty; this, however, is not 
 an invariable rule. Microscopically, in the third form the change in the 
 epithelial cells is found to be composed of an infiltration into the 
 protoplasm of well-defined oil droplets; in the other two the proto- 
 plasm of the cells has undergone a granular change, and the fat drop- 
 lets are very minute particles, indicating a more complete destruction 
 of the cell-mass. But by a careful study of the clinical history, they 
 are easily isolated. The first represents the highest type of destruc- 
 tion; the last, the lowest; and that form which is associated with 
 pregnancy holds the intermediate position. 
 
 Of the three, the intermediate form is the least fatal, the other two 
 
44 CHRONIC PARENCHYMATOUS METAMORPHOSIS. 
 
 standing about equal; the first producing death by itself, the last only 
 by the disease which causes its development. 
 
 In the first and the second, there is a true metamorphotic change, 
 but the last is passive, and simply imbibes fat droplets without de- 
 struction of the renal protoplasm; it is analogous to the fatty liver of 
 similar diseases. 
 
 They are all classed in this group because the change is primary 
 and chiefly located in the epithelial cells; and they are not inflamma- 
 tory in origin, but are due to overwork and impaired nutrition. The 
 last is classed here, not only for convenience, but also and especially 
 from its close external resemblance to the first and the second, and 
 the frequency with which it is met with at the necropsy table. At 
 the same time it should be remembered that the last variety is not an 
 essential lesion, and does not give rise to either rational or clinical 
 symptoms. 
 
CHAPTER IV. 
 
 ACUTE DIFFUSE NEPHRITIS. CHRONIC DIFFUSE NEPHRITIS, 
 FIRST, SECOND, AND THIRD FORMS. 
 
 ACUTE DIFFUSE NEPHEITIS. 
 
 Definition. — Acute diffuse nephritis is that variety in which the 
 intertubular tissue is infiltrated with new cells in addition to a 
 parenchymatous metamorphosis of the epithelial elements. 
 
 There is now every indication of a true inflammatory condition, for 
 there is a migration of the blood-corpuscles into the intertubular 
 tissue and an exudation of all the constituents of the blood into the 
 renal substance, most of which, however, escape from the glands with 
 the urine. 
 
 Etiology. — This lesion is chiefly met with as a sequela of acute 
 diseases, and is especially frequent after scarlatina. It is occasionally 
 developed in connection with severe burns, but it is more frequently 
 produced by sudden and severe exposure to cold; and as the result of 
 irritating diuretics, such as turpentine, cantharides, etc. 
 
 A very large percentage of the cases, however, occur as a complica- 
 tion to or as a sequela of scarlet fever, and when we add to this the 
 cases in connection with diphtheria, the disease becomes in its primary 
 origin almost exclusively one of childhood. 
 
 The cases following sudden exposure to cold or severe burns, and 
 as an exacerbation to a chronic nephritis, are more frequent in adult 
 life. 
 
 Many of the deaths which follow the acute diseases, especially 
 in children, are really due to this complication or sequela, and not to 
 the original disease itself. When this fact is fully appreciated and 
 guarded against, the mortality will decrease. 
 
 During the course of an acute disease of any kind, the renal epithe- 
 lial cells are called upon to perform an unusually large amount of 
 work, and at the same time their nutrition is decidedly impaired. 
 These cells may accomplish this task without a parenchymatous meta- 
 morphosis sufficiently advanced to give rise to clinical symptoms, but 
 they are, nevertheless, weakened, and any little exposure or careless- 
 
4.; 
 
 ACUTE DIFFUSE NEPHRITIS. 
 
 ness on the part oJ' the patient during convalescence, while the renal 
 cells are in this impaired condition, may suddenly interrupt the 
 normal process. An increased amount of work is thus thrown upon 
 these cells, which, in addition to reproducing the parenchymatous 
 metamorphosis, also establishes a true or diffuse inflammatory condi- 
 tion. For these reasons the greatest care should be exercised 
 in guarding the kidneys against these severe strains during the height 
 of the attack, and still more so against damage during convalescence. 
 By remembering these etiological factors, many an acute nephritic 
 
 Fig. .14— Acute Diffuse Nephrites. X 350 and reduced. 
 
 Case of Scarlatina, a, Swollen endothelium of the glomerulus; 6, proliferation of lining cells 
 of glomerulus: c, compressed vascular tuft; d, swollen stroma infiltrated with cells; c, dilated 
 convoluted tubules; g, swollen epithelium peeling off; h, hyaline cast. (Delafield and Prudden's 
 " Handbook of Pathological Anatomy and Histology.") 
 
 attack may be warded off; and in this way, if in no other, the patient 
 may be spared a chronic form of the disease later in life. 
 
 Pathological Anatomy. — The kidneys are usually very much en- 
 larged and sometimes weigh ten ounces (283.496 grams). In rare 
 instances, however, they are not much altered in size. In either 
 case their capsules are non-adherent to the underlying renal 
 substance, the surface of which is found to be smooth and dark 
 after enucleation. The stellar veins of Verheyen are distended 
 with blood, the cut surfaces are dark in color; the cortex and pyra- 
 
ACUTE DIFFUSE NEPHRITIS. 47 
 
 mids of Malpighi are congested and often the seat of ecchymotic 
 spots. Later in the disease the cortex is pale, and often cedematoiis, 
 contrasting strongly with the dark and congested pyramids. The 
 markings are straight and the Malpighian hodies unusually promi- 
 nent. 
 
 On microscopic examination, the epithelial cells are found in the 
 usual condition of parenchymatous metamorphosis, or granular 
 transformation of the cell protoplasm, and the intertubular tissue is 
 swollen, oedematous, and infiltrated with new cells. In the early 
 stage, the vessels are distended with blood, but later on this conges- 
 tion is less marked. There is now an apparent increase in the num- 
 ber of cells, or cell nuclei, covering the Malpighian tuft and lining 
 Bowman's capsule, which, in severe cases, causes a compression of 
 the tuft of vessels within the capsule. This infiltration of the Mal- 
 pighian tuft has been considered diagnostic of the renal lesion 
 which is a sequela to scarlet fever. This, however, does not hold 
 true, for the same condition is found where the nephritic lesion 
 has resulted from other causes. It, perhaps, is more likely to be 
 present on account of the greater severity of the disease in these 
 instances. 
 
 Small extravasations of blood into the glomeruli are often found. 
 Numerous leucocytes are found throughout the section, but not in 
 quantities sufficiently large to simulate a suppurative or pyelo- 
 nephritic condition. A marked difference can be seen between this 
 lesion and the parenchymatous metamorphosis which occurs dur- 
 ing the height of the attack. In the former, all the structures 
 are implicated, and there is every indication of an inflammatory 
 condition, while in the latter only the epithelial cells are involved 
 without any of the lesions common to inflammation, the change 
 being a granular metamorphosis from overwork and impaired nutri- 
 tion. 
 
 The symptoms depend largely upon the cause of the renal lesion, 
 and naturally vary with them. When the patient is attacked with 
 acute diffuse nephritis, and the cause is exposure to cold, or perhaps 
 cannot be discovered, there is usually an initial chill, followed by 
 fever, pain in the back and region of the bladder, difficult and fre- 
 quent micturition, and a very much diminished quantity of urine. 
 Such cases may be divided into groups according to severity. 
 
 a. In very acute cases, these symptoms are rapidly followed by 
 signs of ursemic poisoning, convulsions, coma, and death, which en- 
 sues in from twenty-four to thirty-six hours. 
 
48 ACUTE DIFFUSE NEPHRITIS. 
 
 b. In subacute cases, oedema of the inferior eyelids and feet appears 
 in a day or two after the invasion, followed by general anasarca, while 
 dropsy, abundant or otherwise, may make its a'ppearanoe. The 
 cephalic symptoms are those of the milder type of renal affections, 
 consisting chiefly of pain in the head, drowsiness, and stupid feelings, 
 but delirium rarely occurs. After a few days or weeks, the symp- 
 toms improve, and the patient is apparently cured, although some 
 albumin and a few casts may persist, and be found in the urine for 
 six months or a year. 
 
 c. In still other cases of a milder type, oedema 'and dropsy are the 
 first symptoms that present themselves. There may be some nausea, 
 slight pain in the back and in the region of the bladder, and dimness 
 of vision. These symptoms are followed after a short time by a waxy 
 pallor and a very anaemic condition, the nausea giving place to violent 
 and often persistent vomiting. The patient is much bloated from 
 the anasarca and dropsy, and may become "water-logged." Drowsi- 
 ness and stupor are often quite marked. In these cases, the sight may 
 be impaired from a retinitis, or inflammation of the optic nerve, but 
 more frequently from an imperfect nutritive condition of the optic 
 centres, or what is known as a central lesion. These symptoms, how- 
 ever, gradually disappear, although, as in the former class, the albu- 
 min and casts persist in the urine for a considerable time. 
 
 d. When the acute diffuse nephritis appears as a sequela to scarlet 
 fever, it usually develops on the fourteenth, the twentieth, the twenty- 
 first, or the twenty-second day; that is, from the second or third week 
 after the invasion. This is the time when desquamation is most 
 active, the skin very sensitive, and the patients restless from confine- 
 ment. They slip from a warm to a cold room, or a window is left 
 open, and the child is exposed to a sudden and cold current of air. 
 In this way, almost unnoticed, the surface is unexpectedly chilled, 
 the physiological processes at once interrupted, more work precipitated 
 upon the already weakened kidneys, and the nephritis set in motion, 
 suddenly, and apparently without cause, the increased temperature 
 returns; headache, drowsiness, and stupor make their appearance, 
 and the diagnostic waxy pallor of nephritic disease is developed. 
 There is myalgia, oedema of the face and extremities, followed shortly 
 by general and extensive anasarca, abundant dropsy of the large 
 cavities, and great dyspnoea. In the worst cases the urine is sup- 
 pressed, and convulsions, coma, and death rapidly ensue. 
 
 The urinary symptoms in all the above-described varieties are simi- 
 lar; they are always present, but vary somewhat with the severity of 
 the attack. The following is a synopsis of these symptoms in a typical 
 
ACUTE DIFFUSE NEPHRITIS. 49 
 
 case of acute diffuse nephritis. The urine is diminished in quantity, 
 sometimes suppressed, and dark, smoky or bloody in color, and 
 albumin is abundant. The specific gravity, although the fpaantity of 
 urine passed is small, instead of being high as is the case in the acute 
 parenchymatous form, ranges usually between 1.020 and 1.012. 
 
 Upon microscopic examination, it is found to contain red blood- 
 corpuscles, leucocytes, and epithelial cells; blood casts, small hyaline, 
 nucleated, epithelial, and finely granular casts, with a considerable 
 quantity of granular debris. 
 
 The large amount of blood-corpuscles, and the presence of a large 
 number of blood-casts, are the positive and diagnostic features of this 
 lesion. During recovery, the specific gravity of the urine may rise 
 above normal, and the albumin gradually diminish in quantity. 
 
 Diagnosis. — The only lesion with which it could be confounded is 
 the acute parenchymatous metamorphosis, but from which it is easily 
 differentiated when we remember that the parenchymatous lesion 
 occurs during the attack, while the diffuse nephritis occurs as a 
 sequela. The urine of the parenchymatous variety does not contain 
 blood or blood-casts, but they are abundant in the acute diffuse 
 nephritis, and it is the blood and blood-casts which stamp this lesion, 
 and which are the differential characteristics. 
 
 The prognosis depends entirely upon the severity of the renal dis- 
 ease, as well as the severity of the original attack, also upon a careful 
 study of the symptoms, an early recognition of the disease, and a 
 judicious method of treatment. If the attack be mild in its onset, 
 and the treatment be well directed, the prognosis is favorable; other- 
 wise the reverse will prove true. A very severe case at the onset, if 
 properly handled, may be subdued, and ultimately made to terminate 
 in recovery. 
 
 Those forms of disease which do not occur as a sequela, or compli- 
 cation of scarlet fever, or some of the other acute disorders, are 
 apt to become chronic, and eventually to prove fatal. Quite a num- 
 ber of the mild cases rightly treated will recover. With a clear 
 understanding of the methods of production, and a treatment based 
 upon it, an improved prognosis will result. 
 
 The treatment naturally falls into three headings, the preventive, 
 the management of the acute invasion, and that of the more chronic 
 stage. Under prevention, all that tends to ward off the development 
 of an acute parenchymatous metamorphosis should be vigorously 
 enforced. The skin and bowels should be kept acting freely, thus 
 relieving the strain upon the kidneys. Cold applications to the skin 
 4 
 
50 CHRONIC DIFFUSE NEPHRITIS. 
 
 should be avoided. Non-irritating diuretics should be freely admin- 
 istered, and the saline diuretics avoided. 
 
 During the invasion, when there is renal congestion and threatened 
 suppression of urine, dry cups applied to the loins, and frequently 
 repeated, will be found of service, or wet cups, not repeated, are often 
 very efficacious. Or hydrargyri chloridum mite, gr. ij. (0.1 
 gram), with opium gr. } (0.03 gram), may be given every two 
 hours, followed by castor oil. This plan of treatment is specially 
 indicated when the bowels are constipated. Jalap and calomel, five 
 to ten grains (0.3 to 0.6 gram) each, will be found of service. 
 Elaterium, however, in small and repeated doses, has been found 
 the most efficacious remedy in urasmic conditions, as it appears to re- 
 move from the system the urgemic poison more rapidly and effectually 
 than any other eliminating agent. It produces free and copious 
 watery discharges; keeps down the cedema; greatly relieves the strain 
 upon the kidneys; renders the patient quite comfortable, and is a 
 great aid in effecting a cure. Jaborandi, or its alkaloid pilocarpine, 
 may be used; if the latter, it is best employed hypodermatically, but 
 by some it is considered dangerous in this condition, on account of the 
 shock which it is supposed to give to the system. From observing its 
 action in large doses and in quite a large number of cases, only one 
 deduction is possible: that it is not depressing to any noticeable 
 degree, and is always followed by the most desirable results, both to 
 the physician and to the patient. Recorded observations, however, 
 are quite contradictory on this point, and its action should be care- 
 fully watched. Spiritus astheris nitrosi, digitalis and its preparations 
 may be used for their diuretic and diaphoretic properties; also large 
 draughts of water, demulcent drinks, and some of the mineral waters. 
 Hot-air baths at times may be used, and are often serviceable. 
 
 Digitalis and its preparations are the only safe remedies during this 
 acute stage. They are non-irritating diuretics, and act principally by 
 contracting the arterioles, and increasing the general blood pressure; 
 in this way increasing the pressure upon the glomeruli. They probably 
 have less effect upon the tension of the renal arterioles than on the rest 
 of the circulatory system, otherwise they would diminish instead of 
 increase the flow of urine. Further investigation will probably show 
 that digitalis only acts when there is a venous congestion of the inter- 
 tubular plexus of veins. Some have advanced the idea that this drug 
 has a specific and unexplained action directly upon the kidneys, 
 especially upon the Malpighian tuft. The increased general blood 
 pressure and the condition of the intertubular plexus explains the so- 
 called specific effect. 
 
CHRONIC DIFFUSE NICIMIRITIH. 51 
 
 The potassium salts, here as in acute parenchymatous metamor- 
 phosis of the kidney, are contra-indicated, page 25. 
 
 Opiates, whether admissible in adults or not, are decidedly contra- 
 indicated in nraemic attacks in children. 
 
 After the acuteness of the attack has passed off, and it tends to 
 assume the chronic form, the tinctura ferri chloridi in full doses 
 will be found a most reliable remedy. 
 
 The food should be of the best ; plain, easily digested, nutritious, 
 non-irritating, and such as will yield the least amount of effete 
 material. A simple milk or skim-milk diet often proves most satis- 
 factory. 
 
 During the convalescence, great care should be exercised in keeping 
 the bowels active. One free movement daily should be the rule. The 
 skin also should be kept active by sponging and friction. All expo- 
 sure to sudden changes in temperature and excesses in diet should be 
 scrupulously avoided. By a strict observance of the above rules, the 
 work to be performed by the kidneys is reduced to the minimum, while 
 their nutrition is increased to the maximum, and many cases are caused 
 to terminate in a complete recovery, which otherwise would run into 
 a chronic form of renal disease, and result in an untimely death. 
 
 In this lesion, the plan of treatment detailed on pages 25 and 26 
 will be found to give the most satisfactory results. 
 
 Chronic Diffuse Nephritis. 
 
 Introductory Remarks. — In this group of renal lesions, all the struc- 
 tures of the kidneys are involved. The epithelial cells undergo a 
 parenchymatous metamorphosis, and the intertubular tissue a cellular 
 infiltration and thickening. There are three distinct varieties: in one 
 the kidneys grow large from the major part of the lesion being 
 located in the epithelium; in the other two, the organs are diminished, 
 in size, in one with, and in the other without, a hyaline thickening 
 and expansion of the afferent vessel of the Malpighian coil. 
 
 Chronic Diffuse Nephritis. 
 
 first variety: fourth form of large white kidney. 
 
 Definition. — Chronic diffuse nephritis is an inflammation which 
 involves the interstitial tissue of the kidneys, associated with a 
 chronic parenchymatous metamorphosis of the epithelial cells lining 
 the uriniferous tubules, but which differs from the acute variety in 
 its duration, and in the extent of interstitial involvement. In this 
 peculiar variety, the disease spends its greatest force upon the paren- 
 
52 CHRONIC DIFFUSE NEPHRITIS. 
 
 chyma. It assumes somewhat the type known as chronic parenchy- 
 matous metamorphosis, but it has added to that, the interstitial diffi- 
 culty which now is of an inflammatory nature and not simply an 
 oedematous thickening. 
 
 Etiology. — The exact cause and method of production in the 
 chronic diffuse class cannot be so perfectly traced as in the parenchy- 
 matous group and in the acute diffuse variety. From its infrequency 
 in the tropical and frigid, and its great frequency in the temperate 
 zones, its cause is probably dependent upon the repeated exposure of 
 the surface of the body to sudden and alternating influences of 
 heat and cold, which have a tendency to produce recurring attacks of 
 internal congestion and overwork on the part of the kidneys, until 
 finally this condition is fully established. 
 
 Its frequency among bakers, foundrymen, and engineers points in 
 this direction. Some have ascribed rheumatism as a cause, but the 
 climatic influences which excite the rheumatism appear to be the 
 chief exciting causes of the renal lesion. 
 
 It certainly is common among brain workers who take but little 
 exercise and at the same time live rather highly. In some instances 
 it unquestionably follows an acute attack. Very frequently it is de- 
 veloped without any well-defined cause being ascertained. Eepeated 
 attacks of pneumonia, fevers in general, and all severe diseases which 
 tend to overwork the kidneys are very potent causes for laying the 
 foundation of and paving the way for this variety of renal lesion. 
 
 Pathological Anatomy. — The kidneys are pale in color and may be 
 normal or slightly diminished in size, but as a rule they are markedly 
 enlarged. Their capsules are thickened and slightly adherent, and, 
 upon removal, often bring with them small portions of the underlying 
 renal tissue, but between the adherent spots the surface of the glands 
 may be quite smooth, or only slightly granular. 
 
 The exterior and cut surfaces show numerous small cysts, with here 
 and there a large one. The cortical layer is usually increased in 
 thickness and pale in color, and its markings are wavy, while the 
 pyramids are less prominent than normal. 
 
 Microscopic Examination. — The interstitial tissue is seen to be 
 moderately increased in quantity, and the seat of small round inflam- 
 matory corpuscles. Bowman's capsule is thickened by an inflamma- 
 tory exudation, and the epithelial cells are found in a state of fatty 
 and granular disintegration. The blood-vessels are but little, if at all 
 affected. The only difference between this lesion and that known as 
 chronic parenchymatous metamorphosis, is the marked evidence of an 
 inflammatory exudation and thickening in the interstitial tissue. In 
 
CHRONIC DIFFUSE NEPHRITIS. 
 
 53 
 
 this variety, the major part of the lesion is parenchymatous in char- 
 acter, with only a moderate amount of interstitial involvement, and 
 consequently the kidneys tend to progressively enlarge throughout 
 the course of the disease. 
 
 Symptoms. —In those cases which occur without known cause, the 
 symptoms are very insidious: convulsions and. coma rapidly followed 
 by death may be the first indication; but more frequently its onset 
 is marked by frontal headache, impaired vision, nausea, vomiting, 
 dyspepsia, shortness of breath, weakness, general malaise, oedema, 
 and after a time, a peculiar waxy pallor of the skin, and dropsy 
 or general anasarca. 
 
 In some cases, a persistent diarrhoea, either alone or alternating 
 
 '■&vs 
 
 Fig. 15.— Chronic Diffuse Nephritis. X 350. 
 a, Uriniferous tubule showing marked metamorphotic changes in the epithelium; 6, desqua- 
 mating epithelium; c, new-formed intertubular tissue. 
 
 with periods of obstinate constipation, is a marked symptom. The 
 stomach and intestinal symptoms may be present together or may 
 alternate with each other. The amount of oedema and dropsy 
 varies in the different cases from a slight puffiness under the eyes to 
 a great distention of the skin, and a filling of the large serous cavi- 
 ties with effused fluid; this symptom is almost always present and 
 frequently to a marked degree. 
 
 The dimness of vision may be due to interference with the cere- 
 bral nutrition without any perceptible lesion of the visual apparatus; 
 it may be due to simple neuro-retinitis, to neuro-retinitis accompa- 
 nied by a degeneration of the nerve elements, to the formation of 
 
.">4 CHROXIi DIFFUSE NEPHRITIS. 
 
 connective-tissue patclies in the retina, to emboli, or to apoplexy of 
 the retina. Where any of these lesions occur, there will be no inter- 
 ference with the sense of sight, so long as the macula lutea is not 
 encroached upon. The lesions of the retina are generally symmetri- 
 cal, and occur near the outer side of the optic nerve, appearing first 
 in white spots of small size, and of a quadrilateral shape, which 
 coalesce as they progress, and finally involve the optic disc. Extra- 
 vasations of blood from rupture of the retinal vessels are occasionally 
 seen, and the disc and the retina in its immediate neighborhood have 
 a striated appearance. Later on, the fundus becomes quite yellow, 
 owing to a hyperemia followed by an cedematous infiltration of the 
 retinal tissue, which finally causes a fatty degeneration of its sub- 
 stance, a giving way of the blood-vessels and hemorrhagic extravasa- 
 tions. 
 
 Urinary Symptoms. — The quantity of urine voided varies greatly; 
 at times, it is much less than normal, at others more abundant, or it 
 may be suppressed for several hours. This continued fluctuation in 
 the quantity is one of the chief diagnostic points. Its color is, as a 
 rule, pale. The urine in this group of chronic nephritic lesions has 
 as a characteristic feature a diminution or complete absence of per- 
 ceptible sedimentary deposits, and for this reason casts are often over- 
 looked, or thought not to exist, but a careful study of the lower 
 strata of fluid under the microscope will usually reveal their presence. 
 Neglect of this has often caused a mistake in diagnosis. The specific 
 gravity ranges from 1.025 to 1.012, and may fall as low as 1.005. It 
 is most frequently found to be between 1.017 and 1.010. Albumin, 
 although varying in quantity, is usually present during the whole 
 course of the disease, but it may disappear for days or even weeks, 
 while the casts will be constantly present. Both, however, may dis- 
 appear for a time, or the casts may disappear, and the albumin per- 
 sist. The rule, however, is to find a fair amount of albumin nearly 
 all the time. 
 
 The casts most commonly found are the hyaline, coarsely granular, 
 and fatty, which are generally of large or medium size. 
 
 In acute exacerbations of the disease, all forms and sizes of casts 
 and some blood may be present. Such attacks are frequently mis- 
 taken for an acute and primary diffuse nephritis. 
 
 Prognosis. — Patients with this disease seldom entirely recover, but 
 they may live ten, fifteen, or more years without much discomfort. 
 There is, however, more or less drain upon the system, which renders 
 the prognosis of any acute disease which they may contract particu- 
 larly unfavorable. There is little doubt that the existence of an 
 
CHRONIC DIFFUSE NEPHRITIS. Oi) 
 
 insidious form of this lesion is one of the chief causes for the frequent 
 fatal termination in cases of pneumonia. It also suggests the neces- 
 sity for a closer investigation into the true condition of the kidneys in 
 all acute diseases. An acute exacerbation is likely to occur at any 
 time, and always renders the prognosis bad. 
 
 Treatment. — As our knowledge of the causes of this lesion is some- 
 what obscure, as compared with the parenchymatous group and the 
 acute diffuse form, much less can be accomplished in the way of pre- 
 ventive treatment. All excesses should be avoided. As climate is 
 ascribed as a cause of the malady, the body should be well protected 
 by flannels, so that sudden changes will produce the least impression 
 upon the system. 
 
 The treatment of this and the two following varieties being nearly 
 the same, the three will be spoken of together. 
 
 Chronic Diffuse Nephritis, 
 second variety: second form of small kidney. 
 
 In this, the second variety of chronic diffuse nephritis, the disease 
 spends its force upon the epithelial cells, the interstitial tissue, the 
 arterioles, and the capillary blood-vessels. The greatest intensity of 
 action is located in the intertubular tissue and afferent vessels. 
 There is a marked production of new interstitial tissue, and the small 
 arterioles undergo a hyaline transformation which causes a thickening 
 of their walls and an increase of the lumen. 
 
 The change in the epithelial cells does not compare in extent with 
 that in the intertubular tissue, nor is it as great as that which occurs 
 in the first variety of chronic diffuse nephritis or the chronic parenchy- 
 matous form. There are, however, some primary metamorphotic 
 changes in the epithelial cells, which prevent this lesion from being 
 classed as a sclerotic kidney. 
 
 Etiology. — The cause for this particular form has not been abso- 
 lutely determined. 
 
 The same causes which produce the former lesions appear to act in 
 like manner in this one. 
 
 Believing the peculiar hyaline change met with in the vessels in 
 this form to be diagnostic of a systemic syphilitic taint, and from the 
 fact that a specific history was obtained in most of the cases in which 
 this peculiar lesion was present, the most natural inference is that the 
 syphilitic poison is a factor in determining the character of the lesion. 
 
 In this form of atrophic kidney, we find a similar hyaline change in 
 the small arterioles throughout the body, and usually an hypertrophied 
 
56 CHRONIC DIFFUSE NEPHETTIS. 
 
 heart, but in the next form the vessels are not implicated, and the 
 atrophic heart is the rule. Hence it appears that the cardiac hyper- 
 trophy is due to the general loss of arterial elasticity, and is in no 
 way directly dependent upon the renal circulation, or vice versa. 
 
 The retinal lesions so frequent with this variety and the sclerotic 
 forms, in which there is also a general vascular change, are, like the 
 hypertrophy of bhe heart, dependent upon the impaired condition of 
 the blood-vessels throughout the body, and not to either the renal or 
 cardiac condition alone. The tension upon the circulation is con- 
 stantly fluctuating, and. at the same time, the nutrition of the vascu- 
 lar walls arc impaired, and they soon give way under the unequal strain 
 produced by the cardiac hypertrophy, the loss of arterial elasticity, 
 and the imperfect elimination by the kidneys. 
 
 Si 
 
 Fig. 16.— Section from Cortical Portion Showing Thickened and Expanded Afferent Vessel. 
 
 X 350. 
 
 Pathological Anatomy. — The kidneys are diminished in size; their 
 capsules are thickened and very firmly adherent to the underlying 
 surface. The renal tissue is pale and finely granular upon the 
 exterior. They are small white and granular kidneys. Small cysts 
 are often present. The cut surface shows the cortex to be thinner 
 than normal, and if enough remains, the markings will be wavy. 
 The pyramids are also diminished in size. 
 
 The microscopic examination shows a great increase in the intersti- 
 tial tissue, and tortuosity of the normally straight or collecting 
 uriuiferous tubules. In these tortuous tubes, twisted casts are occasion- 
 ally seen in the sections, and, if discharged with the urine, as fre- 
 quently they are, they appear in the urinary examination as the 
 corkscrew casts. The new tissue is studded with small round inflamma- 
 tory corpuscles. Bowman's capsule also shows evidences of a true 
 
CHRONIC DIFFUSE NEPHRITIS. 57 
 
 inflammatory thickening, due to the production of new tissue. By 
 the contraction of this newly formed tissue, the tuft of vessels within 
 the capsule is often compressed. In this particular form of lesion, 
 there is a marked thickening of the small arteries and afferent vessels 
 of the Malpighian tufts. This peculiar hyaline transformation 
 causes a thickening of the arterial wall and a permanent increase 
 in the lumen of the vessels. 
 
 There is an advanced stage of granular and fatty metamorphosis 
 of the epithelial cells, but the change does not appear to be one due 
 to atrophy from compression, as in the sclerotic kidney, but to in- 
 trinsic changes in the epithelial protoplasm. This positive change 
 in the cell elements is essential to render the lesion diffuse. 
 
 Many of the tubes are found entirely stripped of their epithelial 
 lining, and the remaining basement membrane collapsed and con- 
 verted into fibrous cords, which appear under the microscope as 
 bands of fibrillated connective tissue. 
 
 The occlusion of the tubes in this manner is one of the ways in 
 which the cysts, so frequently seen upon the surface, are formed. 
 The surface of these kidneys may have numerous cicatricial depres- 
 sions, which have been developed by the collapse of one of these cysts, 
 or resulted from the absorption of an infarction. 
 
 The latter mode of formation is the more frequent, but has no 
 special bearing, as they are found in many other varieties and in 
 otherwise normal kidneys. 
 
 Symptoms. — The general symptoms are the same as those of the 
 first variety, the only marked point of difference being in connection 
 with the urine, which is here very much increased in quantity, the 
 daily amount varying between seventy-five and one hundred and 
 fifty ounces. 
 
 This large increase is explained principally by the thickening of 
 the walls of the arterioles. They lose their power of regulating the 
 tension brought to bear upon the capillaries of the glomeruli. There 
 is no longer any method by which the pressure can be equalized and 
 the full and irregular pressure of the circulation is brought to bear 
 directly upon the tuft and, therefore, the water passes rapidly through 
 the walls of the vessels into the tubules. The involvement of the 
 epithelium and the compression of the intertubular plexuses are the 
 causes of the large amount of albumin present in the urine. This as- 
 sertion is sustained by the pathological fact that in all cases in which 
 the epithelial cells are primarily involved, with compression of the 
 intertubular vessels, albumin is always present in large quantities. 
 
 The extent to which these two anatomical portions are involved 
 
58 CHRONIC DIFFUSE NEPHRITIS. 
 
 determine quite positively the amount of albumin discharged. The 
 assertion that the increase in the quantity of water is due to the 
 condition of the arterioles and capillaries is warranted by an abun- 
 dance of clinical and pathological data. In this, as well as in the 
 sclerotic and amyloid varieties, where there is a marked thickening 
 of the walls of the vessels, the quantity of water discharged is 
 always very large. 
 
 In all renal lesions, where the change is primarily in the epithelial 
 cells, with compression of the intertubular capillaries, the arterioles 
 not being involved, the urine is normal or diminished in quantity 
 and the albumin abundant. On the other hand, if no change occurs 
 in the epithelial cells, albumin is absent. 
 
 Prognosis. — The duration of the disease is very uncertain. From 
 a pathological standpoint, involving, as it does, all the structures, it 
 would be short ; but clinically it borders more upon the sclerotic 
 type; and the prognosis is quite as favorable, if not more so, than the 
 first form. 
 
 Treatment. — The treatment of the different varieties of diffuse 
 nephritis will be spoken of together later on. 
 
 Chronic Diffuse Nephritis, 
 third variety: third form of small white kidney. 
 
 Definition. — This variety of chronic diffuse nephritis differs from 
 the other two in that both the interstitial tissue and the epithelial 
 cells are about equally involved, while the glands progressively 
 diminish in size. In this variety, there is comparatively little de- 
 velopment of new connective tissue, but it is given a greater promi- 
 nence owing to the rapid atrophy of the epithelial elements. There 
 is no increased thickening of the arterial walls. 
 
 Etiology. — The causes, so far as known, are similar to those in the 
 two former lesions. Previous attacks of acute disease may have un- 
 duly damaged the renal epithelium. The form of the chronic lesion, 
 whether parenchymatous or diffuse, is as a rule determined by the 
 form and severity of the acute attacks in the past; that anatomical 
 portion of the kidney tissue which suffers the greatest damage during 
 the acute attacks being the portion where the chronic form becomes 
 seated. In this way the different varieties can be accounted for, just 
 as in a machine the part receiving the greatest strain will be the first 
 to give way. 
 
 Pathological Anatomy. — The kidneys are very small, and their cap- 
 
CHRONIC DIFFUSE NEPHRITIS. 
 
 59 
 
 sules are thickened and firmly adherent to the underlying renal tissue, 
 which is very pale, fatty, and granular. Cysts are frequently present 
 upon the surface. The cut surfaces show the cortex to be thin and 
 often almost obliterated. If there is enough left to judge from, the 
 markings are wavy. The pyramids are always pale and atrophied. In 
 macroscopic appearance, they might, easily be mistaken for the sclero- 
 tic variety, but both the external and cut surfaces are paler than nor- 
 mal. This is the small soft kidney. 
 
 Microscopic examination shows an increase in the amount of inter- 
 tubular tissue, which is partly due to a new-formation of connective 
 
 Fig. 17.— Chronic Diffuse Nephritis. Atrophied Kidney, x 350 and reduced. 
 ShowingjsmalTpatches of new connective tissue with atrophy of inclosed tubules, a, new con- 
 nective tissue; b, atrophied tubule containing hyaline casts; c, tube with epithelium peeling off: 
 d, thickened capsule of glomerulus. (Delafleld and Prudden's "Handbook of Pathological 
 Anatomy and Histology.") 
 
 tissue, and partly to the rapid destruction and desquamation of the 
 epithelial elements, with a collapse of the basement tube. Bowman's 
 capsule is thickened by as light amount of newly formed connective 
 tissue, which in some instances, owing to the general shrinkage of the 
 organs, causes compression and collapse of the tuft, followed by 
 atrophy. There is, however, in this variety no involvement of the 
 arterial capillaries, and in this respect it differs from the former 
 lesion. 
 
60 CHRONIC DIFFUSE NEPHRITIS. 
 
 The epithelial corpuscles are extensively involved by a destructive 
 metamorphosis which is both granular and fatty. This extensive de- 
 struction of the epithelial cells, and the contraction of the newly 
 formed tissue, account for both the softness and the great diminution 
 in the size of the gland. 
 
 This form of lesion probably produces the smallest variety of 
 kidney, and one which is soft instead of hard, distinguishing it from 
 the previous form and the sclerotic and gouty varieties. In one in- 
 stance, one kidney weighed one and a half ounces (42.524 grams), and 
 the other only one ounce (28.349 grams). 
 
 Symptoms. — The general or rational symptoms are about the same 
 as in the other forms of chronic diffuse nephritis. There is usually 
 considerable dropsy. 
 
 Diagnosis. — The changes in the urine are the means by which 
 a correct diagnosis is made. The amount of urine voided ranges 
 from fifteen to forty ounces per day, and has the peculiar trans- 
 lucencv common to all forms of chronic diffuse nephritis. It is acid 
 in reaction, and its specific gravity ranges from 1.010 to 1.025, 
 usually being high. In this respect, it resembles a purely paren- 
 chymatous lesion, but its color is pale, while the parenchymatous 
 group, as a rule, yield a high-colored urine. 
 
 Albumin is constant and abundant; this is also true of the paren- 
 chymatous group. In this lesion, all forms of casts are found, and 
 they vary greatly in size; but in the chronic parenchymatous, the 
 large hyaline, coarsely granular, and fatty casts and considerable cast 
 debris, are the distinguishing features. Blood casts may occur in this 
 form, but never in the purely parenchymatous group. 
 
 From the first form of chronic diffuse nephritis it is distinguished 
 by the small quantity and the continued abundance of albumin and 
 casts, and the high specific gravity. 
 
 In the first form, the quantity of urine, the albumin, and casts are 
 constantly fluctuating, while the specific gravity is, as a rule, ab- 
 normally low. 
 
 In the second form, the quantity of urine and the amount of 
 albumin are always large, ranging from sixty to one hundred and 
 twenty ounces per day, casts of the small hyaline and fatty varie- 
 ties being the only kind found, and these in small numbers. The 
 urine also has a specific gravity rarely above 1.010. 
 
 Prognosis. — This is undoubtedly the most fatal form of the diffuse 
 group, after the symptoms become pronounced. The prognosis does 
 not date from the starting-point of the disease, but, in the majority 
 of instances, from the time when the symptoms become sufficiently 
 
CHRONIC DIFFUSE NKI'JI lil'l'IS. 01 
 
 marked to attract the patient's attention and cause him to consult a 
 physician. 
 
 In some, if not in most, of the cases, it is impossible to say when 
 the disease first commenced, and how long it had existed when 'first 
 diagnosticated. Many cases undoubtedly exist for a long time, 
 without attracting the attention of either patient or physician. But 
 a more frequent microscopic study of the urine would unquestionably 
 reveal the lesion much earlier. 
 
 Usually, the disease creeps along in its insidious course until some 
 indiscretion, excess, or overstrain on the part of the individual 
 throws an extra amount of work upon the kidneys, the epithelial cells 
 are damaged beyond toleration, troublesome symptoms declare them- 
 selves; the patient's attention is attracted to these acute manifesta- 
 tions, and a physician is consulted, who at once recognizes the diffi- 
 culty. 
 
CHAPTER V. 
 
 COMPLICATIONS OF RENAL LESIONS. TREATMENT OF 
 CHRONIC DIFFUSE VARIETY. 
 
 COMPLICATIONS. 
 
 There are anumber of conditions associated with the various renal 
 lesions, that are produced directly or indirectly by the kidney disease. 
 There are also other conditions which are concomitant lesions, but 
 which unquestionably act as complications. Some of the symptoms, 
 as they become more aggravated, are classed as such; and for conveni- 
 ence all of them will be considered as complications, and, taken up in 
 alphabetical order, and not with reference to their frequency or im- 
 portance. 
 
 (a.) Ascites, Hydroperitoneum, or Abdominal Dropsy. — This con- 
 dition is a part of the general dropsy, instead of a new and complicating 
 disease, and usually, if moderate in extent, causes little inconve- 
 nience; but when excessive, it crowds up the diaphragm, materially 
 interfering with the respiratory movements, causing dyspnoea, and 
 often increasing the immediate clanger. An associated portal 
 obstruction may also aid or produce ascites, and in this way complicate 
 the renal lesion. 
 
 Treatment. — Unless the abdominal dropsy becomes excessive, it will 
 not necessitate paracentesis abdominis. The ordinary methods for 
 treating the general dropsy with the free use of hydragogue cathartics 
 will generally remove the trouble without an operation. 
 
 (b.) Aneurisms. — The variety here referred to is that commonly 
 known as Charcot's, or the miliary aneurism. These are quite com- 
 mon in the cerebral substance, and have also been observed in the 
 small intestine, stomach, and in the pulmonary tissue. 
 
 By their rupture, both in the stomach and intestine, a fatal termi- 
 nation has resulted from internal hemorrhage, but this is more fre- 
 quently the case in the brain. In this way many of the cases of 
 sudden death, without pronounced urasmic symptoms, are explained. 
 
 The impaired condition of the small vessels is probably brought 
 
COMPLICATIONS OF RENAL LESIONS. 
 
 63 
 
 about by the deteriorated condition of the blood, which diminishes 
 the nutritive supply. This form of aneurism is most frequently met 
 with in connection with those cases in which there is high or increased 
 arterial tension and left cardiac hypertrophy, or in connection with 
 the second form of chronic diffuse nephritis and the sclerotic or inter- 
 stitial variety. 
 
 Their rupture is considered by some to be the only cause of cerebral 
 hemorrhage, not only in connection with nephritic disease, but in 
 every instance. 
 
 Four cases will be cited, illustrating this point. In each, death 
 was rather sudden and unexpected, associated with all the ordinary 
 
 
 Fig. 18.— Miliary Aneurism in the Cortical Substance of the Brain Divided Longitudinally. 
 
 p, Proximal side of vessel, its diameter being 1/54 of an inch; d, distal end of vessel its dia- 
 meter being 1/128 of an inch. The greatest diameter of the aneurism being 1/80 of an inch, 
 its smallest diameter 1/29 of an inch. 
 
 signs and symptoms of internal hemorrhage, and without any symp- 
 tom of a uraemic nature. In two of the cases, the aneurism was 
 located in the wall of the stomach and the hemorrhage poured into 
 its cavity. The history of one of these cases was as follows. The 
 patient was admitted to the hospital for a severe hasmatemesis. The 
 blood vomited was abundant and arterial in character, some was also 
 passed through the anus. Physical examination of the chest gave a 
 negative result. The urine contained albumin and casts, establishing 
 the existence of a renal lesion. Death soon occurred with all the 
 ordinary symptoms common to internal hemorrhages. 
 
6i COMPLICATIONS OF RENAL LESIONS. 
 
 The diagnosis is made by excluding all the other causes for ha?ma- 
 temesis, viz.. ulcer of the stomach, sclerosis of the liver, and all 
 forms of portal obstruction, cancer or toxic inflammations of the 
 stomach, pernicious anaemia, leucocythaemia, purpura hemorrhagica, 
 scurvy or scorbutus, yellow or typhus fever, jaundice, acute atrophy 
 of the liver, pyaemia, pulmonary or cardiac lesions, vicarious menstru- 
 ation, and the bursting of an extrinsic aneurism into the oesophagus 
 or stomach. 
 
 With the rupture of a miliary aneurism in the stomach, the hemor- 
 rhage comes on without premonitory symptoms, aside from those of 
 renal disease; it is abundant and rapidly fatal. Microscopic examina- 
 tion revealed the same condition as represented, Fig. 18, page 63, but 
 the vessel implicated was much larger and, having ruptured, its out- 
 lines were not as perfect. 
 
 In the other two, the aneurism was located in the intestinal tunic. 
 In both there had been a copious hemorrhage into the intestinal canal; 
 while in one of them the blood had also found its way into the peri- 
 toneal cavity. Many similar cases have been noticed, until this lesion 
 has become oue of the recognized causes of death in the chronic 
 forms of renal disease. 
 
 As there are no positive signs by which aneurisms of this description 
 can be recognized until they rupture, they are chiefly of pathological 
 importance in accounting for some of the sudden deaths. 
 
 The ordinary aneurism, in connection with the large vessels, may 
 act as a complication; but it is not dependent in any way upon the 
 renal lesions for its production, and when it does occur, it is a 
 coincident disorder. They may cause troublesome symptoms by their 
 pressure, or sudden death by being ruptured. 
 
 The rupture of a miliary aneurism is usually followed by a fatal 
 issue, and consequently requires uo treatment. The pressure effects of 
 the large aneurism may need attention, and must be treated upon the 
 general principles laid down for such conditions . 
 
 (c. ) Apoplexy or Cerebral Hemorrhage. — This condition is a frequent 
 and fatal complication. It is superinduced in part by the renal lesion 
 causing changes in the blood, which in turn damage the cerebral 
 vessels, and in part by an associated cardiac hypertrophy. 
 
 Hypertrophy of the left ventricular wall and the miliary aneurisms 
 already mentioned easily account for the hemorrhage, or the aneurisms 
 alone may be a sufficient cause. 
 
 Little can be done in the way of treatment for an apoplectic 
 attack. 
 
 (d.) Atheroma of the Vessels in General, or Endarteritis. — This 
 
COMPLICATIONS OK ItKNAL LESIONS. 
 
 63 
 
 condition is frequently spoken of in connection with renal lesions; in 
 some cases it is very pronounced, while in others Lt is altogether 
 absent. From these facts this condition might justly be looked upon 
 as a concomitant lesion, and not necessarily as a complication. Som",, 
 however, hold that there is always hypertrophy or interstitial thicken- 
 ing of the middle coat, especially of the smaller arteries. Repeated 
 examinations of the vessels in connection with renal disease leads to 
 an opposite conclusion, viz., that the one is not directly dependent 
 upon the other. Occasionally the two may be associated, but not as a 
 rule. 
 
 This condition is not often recognized until the necropsy, and con- 
 sequently is not treated. Should it be diagnosticated prior to death, 
 it can only be treated in a general way. 
 
 (e.) Asthmatic Attacks, Dyspnoea, or Urmmic Asthma. — Extreme 
 dyspnoea, or attacks strongly resembling those of asthma, are by no 
 means infrequent in chronic nephritis. These symptoms are most 
 marked during the night, but with the approach of morning the 
 bronchial tubes become moistened by an increased secretion of mucus, 
 and the breathing is easier. During the day the patients remain 
 fairly comfortable, but with the return of night the dyspnoea is renewed 
 and the difficulty in breathing often becomes so severe that the patient 
 is prevented from lying down or getting any continuous sleep. This 
 particular symptom is one of the most aggravating to the patient, and 
 exceedingly troublesome for the physician to overcome. It is due to 
 some portion of the retained and incomplete products of tissue me- 
 tamorphosis acting upon the nervous mechanism distributed to the 
 lungs. The anaemic condition, by diminishing the power of the blood 
 to seize upon oxygen and distribute it to the system, also aids in keep- 
 ing up the dyspnoea. Abdominal dropsy and pleuritic effusion also 
 aid by diminishing the chest space and impeding the respiratory 
 movements. The principal cause, however, is the retained effete pro- 
 ducts which keep up the nervous irritation. 
 
 Treatment. — This complication is one of the most difficult to over- 
 come. Temporary relief will almost always follow a full dose of the 
 muriate of pilocarpine (gr. f) (0.04 gram) hypodermatically. With 
 small and repeated doses, the same effect is occasionally accomplished. 
 By giving a full dose of elaterium, or elaterin, the dyspnoea and 
 asthmatic spasm is often relieved and kept in subjection. It is a 
 good plan to alternate these remedies. Some cases are relieved by 
 full doses of the fluid extract of quebracho. But it must be remem- 
 bered that none of these remedies have a specific effect upon the 
 causation of the asthma, they merely enable the system to relieve 
 5 
 
66 COMPLICATIONS OF RENAL LESIONS. 
 
 itself temporarily of the excitant. This constant drain would natu- 
 rally be thought to hasten the fatal issue, but on the contrary it pro- 
 longs life and renders it far more tolerable. It appears to Bweep 
 away large quantities of water, which carry with it the poisonous ele- 
 ments that are so damaging to the system and constantly keep up the 
 annoying symptoms. The water can easily be replaced, but theother 
 elements are too frequently retained. 
 
 If the effete and poisonous substances are retained and allowed to 
 accumulate in the system, they are liable to suddenly produce a fatal 
 termination. 
 
 At this point it may be well to say that elaterium bas in every in- 
 stance proved the most efficacious cathartic in renal lesions. In some 
 of the cases from which these conclusions have been deduced, this 
 drug was administered daily for several weeks in succession, and in 
 one case from one-half to three-quarters of a grain was administered 
 daily. The method of giving was in pill form (gr. £) (0.008 gram) 
 every fifteen minutes until the bowels commenced to move, or f 
 of a grain (0.04 gram) had been taken. The continued use in this 
 way did not produce any intestinal irritation during life, and at the 
 necropsy the mucous membrane of the intestine was found to be quite 
 normal, so far as any deleterious action of the drug was concerned. 
 
 Many other medicinal agents could be mentioned, but these two 
 are the most certain in giving relief, and have always proved per- 
 fectly safe, but often have to be used continuously in extreme cases. 
 All forms of anti-spasmodics are absolutely useless. 
 
 (f.) Blood Changes. Hydrommia. — The chemical composition of the 
 blood is changed. The specific gravity, corpuscles, and albumins are 
 diminished, but the water is increased in quantity. In some cases, 
 there is an actual increase in the number of the white corpuscles, 
 while the red blood-discs become cedematous and flabby. The urea 
 in the blood is slightly increased. This condition can only be treated 
 by tonics, chalybeates, good food and fresh air; if the renal condition 
 can be improved, the quality of the blood will also improve. 
 
 (g.) Bronchitis. — The acute form may be developed at auy time, 
 run its regular course and terminate favorably, or else become 
 established and chronic in nature; but more frequently it com- 
 mences as a subacute or chronic affection. As both the acute and. 
 especially, the chronic form of bronchial inflammation. as -well as 
 the renal lesions, are common in advancing years, they may be 
 called associated diseases; the bronchitis not necessarily depending 
 upon the renal lesion as a cause, but at the same time acting as a 
 complication and rendering the prognosis less favorable. With this 
 
COMPLICATIONS OF KKNAL LESIONS. 
 
 07 
 
 conception, the bronchitis calls for independent treatment, although 
 the condition of the renal organs should not be lost sight of or neg- 
 lected. The improvement of the bronchitis will often be Followed by 
 an improvement in the kidney disease. 
 
 Treatment. — Undue exposure to cold should be guarded against as a 
 preventive measure, but, when developed, warmth, with tonic expec- 
 torants, will do the most good. The following will be found to 
 speedily relieve these bronchial affections: 
 
 I£ Tincture Opii Deodorati 3 i. 
 
 Ammoniac Carbonatis et 
 
 Ammonias Hydrochloratis aa 3 iij. 
 
 Tincturse Cubebse 3 iv. 
 
 Syrupi Pruni Virginianae q.s. ad § iij. 
 
 M. Sig. 3 i. every three hours in water. 
 
 (h. ) Cardiac Lesions. — Four sets of morbid changes may be found at 
 the necropsy, (a) Hypertrophy without valvular lesion (simple hyper- 
 trophy), (b) Valvular disease, wholly independent of, and originating 
 prior to, the renal disorder, (c) An endocarditis may be excited by 
 the kidney disease, and be followed. by changes in the valves, caus- 
 ing either a stenosis or insufficiency of the valvular orifices, (d) 
 Atrophy and softening. 
 
 (a) Simple hypertrophy, and especially that form which is limited 
 to the left ventricle, has caused much discussion pro et con.; some be- 
 lieving that it is produced by the renal lesion, the change in the blood 
 and blood-vessels, increased tension, etc. ; while others argue that the 
 cardiac lesion is primary, while the kidney lesion is secondary to, and 
 caused by, it. 
 
 In looking over a large number of necropsy records, this fact was 
 noted, that in connection with the parenchymatous group, and in those 
 forms of chronic diffuse nephritis in which there was no general 
 vascular change, the heart was normal or atrophied as in all wasting 
 diseases. But in that variety of chronic diffuse nephritis in which 
 there was a marked thickening and loss of elasticity in the renal and 
 general arterial system, and in the interstitial variety, with a similar 
 vascular change, there was almost invariably a compensatory hyper- 
 trophy of the left ventricle to overcome the general vascular resistance. 
 As only one-third of the renal lesions classed as Bright's are associated 
 with cardiac hypertrophy, it seems reasonable to look for the cause 
 outside of the disturbed renal circulation. In this general vascular 
 thickening and loss of elasticity is found a more potent cause. In 
 
68 COMPUCAHONS OF renal lesions. 
 
 some cases of chronic diffuse nephritis in which the non-eliminating 
 function of the kidneys has come on slowly, and there has been a long- 
 continued blood poisonand mal-nutrition, the vascular walls through- 
 out the system become thickened and non-elastic and cause cardiac 
 hypertrophy. But as Bamberger says: " It is not possible to suppose 
 that destruction or obstruction to the current of blood in a few little 
 vessels in the kidney could produce cardiac hypertrophy, or riceversa." 
 
 On the other hand, there are marked changes in the blood which 
 produce hydroa?mia, diminished nutrition, and a consequent loss of 
 elasticity on the part of the arterial coats throughout the body, which, 
 together with the nervous irritability and the varying arterial tension, 
 so impede the free onward flow of blood that it is, as it were, crowded 
 back upon the heart: this is the most satisfactory explanation of the 
 cardiac hypertrophy. Compensatory hypertrophy is necessitated and 
 developed to overcome the increased obstruction, independent of any 
 change in the renal circulation. Its frequency in the sclerotic variety 
 is unquestionably due to the longer existence of the renal blood 
 .and vascular changes. 
 
 Jn the parenchymatous group and those of short duration, hyper- 
 trophy is not the rule. It has also been claimed that the changes 
 in the heart wall are due to the urea, which is more abundant in the 
 blood, and that it acts as a direct stimulus to the cardiac muscle, and 
 in this way the hypertrophy can be explained. Unfortunately for 
 this theory, it is pretty generally admitted that, in the condition 
 known as urasmia, the cause is not the retained, but the deficient pro- 
 duction of urea. What actually produces the uraemic symptoms has 
 not been clearly demonstrated; but it is some intermediate and incom- 
 pletely formed product of proteid metabolism. Until we can ascertain 
 to a certainty what the irritating substance is, it will be impossible to 
 •determine its influence upon the heart. 
 
 (b) Organic valvular lesions may have existed prior to any renal 
 lesion, and in some cases produced a chronic congestion which ulti- 
 mately resulted in a fully established and chronic kidney disease. 
 This condition has been termed a cyanotic kidney. In such a case 
 as this, the renal lesion is the complication to the cardiac disease. 
 
 (c) On the other hand, the deteriorated condition of the blood, with 
 its contained irritants, may excite an endocarditis which in turn is fol- 
 lowed by organic valvular changes. Now the cardiac lesion compli- 
 cates the renal disease, and in all these instances the proguosis is 
 more serious than with either alone. 
 
 (d) In many instances, the necropsy will reveal a soft, small, and 
 atrophied heart. This is true of the third form of chronic diffuse 
 
COMPLICATIONS OF RENAL LESIONS. 69 
 
 nephritis and the parenchymatous group, and this is due to the pro- 
 gressive and general mal-nutrition. 
 
 The cardiac lesions are to be treated on the general principles which 
 govern those diseases, independent of the renal lesion. Anything 
 which improves the condition of the heart will relieve the kidneys, 
 and cause the general condition of the patient to improve. One of 
 the best cardiac tonics to stimulate the heart's action and increase its 
 nutrition is the following: 
 
 P* Tincture Opii Deodorati 3 iij. 
 
 Tincturas Nucis Vomicae t . , 3 ss. 
 
 Tinctura? Belladonna? 3 iij. 
 
 Tincturse Gentianse q. s. ad 3 iij. 
 
 M. Sig. 3 i. ter in die.- 
 
 (*'.) Cirrhosis of the Liver. — This condition maybe present at the 
 same time as the renal lesion, but usually precedes the kidney trouble. 
 Interstitial hepatitis is more likely to occur with, or act as, the cause 
 which produces the chronic parenchymatous metamorphosis of the 
 kidneys. When it occurs with the diffuse or sclerotic form, it is a 
 coincident lesion. When the two coexist, the interstitial hepatitis 
 greatly impairs the digestive function of the liver, and increases the 
 amount of work to be performed by the excretory structures of the 
 kidneys, and in this way it renders the prognosis more unfavorable. 
 
 For this condition of the liver little can be done in the line of thera- 
 peutics. The food should be plain and nutritious, and all hepatic 
 irritants should be avoided. 
 
 (;'.) Constipation and Diarrhoea. — A form of obstinate and chronic 
 constipation and a kidney lesion often coexist. This condition may 
 be regarded as a urgemic constipation, which is produced by the 
 renal disease. It is often very persistent, and refuses to yield to 
 any form of cathartic, elaterium and croton oil not excepted. It is 
 believed to be due to a paralysis of the muscular tunic of the intestine, 
 which is brought about by the depressing effects of the so-called 
 urgemic poison, whatever this may be. In this way a persistent para- 
 lysis of the intestinal muscular fibres is produced. In other cases, 
 there is an equally persistent diarrhoea, or the two may alternate. 
 The constipation, however, is the more serious, and carries with it 
 greater danger to the patient. 
 
 This complication is very intractable, and by preventing free elimi- 
 nation from the alimentary tract, naturally endangers life. Large 
 and repeated doses of mix vomica, alone or in combination with bella- 
 donna, are very serviceable, especially in the chronic forms. 
 
7<> COMPLICATIONS OP RENAL LESIONS. 
 
 This condition of ten becomes very troublesome for a few days or 
 even weeks just prior bo death, and causes general distress from the 
 accumulation of a large amount of gas within the intestine. An ob- 
 stinate constipation, with suppression of urine, frequently occurs, and 
 [f not relieved, must produce a fatal issue. 
 
 A certain method for relieving these severe symptoms is by the 
 hypodermatic administration of the muriate of pilocarpine, three- 
 fourths of a grain being given at once. It is also well at the same 
 
 O © © 
 
 time to administer cardiac stimulants. This plan of treatment will 
 set all the excretory organs in motion and often prolong life. If full 
 doses of elaterium or other cathartics have preceded the pilocarpine, 
 the symptoms may become alarming, but the patient will ultimately 
 be relieved, a mishap having never been witnessed. 
 
 If the intestinal distention becomes very great, puncture with an 
 aspirating needle or trocar and canula may be practised, or a rectal 
 tube may be inserted and the gas allowed to escape. 
 
 (k.) Eczema. — This variety of skin lesion is occasionally associated 
 with a kidney lesion. It is exceedingly annoying to the patient, and 
 does not readily yield to treatment. The incessant irritation renders 
 it a serious complication. It may be recovered from, but more fre- 
 quently terminates in an erysipelatous inflammation or gangrene, and 
 in this way acts as one cause of death. 
 
 It must be treated upon the principles which govern the manage- 
 ment of all forms of eczema, but an improvement of the renal 
 disease is the chief thing. 
 
 {I.) Emphysema. — This lesion of the pulmonary tissue is by some 
 observers regarded as a frequent complication. It, however, does not 
 appear to be traceable in any direct manner to the renal affection, 
 but is another coincident lesion. 
 
 Little can be done for it in the way of treatment, except to keep 
 the respiratory tract moist and free from mucus. 
 
 (•to.) Endocarditis. — This, with the lesions of the valves produced by 
 it, is a decided and one of the most serious complications produced 
 by renal disease. This inflammatory condition of the endocardium 
 is believed to be caused by the irritating condition of the blood. 
 
 Its treatment is that of the kidney disease. If the renal lesion can 
 be improved, the quality of the blood will also improve, and the endo- 
 cardial lesion will subside or disappear. 
 
 (n.) Erysipelas. — This is a rare complication. It may develop sponta- 
 neously, or be secondary to an erythematous or eczematous inflamma- 
 ation of the skin; and in some instances it follows directly upon the 
 puncturing of the integument for the relief of the excessive oedema. 
 
COMPLICATIONS OF KKNAL LESIONS. 
 
 71 
 
 It is said to be a frequent result of these incisions, while others con- 
 sider it an infrequent occurrence. It, however, docs occur in some 
 cases, and is always to be considered before resorting to the operative 
 method for the relief of the excessive oedema. When developed, it 
 almost always hastens the fatal issue, and little can be accomplished in 
 the way of treatment. 
 
 (o.) Gangrene. — This may follow the eczema or erysipelas, or be 
 developed independently and of itself prove a rapidly fatal complica- 
 tion. 
 
 Treatment is of little avail. Such cases usually terminate in a few 
 hours, or days at the outside. To overcome the unpleasant odor, the 
 affected part should be packed in Puller's earth. 
 
 (p.) Gastric Affections. — There may be only an irritability of the 
 stomach, functional, dyspepsia, or there may be a more pronounced 
 catarrhal condition with marked anatomical changes. The disease 
 may be acute, subacute, or chronic. 
 
 The muscular tunic of the stomach may be hypertrophied or atro- 
 phied. But the morbid changes are more frequently located in the 
 mucous membrane. The interstitial tissue surrounding the gastric 
 follicles is infiltrated and thickened, and with this there may be either 
 an hypertrophy or atrophy of the glands; in the majority of the cases, 
 it is the latter, which is associated with a parenchymatous transfor- 
 mation of the protoplasm of the epithelial cells lining the tubules. The 
 smaller vessels of the stomach may be the seat of miliary aneurisms 
 or of a hyaline infiltration. The latter, however, is rare, unless the 
 renal lesion be associated with prolonged suppuration and continued 
 syphilitic manifestations, probably the latter. 
 
 In all forms of kidney disease, gastric irritability is liable to be 
 developed. 
 
 Symptoms referable to the stomach are quite common in all the 
 acute forms, and with each exacerbation in the chronic forms. When 
 the gastric symptoms continue for a long time and do not yield to 
 treatment, even in the absence of other renal symptoms, they are 
 strongly indicative of the existence of a sclerotic kidney. 
 
 This is doubly true if the patient passes an abnormally large quan- 
 tity of urine with alow specific gravity. 
 
 These manifestations are, strictly speaking, a part of the original 
 disease, and the lesion of the stomach only acts as a complication 
 when it decidedly interferes with digestion and assimilation. 
 
 The symptoms are produced in one of three ways, or by their com- 
 bined action, viz., by au attempt on the part of the gastric epithelial 
 cells t6 eliminate the effete material which should be removed bv the 
 
r2 COMPLICATIONS OF RENAL LESIONS. 
 
 renal organ. In this way the peripheral ends of the nerves are con- 
 stantly irritated and cause the symptoms; or the hyaline infiltration 
 of the vessels may impair the nutrition of the membrane and the 
 
 peripheral nerves. But in the larger numlicr of instances, it is best 
 explained and accounted for by the central irritation of the nervous 
 system, which is constantly being irritated by the incompletely formed 
 
 products of tissue metamorphosis circulating in the blood. The 
 severity and persistence of the nervous manifestations will depend 
 upon the duration of the disease and the amount of damage done to 
 the renal excretory apparatus. If the renal cells can be made to 
 regain their power of elimination, the nervous symptoms, by the aid 
 of nerve tonics, will diminish in severity or disappear. 
 
 The gastric symptoms can be treated by all the stomach and dyspep- 
 tic remedies, but as long as the effete material circulating in the blood 
 is allowed to remain, their efficacy will at best be slight. 
 
 The only hope for relief is in removing the cause. This set of 
 symptoms is most easily and speedily relieved by the eliminative 
 treatment with elaterium. 
 
 The result of this is to carry out of the system a large amount of 
 the poisonous products of tissue waste, and at the same time diminish 
 the amount of work required of the kidneys. The nutrition is im- 
 proved and the renal glands are given a chance to repair the damage 
 already sustained. By following this plan, with a judicious use of 
 diuretics and diaphoretics, the renal lesion in many instances can be 
 materially improved, and the unpleasant symptoms held in check for 
 months, and in some instances for years. 
 
 Pilocarpine and diuretics are of service in severe and acute attacks. 
 Counter-irritation at the scorbiculis cordis always gives some relief. 
 
 (q.) Hemorrhage. — The rupture of the miliary aneurisms already 
 described, or of a large aneurism, may cause a fatal hemorrhage. 
 
 (r.) Hepatic Disease. — Functional hepatitis. This condition has 
 been classed as a complication, but more accurately speaking it is 
 primary, and one of, if not the most frequent, causes for all forms of 
 renal lesions. Preventing as it does the complete transformation of 
 the nutritive and excretory substances, it causes an incomplete nutri- 
 tion throughout the body, and increases the quantity of effete and ir- 
 ritating materials in the blood, thus increasing the amount of work to 
 be performed by the kidneys. "When of short duration, as occurs in 
 connection with the acute infectious diseases, an acute parenchyma- 
 tous lesion will be established; but when of longer duration, a chronic 
 metamorphosis will result, and continue as such until death, or a 
 chronic diffuse nephritis may be established. 
 
COMPLICATIONS OF RENAL LESIONS. T-\ 
 
 The advanced renal metamorphosis, in connection with. diabetes, is 
 a typical illustration of a kidney lesion secondary to a disturbed 
 and incomplete hepatic metabolism. 
 
 The treatment of the functional hepatitis, occurring either prima- 
 rily or secondarily, requires the closest attention. 
 
 In this form of hepatic disturbance, the bile pill mentioned on p. 26 
 will be found of special service; also the general nerve tonic, p. 8!). 
 
 (s. ) Hydropericardium. — Cardiac dropsy occurs as a part of the gene- 
 ral anasarca, or it may be developed in cases where there has been no 
 previous general oedema. It is always a serious and often a fatal 
 complication, compressing as it does an already weakened heart. The 
 spontaneous variety without previous dropsy is the more dangerous. 
 
 The treatment for this condition is to produce a rapid elimination by 
 the skin, bowels, and kidneys, and corresponds closely with that for 
 general anasarca. Brisk cathartics, with the administration of cardiac 
 stimulants, such as ammonia, Hoffmann's anodyne, and alcohol, will 
 be found the safest and most effectual treatment. 
 
 (t.) Headache. — This is sometimes classed as a complication, but it is 
 not so, strictly speaking, but simply an aggravated symptom. 
 
 It is produced by the irritating influences of the retained effete ma- 
 terial in the blood upon the nerve centres. 
 
 This will sometimes yield to iron preparations, to quinine, to the 
 application of hot or cold water, or the two alternately. The breaking 
 of a pearl of amyl nitrite in the mouth will, in many instances, give 
 temporary relief. Many drugs will dispel the pain for a time, but 
 they all fall short of permanent cure, in some of the severer types, 
 morphine may be called for, and its use justified, but great caution 
 should be exercised in using it, for it is not as safe as some have advo- 
 cated, and occasionally may be the cause of a fatal coma. 
 
 The following will often give relief and prevent the necessity for 
 using morphine: 
 
 3 Chloroformi et 
 
 Tincturse Aconiti ail 3 i. 
 
 Chloralis Hydratis et 
 
 Pulveris Camphorae aa 3 i. 
 
 M. Sig. External use. 
 
 This solution applied locally will often give relief and prevent the 
 necessity for using morphine; it is best applied by saturating a cloth 
 with the fluid and binding it on the part where the pain is most intense, 
 and this can be repeated a few times if at first it does not produce the 
 desired effect. 
 
 Eliminating the original poisons which produce the cerebral irrita- 
 
74 COMPLICATIONS OF RENAL LESIONS. 
 
 tion is the only sure method by which a permanent relief can be ex- 
 pected. The prognosis in regard to the headache depends wholly 
 upon our success in increasing the excretory powers of the system. 
 (u.) Hydrothorax. — This, like the pericardia] effusion, may be a part 
 
 of the general anasarca, or an independent affection. If there be much 
 fluid, effused into the pleural cavity, it will compress the lung and 
 cause seriqus dyspnoea, and in some cases materially interfere with the 
 movements of the heart. When developed independently of any gen- 
 eral dr. psy, it may excite an oedema of the lungs, and in this way, 
 cause a sudden and fatal result. 
 
 Occasionally the pleuritic effusion may necessitate a paracentesis, 
 but, as a general rule, it can be modified or caused to disappear by the 
 use of cathartics, diuretics, and diaphoretics, aided by a fly-blister, all 
 being used at once. 
 
 (v. ) Intestinal < 'atarrh. — The same causes which disturb the stomach 
 act in a similar manner upon the intestinal tract, and induce a catar- 
 rhal condition which produces a diarrhoea alone, or with an alternat- 
 ing constipation. 
 
 This condition must be treated upon general principles, remember- 
 ing always the eliminating part. 
 
 (w.) Jaundice. — Functional derangement of the liver may he devel- 
 oped at any time during the course of a renal disease, and give rise to 
 varying degrees of jaundice and constipation with clay-colored stools 
 which, by throwing more work upon the kidneys, materially compli- 
 cate the case, and should be relieved as speedily as possible, by using 
 cholagogue cathartics, such as calomel, podophyllum, phosphate of 
 sodium, etc., or by tonic cholagogues, such as small doses of mercury, 
 ipecacuanha, etc. 
 
 By a tonic cholagogue is meant such drugs or mineral spring waters 
 as have a tendency to increase the quantity and quality of bile pro- 
 duced. The one which most closely imitates nature is the ordinary 
 ox bile. By giving a few grains of the inspissated bile, great relief 
 will often follow. 
 
 A cathartic cholagogue is a remedy which sweeps all excess of 
 bile from the alimentary tract. In this form of hepatic derange- 
 ment the following pill is especially applicable: 
 
 \i Hydrargyri Ohloridi Mitis gr. ii.j. 
 
 Fellis Bovis Inspissati gr. xxiv. 
 
 Quininse Sulphatis gr. xij. 
 
 Extracti Taraxaci 3 ss. 
 
 M. et fiat massa in capsulas no. quindecim dividenda. Sig. One 
 ter in die before meals. 
 
COMPLICATIONS OF RENAL LESIONS. 75 
 
 (x.) Meningitis. — A form of chronic thickening of the pia mater, or 
 chronic meningitis, is frequently associated with all renal lesions 
 which last for any length of time. From a pathological, if not from 
 a clinical standpoint, it should be regarded as a complication, and 
 probably is one factor in causing the continuous headache of kidney 
 disease. 
 
 This lesion is not generally amenable to treatment. 
 
 (g.) Neuro-retinitis. — A chronic inflammation, involving both the 
 optic nerve and retina, is met with in some cases of renal disease, es- 
 pecially in connection with the chronic diffuse nephritis and the scle- 
 rotic varieties. It may cause dimness of vision, and even blindness. 
 It requires no special treatment, for when the nephritic disease im- 
 proves, the same is true for the eye symptoms. A similar condition 
 may be developed with other diseases, so that, taken alone, it cannot 
 be considered as diagnostic of renal trouble. 
 
 (z.) (Edema of the Lungs. — This pathological change usually occurs 
 at some time in the course of the disease. It may develop early in the 
 acute stage; with an acute exacerbation, in connection with a chronic 
 lesion, or it may not occur until late. It may be the determining 
 cause of death, and usually occurs at the end of every case. It is 
 caused by the general hydrsemic condition of the blood, through the 
 nervous system, and as the result of cardiac failure. The symptoms 
 which it gives rise to are rapid and shallow breathing, dyspnoea, and 
 cyanosis. Physical examination reveals sharp, crackling, subcrepi- 
 tant rales over the dependent portions of both lungs, which are often 
 more marked upon one side than the other. These attacks are fre- 
 quently repeated during the course of 'some cases, and, unless promptly 
 treated, may result in an untimely death. 
 
 Treatment. — At the time of the attack, a number of dry cups should 
 be applied to the chest, with the internal administration of volatile 
 cardiac stimulants. This should be followed by the more permanent 
 stimulants, tonics, and eliminating agents, applicable to a general 
 dropsy. 
 
 (aa.) (Edema Glottidis. — This affection occasionally occurs either as 
 part of the general oedema or as a separate and distinct lesion. It 
 gives rise to sudden and dangerous symptoms, characterized by an 
 inability to inhale air and a rapidly developing cyanosis, the expira- 
 tory act remaining unaltered. When developed, unless immediately 
 relieved, it will terminate the life of the patient. 
 
 The treatment consists in the scarification of the cedematous aryteno- 
 epiglottidean folds, or in the performance of tracheotomy. The 
 former is to be preferred if it can be accomplished with safety. The 
 
70 COMPLICATIONS OF RENAL LES1 >NS. 
 
 laryngeal intubation, as recommended by Dr. Joseph R. O'Dwyer, 1 
 migbt be applicable in some of these instances. Dr. Samuel Lloyd lias 
 noticed thai the diminution in the oedema is often followed by a 
 dislodgment of the tube, and if the physician is not on hand to 
 reinsert it or introduce a larger tube, a recurrence of the oodema is 
 the rule. 
 
 (/'//.) (Edema. — General dropsy, or anasarca, when excessive, may be 
 spoken of as a complication. 
 
 The treatment of the condition is by diuretics, diaphoretics, and 
 cathartics, Esmarch's elastic bandage, and a free use of cathartic 
 remedies, as before explained (page 37). In extreme cases, it may 
 be found necessary to puncture the integument, and allow the serum 
 to drain away through the openings, but this is only justifiable as a 
 last resort. Rather than permit the extensive sloughing, which 
 otherwise is likely to ensue, it would be much better to undertake 
 this operative procedure even though the danger of the development 
 of erysipelas and gangrene is great; the latter is almost certain to 
 occur if the extensive oedema remains untreated. 
 
 (cc.) Pericarditis. — This, like endocarditis, is developed during the 
 course of a renal disease. 
 
 It seems to be excited by the irritating excretory products contained 
 in the blood, and may be the first indication of the existence of a 
 renal complication. When it cannot be traced to rheumatism or 
 some other acute disease, the urine should always be carefully exam- 
 ined, and in a large proportion of cases albumin and casts will be 
 found. 
 
 The treatment consists first in removing the exciting cause, to be 
 followed by the principles applicable to pericarditis in general. 
 
 (dd.) Peritonitis. — Inflammation of the peritoneum also suggests a 
 urinary analysis, for it is excited in the same way as the pericarditis. 
 
 Opium, preventing free elimination by the alimentary tract, nat- 
 urally throws more work upon the kidneys, and while it may decidedly 
 improve the peritonitis, it increases the strain upon the renal organs, 
 and materially interferes with their treatment. The question nat- 
 urally suggested is, " Will the kidneys' epithelium stand this extra 
 strain ?" In very many instances, it will not, but a uraemic tox- 
 aemia is developed, which terminates the case. During such a course 
 of treatment, free diaphoresis and diuresis must be maintained, and 
 the kidneys given every possible chance of accomplishing this extra 
 work. 
 
 The above remarks are especially applicable in connection with 
 1 New York Medical Record, Aug. 25th, 1885. 
 
COMPLICATIONS OK IlKNAL LKKIONX. 
 
 77 
 
 abdominal surgery. It has been found at several necropsies in 
 which death followed an abdominal section, that the incision in the 
 abdominal wall and the intraperitoneal wound was in a state indi- 
 cating a rapid reparative process and not one of a septic nature. At 
 the same time, the patients had died with symptoms which are com- 
 monly classed as septicemic. Close investigation, however, revealed 
 the fact that these toxemic symptoms were due to a rapidly develop- 
 ing acute parenchymatous metamorphosis of the kidneys. In every 
 instance, the bladder contained urine in which albumin and casts 
 were abundant and characteristic of this acute parenchymatous lesion. 
 The microscopic sections made from the kidneys revealed the finely 
 
 Fig. 19.— Acute Parenchymatous Metamorphosis of the Kidney Following a Pro- 
 longed Surgical Operation, x 350. 
 
 A, Collecting uriniferous tubule showing degenerating and desquamating epithelium and a 
 cast in the lumen; a, hyaline cast in the lumen of a collecting tubule; B, intertubular tissue 
 thickened by an cedematous swelling; 6, blood-vessels containing blood-corpuscles in the inter- 
 tubular tissue; c, granular cast in the lumen of collecting tubule; superior extremity finely 
 granular, inferior extremity, or that nearest the apex of the pyramid, coarsely granular; d, e, 
 cast in tubule; d, internal end, coarsely granular; e, external end in a state of fatty metamor- 
 phosis. 
 
 granular metamorphosis common to this form of lesion ; and in many 
 instances casts were found in the lumen of the collecting tubules. 
 
 Clinical observation upon this particular point or lesion has shown 
 quite conclusively that in all major surgical operations, but especially 
 those in connection with abdominal surgery, there is a strong ten- 
 dency to the development of an acute parenchymatous metamorphosis 
 of the kidneys. The evidence of this lesion usually appears on the 
 second or third day after the operation, when the quantity of water 
 
COMPLICATIONS OF RENAL LESIONS. 
 
 decreases, the color deepens, the specific gravity increases, and 
 albumin and casts become more or loss abundant. 
 
 If at this point active treatment be instituted with copious draughts 
 of simple or medicated water, the quantity of urine voided will be in- 
 creased, the albumin and casts will be diminished or disappear, and 
 at the same time the specific gravity will fall: if attention is not de- 
 voted to this condition, and if active treatment is not instituted, the 
 septic symptoms will continue, and the cause of death will be a urse- 
 mic toxaemia. 
 
 Careful observations upon this point were made at the Presbyte- 
 rian Eospital by the late House Surgeon. William W. Sherman. 
 especially for this section, who found in several instances this pecu- 
 liar train of symptoms in connection with severe surgical conditions. 
 
 The case in which Prof. William F. Pluhrer ligated the common 
 iliac, and in which an active renal lesion was developed and con- 
 firmed by the necropsy, is another instance of the same kind. 
 
 The way in which this lesion is produced is as follows: 
 
 First. We have the irritating effects of the anaesthetic, together 
 with the primary shock of the operation, both of which have a strong 
 tendency to disturb the nervous mechanism, and in this way alter and 
 render imperfect the metamorphotic processes of the body, and thus 
 increase the amount and irritability of the effete products to be 
 eliminated. 
 
 The damage to the system which results from the administration of 
 ether is induced as follows: 
 
 The anaesthetic action is principally, if not exclusively, brought 
 about by shutting off from the system the normal quantity of 
 oxygen, which causes the blood to become surcharged with carbon 
 dioxide (CO„). In fact, all the anaesthetics appear to have their chief 
 action in their property to deprive the s} r stem of oxygen, for it is well 
 known to all that anaesthesia cannot be produced so long as the 
 system receives its requisite quantity. 
 
 This diminution of oxygen of necessity interferes with the chemico- 
 physiological metamorphosis o-f the body, decreases or arrests nutri- 
 tion, jDoisons the system, and increases the amount of work to be 
 accomplished by the liver and renal glands. 
 
 Experiments further go to show that ether has the property of 
 destroying the red blood-corpuscles, which is also a damage to the 
 blood, and causes the body oxidation to be less complete, so that the 
 products of tissue metamorphosis to be eliminated are very irritating 
 to the renal epithelium. 
 
COMPLICATIONS OK RENAL LESIONS. 70 
 
 The nutrition of the kidneys at the same time is very much dimin- 
 ished or totally arrested. The nervous system is in a state of partial 
 shock attendant upon the operation. 
 
 In the majority of surgical cases, the duration of the etherization is 
 short, and the operation a slight one. In these the system easily 
 sustains the damage and completely recovers. 
 
 But in the minority, the etherization is prolonged, and the operation 
 severe, or a vital part of the body is implicated. Now the prolonged 
 decrease of oxygen and great increase in carbon dioxide (C0 2 ) in the 
 blood, together with the destruction of the red blood-corpuscles, so 
 impairs the nutrition and elimination of the liver and renal glands 
 that a uraemic toxaemia is developed, the symptoms of which have 
 erroneously been called septicaamic. 
 
 These important facts, substantiated by a large number of necropsy 
 examinations, tend to prove that ether is not a perfectly harmless 
 agent. They also teach that the period of etherization should always 
 be as short as possible, if the greatest success is to be attained. 
 
 The above is not an argument in favor of chloroform, for it has 
 all the dangerous effects of ether, as well as an unavoidably de- 
 pressing effect upon the heart, while ether appears to stimulate this 
 organ, thus enabling the system to withstand its ill effects, except 
 when it is unduly prolonged. 
 
 Second. There is also an increase in the amount of effete material 
 to be eliminated, as a natural sequence to the increased nutritive 
 activity necessary for the reparative process. 
 
 Third. The often unavoidable use of opium for the relief of pain in- 
 terferes with the hepatic functions, and in part closes the excretory 
 apparatus of the respiratory and alimentary tract, especially the 
 latter, and thus forces more work upon the skin and kidneys. For 
 these reasons, the metabolism becomes excessive and incomplete, its 
 products imperfect and very irritating to the excretory organs, and 
 especially so to the renal epithelium. As a result, this acute parenchy- 
 matous metamorphosis is established, followed by the so-called septic 
 symptoms which, in the strict sense of the word, are uraemic, or the 
 result of defective elimination. 
 
 The development of this lesion easily explains many of the " septic 
 symptoms" which are developed within a few hours or clays after an 
 operation, and which quickly, and almost without warning, terminate 
 life. It often happens in these cases that the original wound is appar- 
 ently progressing favorably, there being no suppuration nor anything 
 about it to account for the septic condition. Not infrequently, 
 the urine examined prior to the operation is found to be normal, 
 
J>0 COMPLICATIONS OF RENAL LESIONS. 
 
 while thai taken from the bladder forty-eighl hours after the opera- 
 tion is found to contain albumin and casts in abundance, and sec- 
 tions made from the kidneys always reveal the changes characteristic 
 of an acute parenchymatous metamorphosis of the renal glands. 
 
 These pathological, together with the clinical facts, carefully noted 
 by Dr. Sherman, prove quite conclusively that the above method of 
 development is the true explanation for these cases. 
 
 The urinary changes have been ascribed to the disturbed renal 
 circulation, but it seems more reasonable to attribute them to the dis- 
 turbance of the system at large; and if to any vascular area alone, to 
 that of the liver. For the septic symptoms do not occur immediately 
 alter the operation, but after some hours, or one or two days have 
 elapsed. With acute congestion of the kidneys and total suppression, 
 albumin and casts do not always appear in the urine. 
 
 Having observed and studied a large number of these instances, the 
 theory has been developed that, in all surgical cases having any 
 gravity, the renal organs demand especial attention, and should 
 always be prepared ahead for this severe and extra strain. 
 
 Having established the fact that renal lesions are quite frequently 
 excited b} r severe surgical conditions, it suggests, not only the impor- 
 tance of examining the urine prior to every operation, but shows the 
 great necessity for carefully analyzing the urine daily during the 
 height of every surgical case, and also during the period of convales- 
 cence, if the early development of this class of renal lesions is to be 
 recognized. 
 
 Treatment. — For a few days prior to all severe operations, fluids 
 and non-irritating diuretics should be freely administered, for the 
 purpose of washing out the uriniferous tubules, of improving the nu- 
 trition of the epithelial cells, and of placing them in the best possible 
 condition to accomplish this extra work without becoming seriously 
 impaired. During the height of every surgical condition, the renal 
 organs should receive particular attention, and especially when the 
 ether has to be given for a long time, and still more so if opium has to 
 be freely administered; for it is much easier to prevent than to com- 
 bat the lesion when fully established. 
 
 In treating the peritoneal complication of chronic renal lesions, the 
 above facts must always be remembered, otherwise, by the use of 
 opium, we may add an acute to a chronic renal affection, and render 
 death inevitable. 
 
 (ee.) Phthisis. — Pulmonary tuberculosis may occasionally be asso- 
 ciated with kidney disease. By some, it is thought that it is induced by 
 
COMPLICATIONS OF RENAL LESION'S. 81 
 
 renal lesion. This maybe true, but it is probably quite rare. Its 
 treatment is the same as under ordinary circumstances, and the ter- 
 mination is always fatal. 
 
 (ff.) Pleurisy. — An inflammation of the pleura may be induced 
 by the ursemic condition of the blood, in the same way that the other 
 serous membranes are attacked. The inflammatory process may be 
 acute or chronic ; it, however, is more likely to be of the subacute 
 variety, producing a serous exudation. If the effusion be considerable, 
 it compresses the. lungs, and often produces a very marked dyspnoea, 
 and then acts as a serious complication. 
 
 It may be treated by the various eliminating, agents. A large fly 
 blister over the affected side, with free catharsis and diuresis, will 
 usually cause the fluid to be absorbed, but all three must be used at 
 the same time to secure the desired result. 
 
 (gg.) Pneumonia. — All forms of chronic pneumonia are met with 
 in connection with chronic kidney lesions, but they frequently pre- 
 cede the renal disease, and are not induced by it. Nevertheless, they 
 act as complications when present. 
 
 The acute or lobar pneumonia unquestionably acts as a direct cause 
 in producing an acute parenchymatous metamorphosis of the kidneys, 
 and may be one of the remote causes in producing chronic renal 
 lesions. This form of pneumonia often occurs in connection with 
 chronic kidney disease, but it is impossible to say that it is directly 
 excited by the renal affection, or that these patients are specially pre- 
 disposed to lobar pneumonia. One thing, however, is quite certain, 
 that, whenever it does occur in this connection, the prognosis is 
 always bad. The only method of treatment is free and early cardiac 
 stimulation by the ammonia salts aud alcohol, which should be 
 administered at short intervals, and often in very large doses. iSTo 
 specific dose can be given, but the pulse or heart's action must be the 
 guide. Stimulants should be pushed until the pulse falls in fre- 
 quency and increases in force. Ergot will also be found of service in 
 that it steadies the contraction of the arterioles, and renders the 
 general tension more even. Opium would be more effectual for this 
 purpose if it did not prevent elimination. 
 
 By the above method of medication, and the frequent use of dry 
 cups to the chest and loins, many cases will recover which otherwise 
 would terminate fatally. Warm poultices applied to the loins often 
 aid in keeping the kidneys active. 
 
 Digitalis should be avoided in these cases, as it is apt to cause heart 
 failure. 
 
 (Jilt.) Retinal Lesions. — There mav be a simple retinitis without 
 (5 
 
s _ COMPLICATIONS OF EENAL LESIONS. 
 
 involvement of the optic nervej this, however, is rare. A more fre- 
 queni condition is a retardation of the capillary circulation with a 
 tortuosity of the retinal veins: and a dropsical effusion into the disc 
 tissue (•• choked disc "): with this there may be a secondary inflamma- 
 tory effusion and cellular proliferation, or fattv degeneration with the 
 formation of white elevated spots. There may also he found apoplec- 
 tic extravasations, emboli or thrombi of the retinal veins. These 
 lesions may he followed by atrophic changes in the substance of the 
 retina. All these changes may occur without impairment of vision, 
 but, whenever they are located within the field of vision, there will 
 he Borne impairment of sight. At one time certain lesions of the 
 retina were thought to be almost pathognomonic of renal disease, and 
 were described as albuminuric or nephritic lesions of the eye. 
 
 (ii.) UrcBfnia. — A peculiar train of nervous manifestations is de- 
 scribed under this name. It may be considered as a separate disease, 
 as a set of aggravated symptoms, or as a complication of the kidney 
 lesions. The latter is the one preferred, as uraemia is always second- 
 ary to some renal change, and a new factor invariably comes in 
 between the organic lesion and the uremic symptoms. 
 
 It is this intermediate factor which has given rise to an endless 
 amount of discussion pro et con. 
 
 The diseased conditions in which urasmic symptoms are developed 
 are now pretty thoroughly understood; but the exact nature of the 
 uraemic poison, and the modus operandi between its development and 
 effect, is as comjdete a mystery as ever. 
 
 Many theories have been advanced and as frequently refuted. One 
 fact, however, has been quite thoroughly established, which is, that 
 in every instance there is a diminished quantity of urea in the 
 urine, and at the same time there is not a proportionate increase of 
 the urea in the blood. Neither does the injection of urea into the 
 blood produce uraemia. The toxic consequences, therefore, do not 
 appear to be dependent upon the presence of urea in the blood, but 
 to some other and as yet incompletely defined product of tissue 
 metamorphosis, which the kidneys are not calculated to eliminate 
 from the system as speedily as is required. 
 
 Numerous experimental researches have been instituted, but very 
 little exact information has resulted. 
 
 One condition is pretty generally accepted, however, which is, that 
 urea alone is not the cause of the symptoms. 
 
 Frerichs believed that the decomposition of urea in the blood into 
 carbon dioxide (COJ and ammonium carbonate accounted for the 
 trouble. This idea has been disproved by repeated injections of 
 
COMPLICATIONS OF RENAL LESIONS. 
 
 carbonate of ammonium into the blood without producing any 
 uraemic symptoms. 
 
 The ammonia theory is also disproved by experiments which ; ir<> to 
 show that no urea was present in the blood from which the carbon 
 dioxide and carbonate of ammonium could have been developed. 
 
 Some experimenters believe that kreatin, either alone or in com- 
 bination with some undiscovered and incomplete product of^tissue 
 metamorphosis, is the true excitant. 
 
 Again, Traube advanced the theory that it was purely a mechanical 
 process, clue to an cedema of the brain brought about by a varying 
 blood pressure. 
 
 This also has been proven to be erroneous, the cedema being a result 
 and not a cause. 
 
 Much valuable time has been expended in experimental research, 
 and in developing new and ingenious theories, but as yet the exact 
 irritant has not been defined. 
 
 Until the physiologist or the pathologist, or both with their com- 
 bined efforts, can more clearly elucidate the chemico-physiological 
 changes going on in the body between the introduction of the nutri- 
 tive elements, the tissue metamorphosis, the elimination of the result- 
 ing products, and their action upon the system in their incomplete 
 and intermediate state, the subject must in a measure remain in 
 statu quo. 
 
 From the varied manifestations which are attributable to this form 
 of blood-poisoning, it would appear that they cannot be traced to» 
 any single element. But that there are a number of poisonous sub- 
 stances developed during the tissue metamorphosis and the complete 
 formation and elimination of the urea is undoubtedly true. Depend- 
 ing upon the predominance of one or the other of these irritants, we 
 can easily explain and appreciate the great variety of symptoms classed 
 under this common term. 
 
 The uraemic symptoms are often very indefinite, and too numerous 
 to mention in complete detail. Their onset is very uncertain. They 
 may develop as an indefinite and chronic form, or they may be acute 
 and decisive in their nature from the commencement. In the former 
 case, the symptoms are often vague. 
 
 There may be general or localized muscular twitchings which, in 
 either case, may be milcl or severe from the first. 
 
 The voluntary movements are impaired, uncertain, and sluggish; 
 this is also true in regard to some of the involuntary, especially notice- 
 able in the alimentary tract; the heart is often enfeebled in its action; 
 sight is often dim and in some cases approaches to blindness; tinnitus 
 
84 COMPLICATIONS UF BENAL LESIONS. 
 
 aurium aiid severe headaches are quite frequent. Dyspnoea, nausea 
 and vomiting, diarrhoea or relaxation of the bowels, alternating with 
 persistent constipation, are not infrequent. Active delirium, convul- 
 sions ami coma may close the scene. One or more of this list of 
 symptoms may be the first to appear and persist alone for a long 
 time: or it may be of short duration, and then disappear to recur or 
 be replaced by another, or by a group of symptoms, all of which are 
 produced by these indefinite blood poisons. In this way a very great 
 variety of symptoms are developed in a single case, which often leads 
 to an error in diagnosis. 
 
 These remissions and exacerbations are repeated many times, but 
 as the organic lesion progresses, they become more and more pro- 
 nounced, and terminate the case in an acute exacerbation, or more 
 gradually deepen into coma, to which the patient finally succumbs. 
 
 On the other hand, they are acute and decisive from the very onset, 
 and are divisible, from a clinical standpoint, into three sets of cases: 
 
 (a) Those that commence with severe convulsions, and terminate 
 in them, or rapidly pass into coma, to be followed by death. 
 
 (b) Those in which the coma develop's suddenly, and speedily ter- 
 minates life. 
 
 (c) Those in which the comatose and convulsive stages are more or 
 less intermixed, neither absolutely prodominating. 
 
 (a) The convulsive variety is most frequently met with in connec- 
 tion with the sclerotic and gouty forms of renal disease, although it 
 may occur with any variety. Such an attack may be only an exacer- 
 bation of the chronic state, or it may appear -without any previous 
 warning. If the case has been closely watched, a slight elevation of 
 temperature will be found to precede the attack. In some instances, 
 the convulsions are general, and in this respect closely resemble an 
 epileptic seizure, so that during the attack it is occasionally difficult 
 to differentiate between the two. A careful inquiry, however, into 
 the previous history, aud an examination of the urine will usually 
 decide the question. In other cases, the convulsive symptoms will be 
 limited to certain groups of muscles, and closely simulate tetanus. 
 
 The face in either case is usually blanched, but occasionally it may 
 be flushed over the malar processes; the conjunctiva? may be injected, 
 but more frequently they are pale and glassy; the pupils at first are 
 contracted, but later in the attack, the larger proportion are dilated. 
 The urine is often scanty, and occasionally suppressed. Frothy mucus, 
 sometimes tinged with blood, collects in the mouth and around the 
 lips. The integument is dry or moist, but, as a rule, a strong urinary 
 odor emanates from the body. The expired air frequently has a pecu- 
 
COMPLICATIONS OF RENAL LESIONS. 83 
 
 liar odor, which is known as the uraemic breath. Some cases lo e 
 consciousness completely, while others retain their senses to the 
 last. 
 
 This train of symptoms may last for fifteen or twenty minutes only, 
 or he prolonged for several hours, occasionally terminating in re- 
 covery with no subsequent repetition, but more frequently death 
 occurs at the height of a convulsion, or a fatal coma is developed. 
 
 Uraemic convulsions have to be differentiated from epileptic and hys- 
 terical seizures and apoplexy. From epilepsy they are distinguished by 
 the previous history. There is no initial cry. The pallor and con- 
 vulsions are more marked. Uraemia passes into coma; epilepsy is 
 followed by sleep. The urine in uraemia usually contains albumin; 
 rarely in epilepsy. In uraemia, the convulsions are equal on both 
 sides; in epilepsy, they are more marked on one side. 
 
 From apoplexy, by the hemiplegia which follows the unilateral 
 convulsions. In hysteria, there is often a cry, followed by convulsions 
 and a tetanic or cataleptic condition. 
 
 The pupils, face, and temperature remain normal in hysteria, and 
 the patient is always conscious. The limbs are jerked irregularly, 
 the respiratory movements are spasmodic, and a choking sensation is 
 often noted in hysteria, all of which are absent in uraemia. After the 
 hysterical attack, large quantities of pale urine are voided. 
 
 (b) In the second or comatose variety, the symptoms develop with- 
 out warning, or are preceded by slight cerebral symptoms, such as 
 headache, dizziness, etc., which finally culminate in coma and death. 
 
 This condition may occur at any time during the course of a chronic 
 uraemia. Each variety may be recovered from, and no recurrence 
 follow. But, as a rule, it is repeated, and death follows in coma. 
 Here again a slight elevation of temperature may be detected 
 prior to the outburst. In all forms of uraemia, the temperature may 
 run high or be below normal. The face is usually blanched, the eyes 
 pale and glassy, the pupils contracted or dilated — as a rule, the latter 
 — responding slowly to light. Occasionally a flushed face, injected 
 conjunctivae, and contracted pupils are witnessed. The breath- 
 ing is of a peculiar hissing character, produced by the air striking 
 forcibly against the hard and soft palate; it is not of the deep 
 sonorous character which occurs in connection with apoplectic and 
 opium coma. At first, the respiratory movements are accelerated, 
 but soon they become slow and labored. The pulse is increased in 
 frequency, and weak. The coma at first is incomplete, but at the end 
 of a few hours is absolute, and the temperature falls to or below 
 normal. 
 
86 COMPLICATIONS OF RENAL LESIONS. 
 
 This condition lias to be separated from apoplectic, opium, epileptic, 
 and alcoholic coma. 
 
 The unilateral paralysis of apoplexy is the strongest guide; the face 
 is also flushed and the pulse full and strong. In opium coma, the 
 temperature is not altered, the pulse is full and strong, the face 
 flushed and the pupils .contracted, the breathing slow and stertorous, 
 the reverse being true in uraemia. 
 
 From epilepsy, by the previous history and a urinary analysis. 
 
 Prom alcoholic coma it is often exceedingly hard; for the two are 
 frequently associated conditions. In uncomplicated cases, the history 
 and the strong alcoholic breath in one, and urasmic in the other, would 
 easily determine the difference. The skin is cold and clammy in 
 alcoholic, warm and often dry in uraemic coma. 
 
 (c) In that variety to which the term mixed has been applied, the 
 convulsions and coma are so intermixed that it is often impossible to 
 tell which was primary and which the leading feature of the attack. 
 Further than this, the symptoms which may occur have all been 
 enumerated in describing the preceding varieties. The prognosis 
 and treatment will, of course, be the same. In some instances, the 
 first and only symptom of the uraemic toxasmia is a paralysis of the 
 heart's action. 
 
 The treatment of uraemia must be prompt and energetic. Free and 
 repeated use of pilocarpine, elaterium, and hot-air baths, either dry 
 ■or moist, are in order. The loins should be quickly cupped and fol- 
 lowed by a poultice. Diuretics should be freely administered in the 
 form of digitalis, caffeine, tincture of the chloride of iron, Hoffmann's 
 anodyne, or the spirits of Mindererus. 
 
 A very good diuretic pill is the following: 
 
 J* Caffeini 3 i. 
 
 Pulveris Digitalis gr. zl. 
 
 Slrychninae Sulphatis gr. i. 
 
 M. et fiat massa in pilulas no. xx. dividenda. Sig. One every 
 three hours. 
 
 But for a quick action the following solution will be found very 
 prompt and certain: 
 
 1£ Tincturae Ferri Chloridi 3 ss. 
 
 Spiritus Etheris Nitrosi et 
 
 Liquoris Ammonias Acetatis aa | i. 
 
 Aquae q. s. ad 3 iv. 
 
 M. Sig. 3 ss. in a wineglass of water. 
 
TREATMENT OF CHRONIC DIFFUSE NEPHBITIS. 87 
 
 The bromides and chloral hydrate may be given with advantage in 
 some cases; this is especially true in puerperal uraemia. 
 
 In this form, where the spinal centres arc known to be more or less 
 exhausted, large doses of morphine may be administered with advan- 
 tage, but in most of the. other forms of uraemia it will be followed by 
 unfavorable results. 
 
 The puerperal cases, however, are best treated by general blood- 
 letting, and inhalations of ether and chloroform are occasionally of 
 service. In the more gradual or chronic forms, counter-irritation of 
 the scalp or the nape of the neck is often followed by satisfactory 
 results. 
 
 The use of morphine in the treatment of uraemia does not 
 alw T ays seem to be safe, although this method has some strong 
 advocates; while others tell us that it is demanded if there is reason 
 to believe that the spinal centres are depressed, otherwise it is 
 strongly contra-indicated; unfortunately they fail to inform us how 
 we are to differentiate, in urasmic attacks, between the two conditions. 
 The use of morphine, or any of the opiates, would seem, however, to 
 be contra-indicated. The heart should be well stimulated, and 
 oedema of the lungs carefully guarded against by dry cups over the 
 chest. A further discussion of the treatment would be to repeat 
 what has already been said in treating acute and chronic parenchy- 
 matous metamorphosis and other lesions of the kidneys. 
 
 (jj.) Urmnic Blindness. — This is a complication developed during 
 the course of a renal lesion, in which there is no organic change 
 visible, upon ophthalmoscopic examination, in the optic nerves or ret- 
 inae. The dimness of vision, amounting in some cases to total blind- 
 ness, is due to the poisonous influence of the urasmic poison upon the 
 cerebral optical centre. Permanent blindness may also result from a 
 recognizable lesion of the ocular tunics or nerve. 
 
 In either case, little good results from any form of ophthalmic 
 treatment, unless the original cause can be removed. Iodide of 
 potassium has been highly extolled in these optic diseases; but its 
 efficacy is probably due to the great frequency of latent syphilis in 
 the human race, which is favorably influenced by this salt. The satis- 
 factory results so often obtained from the use of iodide of potassium 
 and small doses of mercury in the various forms of renal disease are 
 unquestionably due to their influence upon this often undetected 
 specific taint. 
 
 Treatment. — As the etiology of the group known as chronic diffuse 
 nephritis is somewhat uncertain, little can be done in a direct line of 
 prevention. This much, however, is known, that all excesses tend 
 
88 TREATMENT OF 0HEONI0 DIFFUSE NEPHRITIS. 
 
 to materially damage, not alone the renal organs, but every portion 
 of the body. This fact is especially true during the period of life be- 
 tween the years of twenty and thirty. Having passed this period free 
 from dissipation, and without any severe form of the acute diseases, 
 the prospect for attaining a very old age without a renal disease is at 
 its maximum. It seems reasonable, therefore, to suppose that re- 
 peated attacks of the acute diseases, which perhaps in themselves 
 produce only a moderate amount of parenchymatous metamor- 
 phosis, nevertheless often pave the way for a chronic diffuse nephritis 
 later in life. Consequently, it is the duty of every physician to pre- 
 vent, so far as possible, the development of all acute diseases, and if 
 they do become established, to guard the kidneys against the extra 
 strain during such attacks. By so doing, the parenchyma of the kid- 
 neys may maintain its integrity, and the patient be protected from 
 the development of a diffuse renal lesion later in life. This in itself 
 will be a great gain in prevention. The chronic form frequently fol- 
 lows the acute, and here much can be done in the line of prevention, 
 by simply avoiding the use of all irritant diuretics, many of which 
 now stand first on our lists and are in daily use. 
 
 As climate is among the ascribed causes, the body should be well 
 protected by woollen garments worn next to the skin; for in this way 
 the sudden atmospheric changes have the least deleterious influence 
 upon the system. 
 
 Cold often interrupts the normal metaraorphotic processes of the 
 body, and at the same time produces visceral congestion; in this 
 way it greatly interferes with a complete proteid metabolism, and 
 •throws increased work upon the renal organs, producing a 
 parenchymatous transformation of the renal cells, or a true inflam- 
 mation of the whole organ. Bearing in mind this chain of events 
 and guarding against them, the development or progress of this 
 lesion may be prevented. In the chronic diffuse variety, although 
 the method of production'is not so clearly defined as in the paren- 
 chymatous group, the epithelial cells are involved and undergo 
 a similar change; but in this lesion the nutrition of the cells appears 
 to be primarily impaired, and the metamorphotic process is secondary. 
 Even here the primary source of the trouble appears to originate in 
 part in an incomplete action of the liver. It maybe only a difference 
 in the degree of the irritant, or it may be a difference in quality 
 which determines the variety. 
 
 In all forms of kidney disease, there is a nervous element to be 
 considered as well as the simple metamorphotic changes resulting 
 from the increased eliminative action. The following mixture is 
 
■ ' TREATMENT OF OHEONIC DIFFUSE NEPHBHTS. 89 
 
 found to meet this indication both in relation to the liver and renal 
 glands. 
 
 r> Tincturae JSTucis Vomica? 1 ss. 
 
 Extracti Damianse Fluidi 3 vi. 
 
 Tincturse Gentians? q. s. ad 1 iij. 
 
 M. Sig. 3 i. ter in die after meals. 
 
 Or the same ingredients may be given in pill form. 
 
 $ Extracti JNTncis Vomicae gr. iv. 
 
 Extracti Damiana? gr. xxxij. 
 
 Extracti Gentianse .... 3 ss. 
 
 M. et fiat massa in capsulas no. xvi. dividenda. Sig. One ter in 
 die after meals. 
 
 This form of nerve tonic stimulates both the motor and sympa- 
 thetic nerves distributed to the liver and renal glands, which, to- 
 gether with the bile pills (page 26) and some form of iron, will, in 
 many instances, cause a rapid and total disappearance of all the 
 rational and urinary signs indicative of a renal lesion. 
 
 The two forms of iron which have been found most efficacious are 
 the tincture of the chloride and the albuminate of iron lozenges, 
 manufactured by Mr. Theodore Angelo, of this city. The latter are 
 especially applicable, furnishing a certain amount of albumin with 
 the iron. 
 
 \ In every case, severe mental or physical strains should be avoided, 
 as they always render a renal lesion worse. 
 
 By carefully observing these laws, there will be the least interfe- 
 rence with the physiological processes, the products to be elimi- 
 nated will be more nearly perfect, and the kidneys will be the more 
 likely to remain normal. 
 
 When the lesion has become fully established, the above rules 
 apply with increased force in each and every particular. To pre- 
 vent the dangers from the sudden changes in temperature, it is 
 well for the patient to winter in a tropical climate. The fact that 
 patients do better in warm climates, and the rarity of renal lesions 
 both in the tropical and arctic zones, is strong proof that sudden 
 change in temperature has a decided influence in damaging the renal 
 organs. , 
 
 The diet of patients suffering from a chronic diffuse nephritis 
 should be composed of the most nutritious materials, and of those 
 substances which are the most easily digested, absorbed, and assimi- 
 lated; so that the products of tissue waste shall be as completely 
 
90 i i;i:a tmkxt of chronic ihi-kuse XKPIIRITIS. 
 
 Formed ami as little irritating as possible to the renal tissues in their 
 passage from the blood to the urine. By these means the nutrition 
 of tin 1 kidneys can be increased, and the destructive processes 
 retarded, it' not absolutely arrested. In this May life will be pro- 
 longed, and in some instances a cure he etl'ectcd. 
 
 All stimulating condiments, excesses in alcohol, or in fact any kind 
 of food or drink which is any way irritating or indigestible should be 
 scrupulously avoided, as they all tend in the one direction — to retard 
 nutrition and irritate the kidneys. 
 
 An exclusive milk, buttermilk, or skim milk diet is found to yield 
 the best results in a majority of cases. Of the latter it is especially 
 true. For the starches, sugars, and fats seem to be the principal fac- 
 tors in preventing a perfect proteid metabolism. It would be natural 
 to suppose that a starch and fat diet, with a limited amount of the 
 nitrogenous elements, would most completely overcome the difficulty, 
 but experience teaches the contrary. 
 
 The hepatic cells in their weakened condition may be capable of 
 transforming a sufficient amount of the albuminoids for nutrition and 
 repair, but when the non-nitrogenous are added, they seem to be the 
 first transformed, the hepatic cells become exhausted, and then the 
 albuminoids are incompletely acted upon, and the renal lesion rapidly 
 grows worse; in this way the action of the two is explained. 
 
 The medicinal remedies which have from time to time been extolled 
 for their curative powers upon these lesions are not easy to 
 enumerate. They have all proved about equally useless, and have 
 little or no effect in directly bringing about a cure, except in so far 
 as they aid in improving the general condition, and thus secondarily 
 producing a reparative action upon the damaged renal elements. 
 
 The treatment of renal lesions, therefore, resolves ttself into three 
 general principles or divisions. 
 
 First, the prevention of all extra strains upon the system. 
 
 This part has been dealt with at length under the heading of pre- 
 vention, and consists in aiding the system to perform the physiologi- 
 cal metamorphotic changes with the least expenditure of force. 
 When this is accomplished, nutrition is raised to its highest standard 
 and the system enabled to produce considerable reparative material. 
 
 In addition to what has already been said, the use of tonics must 
 not be forgotten. The best is the tincture of the chloride of iron, 
 wdiich assists in this result by increasing oxidation, and is also a good 
 non-irritating diuretic. 
 
 Second. The accumulation of the effete and irritating substances 
 in the system. These abnormal products interfere with nutrition 
 
TREATMENT OF CHRONIC DIFFUSE NEPHRITIS. 91 
 
 and the reparative, even if they do not hasten the destructive pro- 
 cesses. Nature, therefore, must be assisted in every way possible to 
 rid the system of these damaging products, which have to be elim- 
 inated largely by the kidneys. 
 
 This is best accomplished by a judicious use of diuretics, diaphore- 
 tics, and cathartics, as detailed on pages 35, 36, and 37. 
 
 Third. The treatment of the complications, as enumerated in the 
 first part of this chapter. This often taxes the physician's therapeutic 
 knowledge to the utmost, baffles every attempt, and quickly termin- 
 ates the case by death. Some of the complications are fatal from 
 their onset. 
 
CHAPTER VI. 
 
 ACUTE AND CHRONIC SCLEROSIS OF THE KIDNEYS; GOUTY 
 
 KIDNEYS; HYALINE, ALBUMINOID, OR WAXY 
 
 KIDNEYS; SUMMARY. 
 
 sclekosis of tiie kldneys. clkkhosis or eed atrophy of 
 
 the Kidneys. 
 
 first form of small kidney. 
 
 Definition. — A sclerotic kidney is one in which the primary lesion 
 is almost exclusively confined to the intertubular tissue, which is very 
 much increased in quantity and infiltrated with new cells. This 
 newly formed tissue contracts and ultimately diminishes the size of the 
 kidneys, • which arc dark in color, their capsules thickened and 
 adherent, and the underlying surface rough and granular. The 
 afferent vessels have their walls thickened and the lumen expanded. 
 There is no active lesion in the epithelial cells, but they are dimin- 
 ished by the pressure exerted upon them by the contraction of the 
 new-formed connective tissue, which ultimately causes them to become 
 atrophied. 
 
 An acute interstitial variety has been described by Professor Edward 
 Delafield. 1 
 
 " This is a rare form of nephritis of which the clinical history is 
 still incomplete. One of its most noticeable features is that the 
 patients may have marked drojisy and other renal symptoms without 
 albumin in the urine. 
 
 "The kidneys are very large and succulent, the capsules are non- 
 adherent, the surfaces are smooth, the cortex thick and whitish. 
 
 " The most marked change is the accumulation of white blood- 
 celJs in the capillary veins, and in the stroma between the tubules, 
 while the epithelium of the tubes is but little altered." 
 
 Etiology. — The cause of this peculiar change, known as the chronic 
 
 1 " Handbook of Pathological Anatomy and Histology," Delafield and Prud- 
 den. William Wood & Co.. 1885, p. 386. 
 
SCLEROSIS OF THE KLDNEY3. 93 
 
 form, has not been clearly elucidated. Homo have given fco it the sumo 
 causes as for chronic diffuse nephritis, but these are unsatisfactory, 
 because they do not explain the absence of the parenchymatous 
 metamorphosis of the epithelial cells. It has been attributed to 
 over-indulgence in alcohol, to rheumatism, cardiac hypertrophy, lead 
 poisoning, etc. But there is no very clear connection in any of these 
 instances, for it is quite as often developed in the absence of 
 them all. 
 
 In many instances, the small forms of the diffuse group have 
 
 ■m 
 
 
 
 Fig. 20. — Acute Interstitial Nephritis, x 850 and reduced. (Delafleld and Prudden's 
 " Handbook of Pathological Anatomy and Histology.") 
 
 undoubtedly been mistaken for sclerotic kidneys. This variety is 
 only coincidently associated with the excessive use of liquor. There 
 are comparatively few typical examples in which the clinical 
 symptoms, the urinary manifestations, and the microscopic exami- 
 nation all coincide; but more frequently what is at first thought 
 to be a cirrhotic kidney proves, clinically and microscopically, to be 
 one of the atrophic forms of chronic diffuse nephritis. The results 
 obtained from the study of a large number of necropsies have 
 
94 SCLEROSIS OF THE KIDNEYS. 
 
 demonstrated thai it is the chronic parenchymatous lesion, if any, 
 which can be directly traced to alcohol in excess. 
 
 The very common occurrence of tertiary syphilis, and its ten- 
 dency to produce chronic thickening, may in a measure account 
 for this lesion, if it is not the absolute cause. 
 
 It has been claimed that this variety is more frequent in females, 
 but no special preference as to sex has been clearly demonstrated. 
 
 Macroscopic Anatomy. — The kidneys are very small, their capsules 
 are thickened and closely adherent to the underlying renal surface, 
 which, as a rule, is reddish in color, rough and often contains small 
 cysts. The cut surfaces show the cortex to be thin and dark in color; 
 
 Fig. 21.— Chronic Interstitial Nephritis. X 350. 
 a, Uriniferous tubules lined by normal epithelial cells; 6, uriniferous tubules from which the 
 epithelium has fallen out in mounting the section ; c, dense fibrillated connective tissue studded 
 with new cells; /, small arteriole thickened by a fibrous deposition known as the capillary fibrosis 
 of Gull and Sutton. The large dark spots represent compressed and atrophied tubules. 
 
 the markings, if perceptible, are wavy, and the pyramids of Malpighi 
 small and indistinct. 
 
 Microscopic Examination shows Bowman's capsule to be thickened, 
 the Malpighian tuft often compressed and atrophied, the interstitial 
 tissue between the tubes decidedly increased, and the walls of the ves- 
 sels thickened and their lumen expanded. The epithelial cells are 
 somewhat altered in character, but the change appears to be one of 
 atrophy, due to the pressure exerted upon them by the contraction of 
 the newly formed fibrillated connective tissue, and not to an irritation 
 caused by the elimination of effete and irritating particles, or the 
 effect of inflammatory exudation, as in the parenchymatous and dif- 
 
SOLEKOSIS OF TIIK KIDNEYS. 
 
 95 
 
 fuse forms. In an advanced stage, the epithelial cells have under- 
 gone complete atrophy, the tubules have collapsed, and developed 
 into connective-tissue bands, which appear under the microscope as 
 fibrillated connective-tissue cords. 
 
 In the few typical examples of this variety of lesion, the atrophic 
 changes were most marked near the apex of the Malpighian pyramids, 
 and diminished from that point to the surface of the organ; but 
 were more advanced at one end of the kidney than at the other. This 
 observation suggested the idea that in this disease, for some unknown 
 reason, the lesion began at one end and gradually swept around to 
 the other, as pulmonary lesions extend from apex to base. If this be 
 true, it would in a measure explain the indefinitenessof the symptoms 
 and the sudden death. 
 
 Section showing thickened and expanded afferent vessel entering Malpighian tuft, the tuft 
 being surrounded by a dense mass of fibrillated connective tissue. The open spaces represent 
 transverse sections of the uriniferous tubules compressed by the new tissue, the epithelial lin- 
 ing having dropped out. X 350. 
 
 What epithelium there is left seems to be capable of accomplishing 
 slowly and less perfectly the work which had been performed more 
 rapidly by the normal kidneys. Some effete material is constantly 
 retained in the blood, and naturally explains the vague nervous 
 symptoms. A time comes, however, when so much of the epithelium 
 has been destroyed that a sudden exposure or excess in diet causes 
 an extra strain upon the already damaged organs, which is more 
 than they are able to meet. They rapidly become overworked, 
 paralyzed, as it were, and stop action; suppression of urine ensues, 
 followed by convulsions, coma, and death, or the last may occur 
 without total suppression. 
 
 Symptoms. — The systemic symptoms are very vague; in many in- 
 
96 SCLEROSIS OF THE KIDNEYS. 
 
 stances, when first seen, the patient Is suffering from a uraemic con- 
 vulsion, or is in deep coma. Occasionally, he may come under obser- 
 vation as a dyspeptic, or suffering from dimness of vision, or with a 
 persistent ami often intractable form of facial neuralgia, or an occipito- 
 frontal headache, or he may have a persistent dyspnoea without any 
 pulmonary lesions. In all cases presenting such symptoms, the urine 
 should be carefully and repeatedly examined. In this way an abso- 
 lute diagnosis can often be made, and the life of the patient prolonged. 
 
 The urine in this variety of renal lesion is always very much in- 
 creased in quantity, and the specific gravity is, as a rule, very low, 
 ranging from 1.010 to 1.005. The large quantity of urine is explained 
 by the h valine or fibroid transformation of the smaller vessels. Al- 
 bumin is rarely found, but occasionally a trace may be detected; this, 
 however, is probably due to the slipping through of some of the 
 unassimalated peptones. Casts are not often seen, and are of no 
 marked significance, but occasionally a small hyaline cast may be dis- 
 covered. 
 
 The diagnostic points are the low specific gravity and the general 
 absence of albumin and casts, all of which persist for weeks, months, 
 or years. 
 
 Prognosis. — This is always a fatal lesion. By an early diagnosis 
 and the proper adherence to certain laws, life may be prolonged for 
 ten, fifteen, or twenty years — perhaps longer. In one case this lesion 
 was known to exist for fifteen years. 
 
 Treatment.— There is no medicinal remedy of any value, unless it 
 be the iodides and mercury. The patient should be made to thor- 
 oughly understand that the duration and usefulness of life depends 
 exclusively upon himself. His diet must be of the most nutritious 
 kind, and one easily assimilated. 
 
 All mental and physical excesses, as well as those of eating and 
 drinking, must be rigidly avoided. 
 
 Exposures of all kinds must be guarded against with an ever watch- 
 ful care. 
 
 This, however, will make life somewhat burdensome, but yields in 
 return a chance for many years of fairly good health, with sufficient 
 power for considerable work. But one thing must be remembered: 
 that a deviation from the above rules is likely to be followed at any 
 time, and almost without warning, by an attack of convulsions ol- 
 eoma, from which they may be rallied, but which are equally liable to 
 terminate in death. This unpleasant issue may also ensue without 
 any apparent cause. 
 
 In some instances, a sudden paralysis of the heart is the cause of the 
 
GOUTY NEPHBITTS. 
 
 '•'7 
 
 fatal issue, and such is the true explanation of the many recorded 
 eases of death due to cardiac disease in which no apparent cardiac 
 i is found at the uecro 
 
 Post-mortem observation in connection with the clinical history 
 clearly demonstrates the fact that in some instances the anemic tox- 
 aemia generates a poison which paralyzes at once, and without any 
 premonitory symptoms, either the heart muscles or its nerve centre, 
 and causes an instantaneous arrest of its function. 
 
 In other instances, a cerebral hemorrhage closes the scene. 
 
 The rupture of a miliary aneurism in the stomach or alimeutary 
 canal is occasionally the immediate cause of death. 
 
 GrOTJTY. XePHBIIIS. 
 FOFETH FOEM OF SMALL KIDXEY. 
 
 Definition.— Kidneys in this 'condition do not differ in any re- 
 
 
 ^mm ■ 
 
 :m 
 
 Fig. 23.— §ectiox fkom a Typical Gorxr Kh»-et. x 350. 
 a. Acicular crystals of sodium urate in the uriniferous tubules: 6. uriniferous tubule, epithe- 
 lium normal: c, fibriHated connective-tissue thickening between the tubules. 
 
 spect from those in the conrdi/tion of sclerosis, except that masses of 
 acicular crystals of sodium urate are seen in the uriniferous tubules. 
 Similar crystals are also found in the urine. ■ 
 
 Excepting that the disease occurs in connection with gout, it does 
 not differ in its etiology.- pathology, symptomatology, prognosis, and 
 treatment from renal sclerosis. 
 
98 AMYLOID OR WAXY KIDNEYS. 
 
 Iii t-ast' the patient with gout should develop one of the forms of 
 chronic diffuse nephritis, and have associated with n a similar depo- 
 sit inn of acicular crystals in the renal substance, it might be classed as 
 
 a gouty kidney. 
 
 This classification of gouty kidney is not a distinct ami separate 
 form, hut is described in this way that the reader may more clearly 
 appreciate its exact position. 
 
 The deposition of the sodium urate crystals is a secondary condition 
 and indicates a gouty habit. 
 
 Hyaline, Amyloid., Waxy, Labdaceous, oe Albuminoid 
 
 Kidneys. 
 
 A FOEM OF LAEGE EED KIDNEY. 
 
 Definition. — The hyaline, amyloid., waxy, or lardaceous kidney is 
 one in winch the vascular walls, and especially those of the Malpighian 
 coil, have undergone a complete albuminoid or amyloid metamor- 
 phosis. Here also the afferent vessel of the tuft has its walls thick- 
 ened and its lumen increased in diameter. As a rule, the walls of the 
 blood-vessels are the only part of the organ attacked. 
 
 It is usually preceded or accompanied by a similar metamorphosis 
 of the liver, spleen, and intestinal tract. 
 
 This form of lesion is rare. Kidneys are often thought to he waxy, 
 but they seldom show any reaction when put to the test. 
 
 Etiology. — The ascribed causes are long-continued suppuration, es- 
 pecially in connection with bone and joint lesions, also phthisis, em- 
 pyema, pyelitis, syphilis, ague, and any obscure cachexia. 
 
 It is an open question, however, whether this hyaline or waxy 
 change ever occurs independently of a syphilitic taint; for it not infre- 
 quently happens that necropsies, made in connection with suppurating 
 bone diseases which have lasted many years, show no waxy change, 
 while a short period of suppuration in connection with syphilis will 
 reveal an extensive waxy transformation in one or more organs. 
 
 From these clinical and pathological facts it seems reasonable to 
 consider the syphilitic taint in connection with a suppurative process 
 absolutely essential for the production of this hyaline or waxy meta- 
 morphosis. 
 
 This change in the vascular walls may occur in connection with any 
 of the chronic forms already enumerated, and consequently is no more 
 a separate and distinct renal lesion than the gouty variety; but usually 
 it is the passive metamorphosis which is associated with the amyloid 
 
AMYLOID Oil WAXY KIDNEYS. 
 
 09 
 
 transformation, and the organs grow larger, and are, as: a rule, dark 
 in color from the albuminoid metamorphosis. 
 
 Macroscopic Anatomy. — Usually the kidneys are enlarged and dark 
 in color. Their capsules are normal and non-adherent fco Hi'; under- 
 lying renal surface, which, after enucleation, is Found to be perfectly 
 smooth, unless this change has been superinduced upon a chronic 
 form of diffuse nephritis. 
 
 The cortex is thickened, and the pyramids of Malpighi are dark 
 and distinct. The Malpighian bodies are also quite dark and promi- 
 nent, usually about the size of millet-seeds. 
 
 a. — 1 
 
 Fig. 24.— Waxy Degeneration of Blood- Vessels of Glomerulus, x 350 and reduced. 
 
 a, The tuft is completely transformed into a waxy mass; 6, portions of vascular loops, waxy; 
 c, vascular loops in normal condition; d, convoluted tubules with swollen, degenerated, and 
 peeling epithelium. (Delafleld and Prudden's "Handbook of Pathological Anatomy and 
 Histology. 1 ') 
 
 Microscopic Anatomy. — The walls of the small vessels of the tufts, 
 and small arterioles outside the tufts, are infiltrated with a substance 
 called albunjinoid material; a change which may involve all the 
 vessels of the kidneys. The afferent vessels are thickened and 
 expanded by this amyloid change in their walls. The thickening 
 and dilatation are quite marked even early in the development, 
 and become more and more marked as the disease becomes more 
 
100 
 
 AMYLOID OE WAXY KIPN l\ 8. 
 
 advanced. Later there may be some increase in the interstitial tis- 
 sue, followed by a fatty infiltration of the epithelial corpuscles. This 
 condition may be developed in conjunction with a chronic diffuse 
 nephritis: in such instances the change is more complex, aud the 
 symptoms are dependent upon the predominating lesion. 
 
 The maeroscopic test for amyloid or waxy transformation is a 
 change in color upon the addition of a solution of iodine to the cut 
 surface of the organ. If this waxy condition has occurred, those 
 portions which are the seat of the amyloid change will turn a dark 
 mahogany color when the iodine solution comes in contact with the 
 affected portion. 
 
 The most delicate test for microscopic examination is the methyl- 
 green, originally described by Curschman.' 
 
 
 &.Y& 
 
 Fig. 2").— Early Stage of Waxy Metamorphosis of the Kidxeys, Stained with Methyl- 
 
 C4reex. X 350. 
 
 a, Transverse section of blood-vessels showing a thickened wall and expanded 'lumen; b, uri- 
 niferous tubule not affected by amyloid change; c, afferent vessel of Malpighian tuft with 
 thickened walls and expanded lumen from waxy change; d, Malpighian tuft showing partial 
 waxy metamorphosis. The darker rings indicate the waxy charge. 
 
 It is best applied as follows: the specimens are soaked for several 
 hours in a two-per-eent aqueous solution of methyl-green, then Mashed 
 in water until the deep-green color commences to assume a decided 
 rose tint; they are then mounted in equal parts of glycerin and water. 
 
 When examined microscopically, this rose color, indicative of the 
 seat of the amyloid change, is found to be confined to the walls of the 
 smaller vessels and those of the Malpighian coil; the intervascular 
 
 Curschman, Archiv f. Path. Anat., lxxix., iii., 1880. 
 
AMYLOID OB WAXY KIDNEYS. 1 OL 
 
 portion or parenchyma remaining green and free from any waxy 
 transformation. 
 
 Symptoms. — These are not marked, and are usually inseparable 
 from those accompanying the exhausting processes in general. Late 
 in the disease, cephalic symptoms may present themselves in the form 
 of a slight wandering of the mental faculties, sometimes reaching to 
 a mild delirium. There is usually diarrhoea, but this is not always 
 marked, unless the vessels of the intestine have undergone the same 
 change as those of the kidneys. There is almost always enlargement 
 of the liver and spleen, but oedema is seldom present, and even 
 then only to a slight degree. 
 
 In all the diseases of the kidneys, the oedema is, in a large measure, 
 directly dependent upon the quantity of water discharged from the 
 body; consequently, when the quantity of urine voided is large, the 
 oedema is slight; but when small, the reverse is true, and general 
 anasarca is frequently developed. 
 
 Diagnosis. — The quantity of urine voided daily is very large, and 
 the specific gravity unusually low, ranging between 1.005 and 1.001. 
 A trace of albumin and hyaline casts may occasionally be found, but 
 both are rare. 
 
 The previous history and the very low specific gravity are the diag- 
 nostic points of the disease. 
 
 Prognosis and Treatment. — There is little or no hope for recovery, 
 unless the cause can be removed; if this can be effected, the kidneys 
 will probably return to their normal condition. This, however, is a 
 hard question to decide, as we have no way of confirming the accuracy 
 of our diagnosis if the patient survives. The prognosis nevertheless 
 rests upon the primary disease, and not upon the renal lesion. The 
 treatment also refers entirely to the primary disease; an improvement 
 in that will of necessity retard the renal lesion, and tend to establish 
 a more normal condition of the kidneys. 
 
 If, on the other hand, the syphilitic taint be the chief and deter- 
 mining cause, a strict anti-syphilitic line of treatment should be 
 insisted upon, and the number of amyloid kidneys met with will 
 then be less frequent. 
 
 Summary. — The foregoing classification of renal lesions is not 
 wholly new, but its modification and presentation in this concise 
 pathological and clinical form is the result of a careful study of a 
 large number of clinical cases, and the pathological data furnished by 
 several hundred necropsies. 
 
 Each lesion is believed to be separate and distinct from the com- 
 
102 AMYLOID OK WAXY KIDNEYS. 
 
 mencf men! ; there is not first a parenchymatous enlargement, followed 
 by a contraction or cirrhotic stage, as formerly taught. 
 
 The chronic parenchymatous group may need a word of explana- 
 tion, as ii resembles the chronic diffuse variety in some respects, hut 
 a careful analysis of the clinical and urinary symptoms, as well as the 
 microscopic changes, clearly establishes its identity as a separate and 
 distinct class. A long-continued lesion of the epithelial cells must, 
 of necessity, produce some change in the intertubular tissue, but from 
 the method of its production, and the fact that the major part of the 
 lesion i- primarily in the epithelial cells, and not of inflammatory 
 origin, it is established as a separate and distinct group. It has been 
 frequently, but wrongfully, classed as a diffuse lesion. 
 
 The same holds true in reference to the sclerotic type, for the 
 primary lesion originates in and is principally confined to the inter- 
 tubular tissue, while the epithelial cells suffer a slight change, but 
 3 T et this should not be classed as a diffuse lesion. 
 
 By an observation of the principles laid down for each, repre- 
 sentative cases have been repeatedly diagnosticated at the bedside, 
 and in over a hundred consecutive cases, the necropsy has con- 
 firmed the diagnosis. Most of the drawings illustrating the differeut 
 lesions are from sections made from these cases. 
 
 By some, chronic congestion would be included in the class com- 
 monly called Bright's: but it is here omitted, as it is generally con- 
 ceded that it does not give rise to albumin aud casts until structural 
 changes have been developed in the epithelial cells or intertubular 
 tissue, or both; then we have one of the lesions already enumerated. 
 In this light the chronic congestion becomes a cause of renal disease, 
 and in no sense an intrinsic kidney lesion. 
 
 This arrangement in part duplicates some of the lesions, but from 
 their clinical differences, they appear to deserve this distinct multi- 
 plicity. 
 
 This classification is based upon the more recent theory that the 
 kidney progressively enlarges or decreases in size from the inception 
 of the disease until its termination, and not upon the old idea of pro- 
 gressive enlargement followed by rn'ogressive diminution in size. A 
 careful study of the clinical symptoms in connection with the necropsy 
 findings clearly demonstrates the identity of each of these varieties. 
 This classification is based upon the study of several hundred post- 
 mortem examinations, in which more than one hundred had one of 
 the active forms. 
 
 It should always be remembered that the exact kind of lesion can- 
 
AMYLOID OK WAXY K 1 1 >N K V 8. 1 03 
 
 not be determined by one analysis or a single sign or symptom, but 
 only by an accurate appreciation of the causation and method of pro- 
 duction, together with an analytic study of the clinical history and the 
 sum total of the results of several examinations of the urine. When 
 this is accomplished, the exact variety can be determined with a won- 
 derful degree of precision, and the size and the exact condition of the 
 kidneys predicted with an astonishing accuracy. 
 
 For the large number of distinct renal lesions that can be recog- 
 nized during life, as well as at the necropsy, the term Bright's dis- 
 ease no longer seems appropriate; but if it is desirable in honor of the 
 discoverer to still retain his name, it would be better, as Prof. Andrew 
 H. Smith and others have suggested, to speak of the class as Bright's 
 diseases, as there is no longer a Bright's disease. 
 
 By this arrangement it is quite evident that the quantity of albumin 
 discharged with the urine, in renal lesions proper, bears a direct rela- 
 tion to the amount of retrograde change in the epithelial protoplasm. 
 When this epithelial metamorphosis is slight, the quantity of albumin 
 is small; but when the epithelium is extensively implicated, its 
 amount is large. Although the physiologists teach that albumin 
 makes its escape through the vascular walls of the Malpighian coil, 
 its transudation in connection with the renal diseases appears to 
 be directly dependent upon the integrity of the epithelial cells. 
 When the epithelial metamorphosis is extensive, there is a large 
 amount of effete material retained in the blood, which, together 
 with the cause of the kidney disease, greatly impairs the nutrition 
 of the wall of the vessel composing the Malpighian tuft. It loses its 
 power to hold the serum albumin within its lumen, and it is forced 
 through into the uriniferous tubule with the water. With a slight 
 retrograde change, less effete material is retained, the walls of the 
 blood-vessels retain a higher degree of integrity, and prevent so large 
 an escape of albumin. 
 
 The quantity of urine discharged also is in direct relation to the 
 change in the afferent vessels of the Malpighian coil; for in every 
 lesion where this afferent vessel of the Malpighian coil has a thickened 
 wall and an expanded lumen, the quantity of water discharged is con- 
 stantly large, but in all those lesions in which the afferent vessel 
 remains unaffected, the quantity of urine discharged is invariably 
 normal or more often perceptibly diminished. The diabetic parenchy- 
 matous metamorphosis will be discussed in detail in the chapter 
 •devoted to that disease. 
 
1(4 
 
 AMYLOID OK WAXY KIDNEYS. 
 
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CHAPTER VII. 
 
 RENAL HEMORRHAGE. H,EMATOGLOBINURIA. ANAEMIA. 
 RENAL HEMORRHAGE. 
 
 Hemorrhage from the kidneys cannot be classed as a distinct dis- 
 ease, dependent, as it is, npon so many- other renal affections which 
 usually have marked symptoms of their own. But it is often desir- 
 able, especially in medico-legal cases, to differentiate between it and 
 hemorrhage from other parts of the genito-urinary tract. 
 
 Etiology.- — The causes of renal hemorrhage are quite numerous. 
 They are cancer, sarcoma, tubercle of the glands, suppurative neph- 
 ritis, irritation of crystals, acute diffuse nephritis, purpura hemor- 
 rhagica, scorbutus, scurvy, pernicious anasmia, leucocythaemia, erup- 
 tive fevers, yellow-fever, phthisis, parasites, acute and chronic con- 
 gestion, injury with or without rupture of the renal substance, 
 embolism and thrombosis of the renal vessels, and infarctions. Over- 
 doses, and sometimes even large doses, of certain medicines such as 
 turpentine, cantharicles, squills, and all forms of irritating diuretics, 
 are liable to produce this result. 
 
 Pathological Anatomy and Symptoms.— No pathological changes 
 are developed in the kidneys which cannot be referred to the exciting 
 or irritating agent. Under the microscope, blood will be found in the 
 uriniferous tubules, and the blood-vessels will be congested. The 
 changes due to whatever disease it may complicate will also be observed. 
 
 The symptoms also are those of the cause, and previous to death 
 the urinary manifestations only can be relied upon for a positive 
 diagnosis. The urine is red in color, the density of the shade de- 
 pending upon the quantity of blood contained. The reaction is 
 usually alkaline; albumin is present, and the specific gravity is high. 
 
 When examined by the microscope, varying quantities of blood-cor- 
 puscles and blood-casts are present. All of these symptoms, except 
 the presence of blood-casts, may appear in the urine without the" 
 hemorrhage being necessarily renal in origin. But if blood-casts 
 are found, and especially if numerous, some of the blood at least can 
 be positively asserted to have come from the kidneys. Nephritic 
 
106 ll.KM()i;i.oi;iMi;iA. 
 
 hemorrhage, on the other hand, may also occur, and blood-casts be 
 absent in the urine; in such a rase, a positive diagnosis is impossible. 
 Therefore, in a medico-legal case, it would be impossible to say that 
 the blood did not come from the kidneys, in the absence of these 
 blood easts. Hut when blood-casts are found in the urine, a positive 
 assertion regarding the source of the blood can be made. 
 
 Prognosis. — In itself tins affection is not serious, but it always 
 renders the prognosis of the exciting disease or injury more unfavor- 
 able. 
 
 Treatment. — Little or nothing can be done in the way of treatment, 
 excepl that which may be indicated by the cause. Ergot in small 
 and repeated doses is of service, if not contra-indicated by some other 
 condition. The same is true of gallic acid; this, however, is liable to 
 produce temporary retention, which is always an objection to its use 
 as an internal hemostatic. 
 
 The hemorrhage, however, except in traumatic injuries, is rarely of 
 sufficient importance by itself to necessitate any special or independent 
 treatment. 
 
 HEMOGLOBINURIA. 
 
 Definition. — Hemoglobinuria is a condition in which dark-colored 
 urine which contains haemoglobin, with but few, if any, blood-corpus- 
 cles, is excreted by the kidneys. There may be only one attack, or 
 there may be several which follow one another with a certain degree 
 of regularity. It is then known as periodic hemoglobinuria. 
 
 Etiology. — This is still a mooted question. This kind of urine has 
 been met with in connection with a number of dissimilar conditions, 
 which naturally renders its actual causation extremely doubtful. It 
 has made its appearance after muscular exertion, as recorded in the 
 case of soldiers after a prolonged march, and occasionally after other 
 forms of muscular fatigue; after mental excitement in connection with, 
 or as a sequel to, various diseased conditions, viz. : malaria, syphilis, 
 rheumatism, malignant and septic fevers, putrid and typhus fever, 
 purpura, scurvy, phthisis, etc. After the use of, or poisoning by, 
 naphthol, pyrogallic acid, arseniuretted hydrogen, carbon anhydride, 
 chlorate of jsotassium, etc. The precise relation of cold as a causative 
 agent is yet uncertain, although there is considerable proof in favor of 
 its acting as a secondary excitant, if not as a direct cause. 
 
 The theory of Ponfick appears quite rational, 1 viz., that a condi- 
 tion of hemoglobinuria is produced by or is attributable to a destruc- 
 
 1 Berliner Klinisehe Wochensclnift, No. 26, 1883. 
 
HEMOGLOBINURIA. 107 
 
 tion of the red blood-discs; that this condition is divisible into three 
 forms, dependent upon intensity and in which the corpuscular debris 
 is disposed of in as many different ways. In the first or mildest form, 
 the detritus accumulates in the spleen, which causes an enlargement of 
 that organ. 
 
 In the second or intermediate degree, the liver secretes an excessive 
 quantity of bile (hypercholia), and in this way relieves the system. 
 
 In the third or severest form, the corpuscular debris is excreted 
 from the plasma of the blood by the epithelium of the kidneys, and 
 gives rise to the condition known as hsemoglobinuria. 
 
 The enumerated causes certainly point in this direction. 
 
 If this theory be true, it offers a very rational and satisfactory ex- 
 planation for the unusually high-colored urine in pneumonia and the 
 : severe forms of blood diseases. It would appear, therefore, that a par- 
 tial hsemoglobinuria, resulting from the destruction of the red blood- 
 discs, is the true explanation of the high-colored urine. 
 
 The hepatic portion of this theory also affords a tangible reason for 
 the icterus in this class of diseases. 
 
 The splenic portion of the theory explains the universal enlarge- 
 ment and the metarnorphotic changes so generally met with in con- 
 nection with that organ. 
 
 The renal portion explains the development of this peculiar urine, 
 and accounts for the precise changes in color with every fluctuation 
 of the acute diseases. 
 
 Pathological Anatomy. — The necropsies that have been made upon 
 persons who have died, during an attack of acute or periodic hsemo- 
 globinuria, have been so few that nothing positive has been deter- 
 mined concerning this condition. If the above assumptions be true, 
 little would be expected in the way of change in the organs. We 
 would naturally expect to find a parenchymatous transformation in 
 the glandular organs, and this may be one grand cause in producing 
 these changes. It is certainly reasonable to believe that destruction 
 of the red blood-corpuscles takes place in some part of the body, and 
 that this destruction, in quite a number, if not in the majority, of 
 the cases, is directly excited or influenced in some way by undue ex- 
 posure to cold. 
 
 It has been suggested that there must be a condition of the nervous 
 mechanism, by which it either does not permit of a healthy formation 
 of the red corpuscles, or is so markedly sensitive that it affects these 
 elements of the blood. 
 
 The very fact that certain chemical and medicinal agents, when 
 hrought in contact with the blood-discs, rapidly decompose them, 
 
L08 H.KM-K.l.olUNlKIA. 
 
 and the association of this disease or change in the urine with many 
 of the acute blood diseases, points strongly to some blood poison. 
 whatever it may be, as the agenl which excites the destruction of the 
 red blood-corpuscles and causes the appearance of the haemoglobin in 
 
 the urine. The observations of Boas and others make it possible that 
 the destruction of the red blood-discs takes place in those parts of the 
 body which are most exposed to the severe action of these elements. 
 Tlir whole Bubject, however, aside from its occurrence, is somewhat 
 in a state of uncertainty. 
 
 Symptoms, — The attacks may not be paroxysmal, hut in the majority 
 of instances they are; hence the name paroxysmal hemoglobin- 
 uria. They begin with a slight chill or shivering sensation, followed 
 by a rise in temperature, which in one recorded case rose to 103° F., 
 or 39.4° C; and in another to 104° F., or 40° C. As the paroxysm 
 subsides, the temperature falls, and in this respect it simulates the 
 malarial diseases. The urine voided during the attack, or early in 
 its subsidence, is found to contain albumin; a little later, the urine 
 passed is dark in color, resembling port wine, or even of a deeper 
 hue. At the end of a few hours it will have returned to its normal 
 color and composition. In other cases, this peculiar urine persists for 
 several days, or even weeks. 
 
 Microscopical Examination. — Very little that is abnormal is found - 
 in some, a few blood-corpuscles are detected; while in other samples, 
 they are entirely absent. Occasionally, a few hyaline casts may be 
 found, but their occurrence is exceedingly uncommon. By a spectro; 
 scopic analysis of the urine, every evidence of haemoglobin will be 
 found. This, however, is not a practical test for the general practi- 
 tioner. 
 
 Its presence may also be ascertained by Heller's or the guaiac test, 
 see section on blood. 
 
 In some of the recorded cases, there has been a recurrence of these 
 attacks at varying intervals for a long period. In one, the patient 
 was closely observed for several years. He was subjected to cold 
 foot baths, which invariably and quite rapidly brought on a recurrence 
 of the symptoms. These urinary changes have been thought to take 
 the place of a malarial chill. 
 
 Only one case in which the symptoms in any way approached this 
 condition has been directly observed, but opportunities have offered 
 for the examination of several samples of the urine from such patients. 
 In the instance cited, the urine looked bloody; but compared with its 
 color and general microscopic appearances, it contained so few of the 
 
ANiEMIA OF THE KIDNET8. L09 
 
 red blood-discs, that practically it might he said that there; were hoik; 
 present. 
 
 Several times the question has been asked: "How would you ac- 
 count for black urine, without any other symptoms resembling a 
 malarial attack, in persons suffering previously from malaria, and in 
 whom the voiding of this kind of urine appeared to replace one of 
 the paroxysms ?" 
 
 This query has most frequently come from physicians practising in 
 decidedly malarial sections of the eountry and they must have been 
 instances of hemoglobinuria. 
 
 As a spectrum analysis is not very convenient or practical, and the 
 chemical tests are somewhat uncertain, the examination is often 
 negative. 
 
 Satisfactory methods for the detection of haemoglobin cannot always 
 be instituted to confirm the diagnosis. But the sudden discharge of 
 such dark urine, and an absence of the red blood-corpuscles when ex- 
 amined microscopically, would warrant the diagnosis of this trouble. 
 Carbolic-acid poisoning occasionally causes the discharge of black or 
 very dark urine, but the two could hardly be confounded. It is pos- 
 sible that the dark urine of carbolic-acid poisoning is only a form of 
 hemoglobinuria produced by the action of this acid. 
 
 Prognosis. — So far as this symptom is concerned, there appears to 
 be no immediate danger, as very few cases are recorded in which the 
 patient died at the time of the attack. 
 
 Treatment. — This depends largely upon the pre-existing condition. 
 If traceable to a malarial origin, quinine or some of the cinchona 
 alkaloids, as in all miasmatic affections, will yield the best results. 
 When attributed to a syphilitic taint, the combined use of mercury 
 and the iodide of potassium offers the best prospect of recovery, and 
 naturally tends to prevent recurrence. 
 
 In connection with the acute blood diseases, no special treatment is 
 called for, further than that of the general disease with which it is 
 associated. When there is a tendency to recurring attacks, all exposure 
 to cold and sudden changes in temperature must be avoided. Warm 
 woollens must be worn next to the skin, and this is especially true with 
 regard to the winter season. The general nutrition should be improved 
 by chalybeates, tonics, good food, and pure air. 
 
 ANEMIA OF THE KIDNEYS. 
 
 Definition. — This is a condition of the kidneys in which the organs 
 are found to be extremely pale, and the vascular areas devoid of blood. 
 
110 A.VKM1A OF THE KIDNEYS. 
 
 Etiology. — This abnormality is caused by pernicious anemia, pur- 
 pura hemorrhagica, Leucocythsemia, excessive haemorrhage cither ex- 
 ternal or internal, and with wasting diseases in general. 
 
 Macroscopic Anatomy. — The kidneys remain about normal in size. 
 The principal change is the extreme pallor, both of the cortical and 
 the medullary portion. 
 
 Microscopic examination shows the capillaries free from blood and 
 empty, and the epithelial cells arc pale and granular. 
 
 Symptoms. — There are none specially referable to the kidneys, but 
 those of the condition with which it occurs. 
 
 Its treatment is that of the condition by which it is produced. 
 
CHAPTER VIII. 
 
 ACUTE CONGESTION. CHRONIC CONGESTION. 
 
 Acute Hyperemia of the Kidneys, 
 determination of blood to, or acute congestion of the 
 
 KIDNEYS. 
 
 Definition. — Hyperemia of the renal glands may be due to the 
 determination of more blood to the kidneys than the normal quantity, 
 or it may be due to a temporary obstruction which prevents the venous 
 return. 
 
 Iu the variety which is commonly called acute congestion, there is 
 an abnormal influx of arterial blood, and a consequent dilatation of 
 the arterial capillaries from the cardiac side. 
 
 Etiology. — Acute congestion may be caused by irritation or par- 
 alysis of the vaso-motor nerves, by acute inflammation of the kidneys; 
 the blood-poisoning of various diseases, as in scarlet fever, small-pox, 
 measles, etc. (if a marked parenchymatous metamorphosis is not 
 developed), or by a diffuse nephritis; exposure to cold, and in malarial 
 attacks. With the last, congestion is very marked in the kidneys as 
 well as in the other visceral organs. It is also produced, by irritating 
 diuretics, such as cubebs, copaiba, turpentine, cantharides, potassium 
 nitrate, etc., and by carbolic-acid poisoning. Digitalis practically 
 produces acute hyperemia, like cold, by increasing the general 
 systemic and diminishing the renal tension, and in this way an 
 increased volume of blood is forced upon the kidneys. This is the 
 true explanation for the diuretic action of digitalis. But it only acts 
 well when there is slight obstruction in the intertubular plexus. Con- 
 cerning vaso-motor paralysis as a cause, its exact modus operandi is 
 not clearly explained; but with the high arterial tension of the general 
 arterioles outside of the splanchnic arcade, there appears to be a corre- 
 sponding dilatation of the renal arterioles, and certain drugs appear 
 to cause a dilatation of the splanchnic arcade and not of the arterioles 
 in general. Diabetes insipidus and polyuria are both instances asso- 
 ciated with renal vaso-motor paralysis. 
 
1J2 
 
 ACUTK HYPEREMIA OK THE SIDNEYS. 
 
 Pathological A mil mini. Macroscopic Appearances. — The kidneys are 
 normal in size, or slightly enlarged; their capsules are not thickened 
 nor adherent to the underlying renal suface, which is smooth and 
 dark in color. The cnt surfaces also are darker than normal. The 
 epithelial cells of the cortex and pyramids arc unchanged, except in 
 color, which is deepened. The renal substance is abnormally soft, 
 and the vessels arc engorged with blood. Throughout the cortex 
 dark-red points are plainly visible to the unaided eye. and represent 
 the location of congested Malpighian tufts. Bloody serum often 
 exudes from the incisions made in its substance. 
 
 
 
 A 
 
 Fig. 26.— Acute Renal Congestion with Infarctions. 
 A, Pyramidal portion deeply congested; B, cortical portion deeply congested; a, occluded 
 vessels; 6, Malpighian corpuscle congested. 
 
 Microscopic examination shows the blood-vessels to be distended 
 with blood, which is principally located in the arterial side and in the 
 capillary loops of the glomerulus, the walls of which, in some instances, 
 have given way and permitted of small extravasations within Bow- 
 man's capsule, the effused blood passing into the uriniferous tubules. 
 Extravasations may also occur from the small vessels before the tufts 
 are reached, but this is the exception. Occasionally a tubule may be 
 found that is packed full of red blood-corpuscles for a considerable 
 distance, or they may contain hyaline plugs or casts. All these changes 
 
ACUTE HYPEREMIA OF THE KIHNEYS. 113 
 
 .are sometimes present in it single field. Some of the epithelial cor- 
 puscles are a little opaque, but the change in their protoplasm is not 
 marked, and rarely reaches the condition known as cloudy swelling. 
 
 Ecchymotic spots are sometimes found in the pelves of the kidneys. 
 
 Symptoms. — The general or rational symptoms will be those of the 
 exciting disease rather than those which are directly referable to the 
 renal lesion proper. In that form traceable to cold or irritating 
 diuretics, the disease may be ushered in by a chill or strangury, great 
 pain in the loins and hypogastric region, and some febrile movement, 
 associated with or followed by almost, if not total, suppression. The 
 condition of the urine is the diagnostic element. Urinary Examina- 
 tion. — The urine will be diminished in quantity, high colored, with an 
 increased specific gravity, and it will contain blood and albumin, or 
 both may be absent. Under the microscope, blood and blood-casts 
 and hyaline casts will usually be found; also, an abundance of the 
 urates. These symptoms may last for a few hours only, or be pro- 
 longed for several days and finally terminate in recovery, or degener- 
 ate into a more chronic form of renal lesion. The albumin in this 
 disease comes largely from the blood-corpuscles, or is forced through 
 by mechanical pressure. The presence of blood in the urine is not 
 diagnostic, for urine which does not contain blood-casts cannot be 
 said to come from the congested kidneys, however marked the other 
 symptoms may be. On the other hand, congestion, even with suppres- 
 sion, can and does occur, and neither blood nor albumin are found in 
 the urine; such cases are somewhat rare but severe when they do 
 occur. As the congestion subsides, the first urine passed will be 
 heavily loaded with urates, but does not contain albumin or casts. 
 
 Prognosis. — In this form the congestion usually subsides sponta- 
 neously, the prognosis being almost always favorable. There are, 
 however, instances, especially those produced, by malarial poisoning 
 or some irritating diuretic, in which the functions of the kidneys are 
 entirely arrested, and if not speedily relieved, the patient will die 
 from suppression and the consequent uraemia. 
 
 Treatment. — This must be more or less vigorous, depending upon 
 the severity of the attack. In some cases, none will be necessary; in 
 others, rest in bed will be all that is required. Dry or wet cups should 
 be applied to the loins, to be followed by a warm poultice. A drastic 
 cathartic is always in order, ten or twenty grains (0.6 gram, 1.4 
 gram) each of calomel and jalap is one of the best. If a relia- 
 ble preparation of elaterium can be obtained, it is better than the cal- 
 omel and jalap. It should be used in one-eighth grain (0.008 gram) 
 doses, every fifteen or twenty minutes, until three-fourths of a grain 
 
114 mriKKMlA OF THE KIDNEYS. 
 
 (0.018 gram) have been given, or the intestines have commenced to 
 move. After the attack has reached its height, and there is a fall in 
 the blood tension, digitalis is to be nsed freely, and in full doses. As 
 there is apt to be nausea or vomiting, and difficulty in retaining any- 
 thing in the stomach, the tincture will be found the most reliable. 
 This preparation maybe given in ten minim (0.G c.c.) doses every 
 tli roe hours, until the renal secretion is started, and then less fre- 
 quently. 
 
 In cases threatened with uraemic convulsions and coma, a full dose 
 of pilocarpine, administered hypodermatically, will be necessary to 
 prevent impending death. By a judicious administration of these 
 medicinal agents, a case of uncomplicated renal congestion will sel- 
 dom prove fatal; but, if superimposed upon a chronic kidney disease, 
 the best directed remedies will many times prove inadequate. 
 
 Hyperemia of the Kidneys, 
 passive or chronic congestion of the kidneys. 
 
 Definition. — Hyperemia of the kidneys is an active or passive con- 
 dition, the latter having an acute or chronic character. 
 
 In the active, there is an abnormal influx of arterial blood to, and a 
 consequent dilatation of, the arterial capillaries ; but in the passive 
 congestion, there is some obstruction to the venous current, which 
 prevents the normal escape of blood from the kidneys, and causes an 
 engorgement of the renal veins. 
 
 Etiology. — This lesion is purely mechanical in origin. It is often 
 due to some lesion of the heart, especially pulmonary insufficiency, 
 mitral stenosis or regurgitation, more often the latter, fatty degene- 
 ration and dilatation or endocarditis — in fact, all conditions in which 
 there is an interference with the cardiac and pulmonary circulation, 
 which forces the blood back upon the general venous circulation. 
 Occasionally it is associated with adhesive pericarditis, or an exten- 
 sive hydropericardium. The following diseases of the lungs will 
 produce it, viz., emphysema, chronic interstitial pneumonia, pleurisy 
 with effusion, also aneurisms of the aorta, and tumors of the medias- 
 tinal spaces or abdominal cavity, which press upon the inferior vena 
 cava above the renal veins. Tumors pressing upon the pulmonary veins 
 act in like manner. 
 
 The gravid uterus is another cause of a temporary form of chronic 
 congestion of the veins of the kidneys. 
 
 Thrombosis of the inferior vena cava or renal veins may be included 
 among the causes. 
 
HYPEK^MIA OF THE KIDNEYS. 115 
 
 Pathological Anatomy. Macroscopic Appearances. — In this, the 
 chronic form, the kidneys maybe smaller, of the ordinary dimensions, 
 or considerably larger than normal, the latter being: the rule. A pe- 
 culiar feature is their extreme hardness, which has been called a 
 " stony hardness." The capsules of the organs are about normal in 
 thickness, and non-adherent to the underlying renal tissue, which i& 
 usually quite smooth after enucleation. 
 
 It may occasionally appear lobulated, but this is due to remnants of 
 the foetal lobules becoming more apparent by the congestion and en- 
 largment. The stellar veins of Verheyen are remarkably prominent. 
 The cut surfaces have a succulent appearance, but in reality are quite 
 firm. Both the cortical and medullary portions are dark in color, and 
 this is more marked in the pyramids than the labyrinth; the mark- 
 ings of the latter are sharply defined and straight. The Malpighian 
 bodies are quite prominent, but not so decided as in the acute form. 
 
 Microscopic Examination. — The veins are found under the micro- 
 scope to be very much congested, but now the engorgement is most 
 marked in the large veins and interlobular plexuses, the tufts and 
 arterial capillaries being comparatively free. The epithelial cells of 
 the tubules are moderately swollen, opaque, approaching toward a 
 granular transformation, and by their enlargement often diminish 
 the lumen of the tubules both in the medullary and cortical portions. 
 This change is most easily recognized in the straight and collecting- 
 tubules as a distinct lesion; the lumen often contains hyaline plugs 
 resembling casts. This cast-like substance is seldom, if ever, found 
 in the convoluted tubules. There does not appear to be any inflam- 
 matory new formation in the interstitial tissue, but the change ap- 
 pears to be a nutritive one, by which more material has been brought 
 to the organ than is absolutely required. As a consequence, the sub- 
 stance of the glands absorbs these nutritive elements in abnormally 
 large quantities and hypertrophies, without the intervention of any 
 truly inflammatory process. An inflammatory action may at any time 
 be engrafted upon this lesion. This is more likely to be the case 
 than if the organs were normal. Bowman's capsule, and in fact every 
 part, may be thickened. This condition has been considered as one 
 form of that large list usually classed under the common term Bright's. 
 But, as already stated, it is, more strictly speaking, a direct cause of 
 the renal lesion. 
 
 Symptoms. — Aside from the urinary indications, there are no 
 definite characteristics by which this disease can be diagnosticated. 
 Such cases present a large variety of symptoms, all of which, however, 
 are directly traceable to the pre-existing lesion, which is producing 
 
116 HYPEREMIA OF THE KIDNEYS. 
 
 the kidney trouble. Associated with these we find positive alterations 
 in the urine, which readily indicate the true nature of the disease. 
 
 Diagnosis. — With chronic obstruction to the venous return, the 
 oedema will first appear in the lower extremities, and gradually work 
 up to the large serous cavities and superior extremities; while in 
 primary renal disease the oedema is first noticed under the eyes, and 
 later in the extremities. 
 
 Urinary Changes. — With chronic congestion we find the urine very 
 much diminished in quantity, with a high specific gravity, 1.025 to 
 1.030 or higher; of a very dark color and often heavily loaded with 
 urates. Albumin and blood-corpuscles are quite common, and occa- 
 sionally blood-casts are present. The quantity of albumin is usually 
 small, and this may be accounted for in two ways. It may be due to 
 an incomplete metabolism of the proteids, and a filtration of the undi- 
 gested albuminates, and to mechanical pressure which is very greatly 
 increased by the venous obstruction; as the pressure rises and. the 
 metamorphotic changes in the epithelium become more extensive, the 
 amount of albumin in the urine increases. Casts are infrequent, but 
 occasionally a small hyaline, a finely granular, or blood-cast, may be 
 present; still more rarely a fatty cast can be added to the list. The 
 blood-cast, however, is the only variety which is positive evidence that 
 the blood originated in the kidneys. The diminution in the quantity 
 of urine will progressively grow less until a condition, similar to acute 
 suppression, is developed. This will often give rise to a uraemic at- 
 tack, which, if not immediately relieved, will cause death either in 
 convulsions or coma. 
 
 The kidneys, thus constantly impaired, are quite likely upon the 
 slightest provocation to become the seat of a more acute process. 
 Necessarily, therefore, excesses in eating or drinking, severe attacks of 
 indigestion, or a sudden yet moderate exposure to cold, will often ex- 
 cite an acute congestion or inflammation of the renal glands. In this 
 way, the acute exacerbations which frequently occur, and in which 
 there is a discharge of bloody urine, are explained. The urine will 
 now be small in quantity, highly albuminous, and contain epithelial 
 and blood-casts, often in abundance. Exacerbations occur frequently, 
 until finally they prove fatal. During the remissions, the casts will 
 entirely disappear, and often only a trace of albumin continues, but 
 the quantity of urine usually remains small, high colored, and of high 
 specific gravity. 
 
 Prognosis. — Naturally this depends, first, upon the severity of the 
 primary disease and the influence of treatment; second, upon the fre- 
 quency and the severity of the acute exacerbations and the concurrent 
 
HYPKK/EMIA OF THE KIDNEYS. 117 
 
 renal lesions. Death seldom results from the effects of this disease 
 simply, but is caused by one or more complicating influence . 
 
 Treatment. — In determination of blood to the kidneys, the treat- 
 ment required is often quite active, but in the passive or obstructive 
 variety the reverse is true. All medicinal agents which tend to im- 
 prove the pre-existing disease will improve the condition of the kidneys. 
 If the renal congestion be dependent upon an irreparable damage to 
 the heart or pulmonary organs, or to a tumor pressing upon the veins 
 which cannot be removed, little or no relief can be expected from in- 
 ternal medication. Unless the cause can be removed, the congested 
 condition of the kidneys must remain. 
 
 Digitalis is not called for, but contra-indicated, as it tends to in- 
 crease the pressure upon the tuft of vessels constituting the glomer- 
 uli. It will, undoubtedly, cause an increase in the quantity of water 
 discharged, but it does not overcome the venous engorgement. On 
 the other hand, it tends to increase the congestion, and diminishes 
 the excretory and nutritive power of the renal glands. 
 
 The sending of more blood to the kidneys must be guarded against, 
 and a free escape favored in every possible way. This is best accom- 
 plished by acting upon the bowels and skin, with a few dry cups 
 applied to the loins, and followed by a warm poultice. 
 
 As a rule, most of the diuretics are theoretically contra-indicated* 
 and in most instances have proven themselves practically of no avail. 
 
 Jalap, calomel, and elaterium are often serviceable. Small doses of 
 pilocarpine frequently administered are also useful. 
 
 In the acute stage of an exacerbation, the treatment must be active; 
 prompt catharsis and diaphoresis will often relieve the symptoms and 
 prolong life. 
 
CHAPTER IX. 
 
 PYELO-NEPHRITIS. PYELITIS. PYONEPHROSIS. 
 
 Pyelonephritis, 
 suppurative nephritis. surgical kidneys. 
 
 Definition. — This is an intense inflammatory condition of the kid- 
 neys, terminating in the formation of pus, which may be localized or 
 diffused throughout the substance of the organs. The term surgical 
 kidney is especially applicable to this lesion when it is directly trace- 
 able to a surgical operation, as is often the case. In fact, it is one of 
 the " bugbears " of genito-urinary surgery. 
 
 Etiology. — The causes of pyelo-nephritis are, injuries, deposition of 
 crystals in the uriniferous tubules or pelves of the kidneys; renal 
 parasites, renal calculi, pyelitis, lodgment of calculi in the ureters, 
 cystitis, cystic calculi, tumors obstructing the ureters or neck of the 
 bladder, enlarged prostate, prostatic calculi, inflammations and 
 abscess, urethral calculi and strictures, and all operations upon the 
 genito-urinary tract, gonorrhoea, urethral chancres and chancroids, 
 pyaemia and septicaemia; it also occurs in connection with paraplegia 
 and hemiplegia. The more common, however, are cystitis, alone or 
 associated with calculi, stricture of the urethra, enlarged prostate, 
 operations upon the genito-urinary tract, and gonorrhoea. 
 
 Pathological Anatomy. — This lesion, for convenience of descrip- 
 tion, will be divided into three stages. In the first or early development, 
 the kidneys, to all outward appearances, are simply congested. This is, 
 however, more marked than in an ordinary and simjfle congestion. 
 "When the organs are laid open, the mucous membrane of their renal 
 pelves is congested and covered with mucus and little patches 
 of a fibro-plastic exudation, which are adherent to the membrane. 
 This condition has been described as a diptheritic pyelitis. 
 
 "When such kidneys are examined under the microscope in thin 
 sections, lymphoid corpuscles will be found quite abundant between 
 the tubules, but usually localized in small foci; the intervening 
 tubules remaining nearly normal, while in places minute abscesses are 
 
PYKLO-NKr/IUITJS. 
 
 119 
 
 found. But as the disease progresses to what may be termed its 
 second stage, and the one most frequently seen at the necropsy, the 
 surface is studded with clumps of white points, varying in size from 
 a pin's head to a walnut. These larger spots look like ahscesses just 
 underneath the renal capsule. Upon cutting into one, it is found to 
 •consist of purulent matter. These little abscesses are scattered all 
 through the kidneys, but are usually more abundant in the cortical 
 portion and near the surface. 
 
 Upon microscopic examination, what was an inflammatory focus in 
 the previous stage, has developed into a localized purulent centre, 
 which has no limiting wall of fibro-plastic material. 
 
 The tubules lying in the continuity of these abscesses have been 
 
 Jiliil 
 
 Fig. 27.— Pyelo-Nephritis or Surgical Kidney, x 350. 
 a, TJriniferous tubule showing parenchymatous metamorphosis; 6, diffuse suppurative zone; 
 c, cedematous intertubular tissue. 
 
 liquefied and destroyed by the solvent power of the pus, so as to be 
 completely cut across, and open abruptly on either margin of the 
 abscess. The contents of one of these purulent centres are pus, gran- 
 ular detritus, and degenerating renal epithelium. 
 
 In still more advanced cases or the third stage, two or more of these 
 purulent centres may have coalesced, until one-half or two-thirds, or 
 even a whole kidney, may have become converted into a large sac of 
 pus, having the capsule of the kidney for its limiting wall. Xow the 
 contents will be composed almost exclusively of pus, all evidence of 
 the renal substance having been destroyed. 
 
 Associated with this condition and acting as a complication, there 
 
120 PYELO-NEPHBITIS. 
 
 is an Inflammation of the bladder or ureter, most frequently the 
 former. 
 
 It has been said that each purulent centre is due to the action of 
 microbes, but as yet this has not been satisfactorily authenticated. 
 
 Symptoms. — In this peculiar lesion, the symptoms are exceedingly 
 are, and naturally vary with, or are masked by, those of the lesion 
 which causes the disease. 
 
 Willi any of the above-enumerated causes, a chill or a series of 
 rigors may he developed. If due to a renal calculus, there may lie 
 severe pain, deep seated in the region of the kidneys. The urine may 
 be unchanged, and the patient die a.t the end of a few days. When 
 it follows a paraplegia, its occurrence is a little more clearly defined 
 by the retention of the urine, its alkaline decomposition and cystitis, 
 followed by the rigors. 
 
 In every instance, the chills are followed by some febrile movement 
 with great depression, sweating, rapid and feeble pulse, hurried res- 
 piration, a dry and coated tongue, loss of flesh and strength, and a 
 diminution in the quantity of urine voided. The patient falls rapidly 
 into a typhoid state, and dies at the end of tw r o or three days. 
 
 The urinary changes are very obscure, and do not give any signs 
 upon which to base a diagnosis with any degree of certainty. The 
 reason for this is, that the pre existing condition in itself, often induces 
 a diminution in the quantity of urine secreted, together with the ap- 
 pearance of pus and albumin. This lesion is not marked by the 
 appearance of a large quantity of blood, and there is no discharge of 
 characteristic casts. 
 
 A careful consideration of the producing lesion, and a close study 
 of the clinical history and symptoms, will usually enable the examiner 
 to surmise quite accurately, if not to positively diagnosticate this con- 
 dition; and this supposition will frequently be confirmed at the 
 necropsy. 
 
 Prognosis. — This lesion is of special interest in connection with 
 surgical operations, as it is often developed just prior to, oris directly 
 induced by the operation. In either instance the result is fatal. 
 This is one of the great dangers in genito-urinary surgery and one 
 which is unavoidable by the surgeon. 
 
 Treatment. — Perhaps the immediate performance of nephrotomy 
 or nephrectomy w r ould save the life of the patient in some few in- 
 stances, but as the disease usually attacks both kidneys at the same 
 time, the operation is not admissible from a practical standj^oint. 
 Further, the operation has not yet been proven to be a practically suc- 
 cessful one, but on the contrary is rather losing favor. Evacuation 
 
PYELITIS. 1^1 
 
 of the pus may be accomplished by aspiration, but so long as the 
 cause remains, little or nohting can be accomplished. The only 
 way by which any good can justly be expected is in the line of 
 prevention. 
 
 The liability of this condition being developed as a sequel to the 
 above-mentioned diseases should always be remembered, and steps 
 taken to prevent the cause if possible. Considerable can be accom- 
 plished in this line, especially in connection with enlargement of 
 the prostate gland, paraplegia, hemiplegia, etc. In these, the genito- 
 urinary tract should be kept empty and clean, and in this way alkaline 
 decomposition of the urine followed by a cystitis will be prevented, 
 and the fatal issue retarded or avoided. 
 
 PYELITIS. 
 
 Definition. — Pyelitis is an inflammation of the pelves of the kidneys 
 and of their calices. It may attack one or both organs at the same 
 time. 
 
 Etiology. — Sometimes, though rarely, it occurs after exposure to 
 cold, but its most frequent cause is the irritation of renal calculi in 
 the pelves of the kidneys, or the presence of decomposing urine in the 
 renal pelvis, due to some obstruction either in the urethra or blad- 
 der. Unduly acrid or acid urine may excite it. A mild form is 
 sometimes excited by any of the varied forms of renal disease, and 
 occasionally it occurs during pregnancy. It may also result from a 
 cystitis, gonorrhoea, and all inflammatory conditions of the urinary 
 tract by an extension of the inflammatory process. With gonorrhoea, 
 the inflammatory process in the renal pelvis will suddenly develop, 
 without any apparent involvement of the intervening portion of the 
 urinary tract. Pyelitis may be excited by turpentine, cantharides, 
 squills, and the many forms of irritating balsams, resins, etc., as well 
 as by all acrid substances excreted by the kidneys. 
 
 A mild form of this disease is sometimes developed in the typhoid 
 stage of cholera, in typhus fever, diphtheria, and all the exanthemata. 
 
 A hemorrhagic variety has been described, in which there is frequent 
 and sometimes extensive hemorrhage into the renal pelvis. This 
 condition occurs in connection with scurvy, purpura hemorrhagica, 
 pernicious anemia, and leucocythasmia. 
 
 Pathological Anatomy. — The mucous membrane is very much con- 
 gested and dotted with ecchymotic extravasations, and at places the 
 epithelial surface is completely destroyed. In the most acute stage, 
 there is little or no discharge, but as the disease advances and becomes 
 
122 PYELITIS. 
 
 more chronic, a muco-purulent secretion is given off, and the mem- 
 brane is relaxed and swollen. As the inflammation advances, the 
 pelvis and infundibuli become enlarged and their walls thickened: 
 the color of^the mucous membrane changes to a grayish-white or slate 
 color, and its surface is traversed by delicate capillaries. Should 
 therein' much mechanical irritation, ulceration is liable to be devel- 
 oped, which may cause rupture of the wall, and the urine be extra- 
 vasated into the surrounding tissue, the peritoneal cavity, or into some 
 of the neighboring organs, inflammation and previous adhesions 
 having been formed. 
 
 The walls of the pelvis may be very much distended by the retained 
 urine and accumulated pus, and the kidneys may undergo atrophy, 
 as in hydronephrosis. Occasionally the fluid becomes entirely ab- 
 sorbed, the pelvis may shrivel into a hard capsule for its own inspis- 
 sated contents, and the ureter become converted into a fibrous cord, its 
 lumen having been obliterated. In certain cases where the inflamma- 
 has been very severe, a fibro-plastic exudation is thrown out upon the 
 surface of the mucous membrane, and this has been termed a diphthe- 
 ritic pyelitis. 
 
 Symptoms. — It must always be remembered that the symptoms 
 of pyelitis are often masked by those of its cause. It usually begins 
 with a chill, sometimes a series of rigors, followed by a rise of tempera- 
 ture of about three degrees Fahrenheit; pain in the back, increased 
 on pressure and often radiating down along the course of the ureter. 
 There is often nausea and vomiting, together with a continual desire 
 to micturate, and pain on attempting to do so. As the disease pro- 
 gresses and becomes more chronic, the lassitude from which these 
 patients suffer increases. 
 
 Hectic is finally developed and death ensues, either from exhaustion 
 or a form of septicemia, or by the combined action of both. 
 
 In those cases due to a renal calculus, the pain in the loins is the 
 most prominent symptom. 
 
 Another quite diagnostic symptom is the alternating discharge of 
 the clear or normal urine, and that charged with pus. 
 
 Urinary Examination. — The urine is usually increased in quantity, 
 owing, perhaps, to the moderate hyperemia of the kidneys always 
 associated with this disease. The specific gravity is somewhat above 
 normal, from 1.025 to 1.030; and its reaction is alkaline. Under the 
 microscope, it is found to contain blood, pus, and epithelial cells. 
 
 Great stress has been laid upon the character of the epithelial corpus- 
 cles in the urine and their diagnostic significance in reference to 
 pyelitis. But from the observations of Dr. Credon and others, it has 
 
PYELITIS. 1 23 
 
 been clearly proven that there is no difference in the size and shape of 
 the epithelial cells in the different regions of the genito-urinary tract. 
 For this reason, it becomes absolutely impossible to base any positive 
 diagnosis of pyelitis upon anything found in the urine with the 
 microscope. Albumin will always be found on account of the pus 
 present. 
 
 In some cases, the urine and the pus is retained in the pelvis of one 
 kidney for a time, and the urine excreted by the other kidney will 
 appear normal, or the two will alternate. 
 
 In other instances, the urine is permanently retained in the pelvis of 
 one kidney; under such circumstances, there will often be formed a 
 pyelo-nephritic tumor in the lumbar region, which will produce a 
 bulging of the side between the crest of the ilium and the twelfth 
 rib. There will be deep-seated fluctuation which can be detected 
 upon palpation; with tenderness upon pressure, and flatness upon 
 percussion, except when the tumor is crossed by the colon containing 
 gas. If tapped, a sero-purulent fluid may be obtained, but with all the 
 above symptoms the urine may remain normal or free from pus. 
 
 A mild form of pyelitis is far more frequent than the severe type 
 just described. It is often mistaken for and treated as a cystitic in- 
 flammation. 
 
 This variety is often chronic, when it unquestionably acts as an ex- 
 citing cause for the development of intrinsic renal lesions. Its char- 
 acteristic symptoms are the passing of pale acid urine, which has a 
 low specific gravity and contains albumin and pus-corpuscles. The 
 urine from a case of chronic pyelitis contains a fair amount of pus, 
 while the reaction remains strongly acid; with a cystitis, the urine 
 contains pus in abundance, but the reaction is alkaline. 
 
 From the study of a large number of these cases, this conclu- 
 sion has been formulated. When a patient has increased micturition 
 and has to rise several times during the night to empty the bladder, 
 and the urine passed is strongly acid, with a considerable quantity of 
 pus and some albumin but no casts, the inflammation is located in 
 the pelves of the kidneys. 
 
 These cases are frequently kept up by an undue acidity of the urine. 
 
 Diagnosis. — This is exceedingly difficult to make with certainty. 
 If the patient has, along with the above symptoms, alternating inter- 
 vals of purulent and clear or normal urine, the diagnosis of pyelitis 
 is pretty certain to be confirmed at the necropsy. This phenomenon 
 occurs in connection with those cases due to renal calculi or plugging 
 of the ureter with mucus or inspissated pus. On the other hand, it 
 should be remembered that this fluctuation is not always present. 
 
124 PYELITIS. 
 
 The continuous discharge of acid urine containing pus is positively 
 diagnostic of pyelitis. 
 
 Prognosis. — This depends in a great measure, if not wholly, upon 
 
 the exciting cause. When it is a complication of chronic cystitis, 
 enlarged prostate, urethral stricture, and operations upon the genito- 
 urinary tract, the prognosis is very unfavorable, to say the least 
 When pyelo-nephrosis occurs, the tumor may disappear, the sac be 
 obliterated, and the patient recover, but it ruins one kidney; if this 
 does nol take place and no rupture follows, death may be expected 
 from exhaustion or septic toxaemia. Should the sac rupture, the 
 prognosis will depend upon the seat of the extravasation; if it is into 
 the peritoneal cavity or retroperitoneal areolar tissue, death will 
 ensue from shock, peritonitis, or septicaemia; if externally or into the 
 alimentary tract, the patient may and frequently does recover. If 
 both kidneys are the seat of a pyelitis, the case is almost certain to 
 terminate fatally, hut when only one is implicated, there is always a 
 chance for recovery. 
 
 Treatment. — During the onset of the disease, wet or dry cups to 
 the loins, followed by warm poultices, should be employed and mor- 
 phine should be injected hypodermatically if the pain be very severe 
 and unbearable; considerable care, however, must be exercised in the 
 use of opium in any form, for in some it certainly does excite a 
 fatal uraemia. Alkaline and demulcent drinks should be administered 
 freely, as they diminish the irritability of the urine. 
 
 The following mixture has been found one of the most valuable of 
 all, not alone in inflammations of the renal pelvis, but in all forms 
 of catarrh and inflammation involving any portion of the mucous 
 membrane of the urinary tract. This statement is especially true in 
 regard to the bladder. For it appears quite clear that a large propor- 
 tion of the inflammatory conditions of this canal, not due to a cal- 
 culus or some mechanical obstruction, are in a great measure depend- 
 ent upon a depressed or over- worked condition of the lumbar portion 
 of the spinal cord, and to a similar condition of the abdominal sympa- 
 thetic system, and especially of the hypogastric, renal, and vesical 
 plexuses, in connection with an acid condition of the urine. 
 
 If we overcome these three difficulties, restore the cord and 
 sympathetic system to their normal state, and remove the irritability 
 of the urine, the inflamed mucous membrane will by nature's 
 intrinsic reparative powers be speedily restored to its normal con- 
 dition. 
 
 This combination fulfils these three indications and is usually fol- 
 lowed by immediate relief: 
 
PYELITIS. 125 
 
 I£ Extracti Damianae Fluidi 3 vi. 
 
 Extracti Hyoscyami Fluidi 3 iij. 
 
 Potassae Bicarbonatis 5 88. 
 
 Acaciae q. 0. 
 
 Aquae destill q. S. ad § iij. 
 
 M. Sig. 3 i. four times a day in water. 
 
 By the addition of the mucilage, the insoluble extracts form with 
 the alkali an emulsion. The damiana is one of the most powerful 
 stimulants to a depressed or over-worked spinal cord; while in health 
 it has but little, if any, influence. The so-called autispasmodic 
 action of hyoscyamus is due to its power to stimulate a weakened 
 sympathetic system, and in these cases it acts by this stimulating 
 property, and raises the depressed and irritable hypogastric and 
 renal plexuses to their normal standard and activity. The alkali 
 renders the urine less irritating. 
 
 The hyoscyamus and potash are not new agents, but the damiana is, 
 and it is a remedy greatly needed in many of these cases, for they are 
 frequently excited by venereal excesses. Hot baths, especially hip 
 baths, and perfect rest must be insisted upon. One of the best 
 methods for a medicated sitz-bath is to put a bunch of wormwood in 
 a chamber or other receptacle in a closed water-closet chair, and then 
 pour on it some boiling hot water, and have the patient sit over the 
 steaming decoction. This valuable suggestion was made by Prof. 
 Satterthwaite. 
 
 If the disease becomes chronic, with the excretion of large quanti- 
 ties of pus, astringents, especially gallic acid, will be found useful, and 
 in all a nutritious non-stimulating diet must be enforced. 
 
 In case pyonephrosis makes its appearance, aspiration is the only 
 mode of treatment at first, both to prove the correctness of the diag- 
 nosis and to lessen the immediate danger from rupture into some 
 locality where a fatal result would be almost certain to ensue; later, 
 if the tumor reappears, it may be expedient to make a free and per- 
 manent opening through the abdominal wall. 
 
 Counter-irritation to the lumbar region in the form of actual cau- 
 terization is often followed by a great improvement. 
 
 As an undue acidity of the urine often exists and keeps up the 
 inflammatory action, the digestive apparatus requires attention, that 
 the quantity of uric acid produced may be diminished. 
 
 The inspissated bile pill will be found a most effectual remedy, see 
 p. 26. 
 
126 PYONEPHROSIS. 
 
 PYONEPHROSIS. 
 
 Definition. — Pyonephrosis is that condition in which a pyelitis has 
 become chronic, the ureter occluded, the renal pelvis distended with 
 pus, and the kidney-tissue liquefied and destroyed. 
 
 Etiology. — The indirect causes are those which excite a pyelitis, but 
 tlie direct cause is the occluding of the ureter. In fact, it is one of 
 the ways in which a pyelitis may terminate. 
 
 Pathological Anatomy. — The mucous membrane of the pelvis of 
 the kidney is thickened, the ureter occluded, and the pelvis, infundib- 
 nla, and calices over-distended with pus. The renal substance is 
 gradually encroached upon, the papilla? flattened and destroyed, and 
 finally the Malpighian pyramids and the cortical arches are completely 
 obliterated. 
 
 The capsule of the kidney becomes distended and thickened, and 
 forms the wall of a sac containing pus and granular debris. 
 
 Symptoms. — It is preceded by all the symptoms of an ordinary pye- 
 litis, followed by a disappearance of the pus in the urine, and the pro- 
 gressive development of a tumor in the lumbar region. 
 
 The tumefaction is upon one side or the other, and occupies the 
 space between the crest of the ilium and the floating ribs. As a re- 
 sult, the abdomen becomes unsymmetrical. On palpation, a deep- 
 seated fluctuation and considerable pain are found to be present. Upon 
 percussion, an increased area of dulness is easily detected, which is 
 often crossed by a resonant zone, indicating the position of the colon. 
 Aspiration will give evidence of pus or purulent debris. 
 
 Diagnosis. — This rests upon the previous history, and the removal 
 of purulent matter by a trocar or aspirator. 
 
 Prognosis. — Recovery is possible if the sac bursts into the alimen- 
 tary tract, or externally through the abdominal parietes. 
 
 In case it bursts into the retroperitoneal tissue or peritoneal cavity, 
 death speedily ensues. 
 
 In other instances, there is no rupture, the suppurating foci con- 
 tinue, and the patient dies from exhaustion. In still others, the for- 
 mation of pus ceases, absorption takes place, the sac contracts down 
 upon a cheesy mass, and recovery results. 
 
 Treatment consists in good food and tonics, aspiration, nephrec- 
 tomy or nephrotomy. 
 
CHAPTER X. 
 
 HYDRONEPHROSIS. RENAL CALCULI. 
 
 HYDKONEPHKOSIS. 
 
 Definition. — Hydronephrosis is that condition in which the pelves, 
 infundibuli, and calioes of the kidneys are distended with urine, owing 
 to some obstruction in the urinary passages, almost invariably of 
 the ureter, followed by complete or partial atrophy of the renal sub- 
 stance. Both pelves are seldom affected at the same time. 
 
 Etiology. — Congenital malformations play an important part in the 
 causation of this condition, and are often associated with deformities 
 elsewhere, such as hare-lip, imperforate anus, etc. The causes, how- 
 ever, which occur afterbirth, and which may be called acquired, are 
 the impaction of calculi, inflammation in the walls of the ureter ob- 
 literating its lumen by contraction, pressure by tumors, morbid 
 growths or displaced organs, as the uterus or enlarged ovary, pelvic 
 peritonitis with exudation of fibro-plastic material, inflammation of 
 the bladder involving one or both orifices of the ureters, and obstruc- 
 tions of the urethral canal. Hydronephrosis is usually unilateral, but 
 where the cause exists below the cystic orifice of the ureters, it becomes 
 bilateral and of a more serious nature. Even then it is more marked 
 upon one side than the other. 
 
 Pathological Anatomy. — Obstruction of the ureter is followed by 
 dilatation of its lumen, and an increase in the thickness and 
 fibrous density of its wall. The renal pelvis progressively enlarges, 
 and at the same time there is a progressive atrophy of the renal sub- 
 stance, due to the continued and increasing pressure of the continu- 
 ally effused fluid. The kidney-tissue never disappears entirely, but it 
 can be found either in a thin stratum or iu isolated patches upon the 
 wall of the cyst, which, like the wall of the ureter, is converted into a 
 thick and fibrous layer. 
 
 The cyst in some cases becomes quite large, measuring several 
 inches in diameter; it is usually single, but in some rare instances it 
 is multilocular. These multilocular formations are due to an irregu- 
 lar dilatation of the uriniferous tubules. Their fluid contents are light 
 
128 HYDRONEPHROSIS. 
 
 in color, and somewhat cloudy, low in specific gravity, alkaline or 
 central in reaction, rarely acid, and almost always contain albumin 
 and all the salts usually found in the urine, excepting, perhaps, urea 
 and uric acid, which are sometimes absent. In rare instances, the 
 contents of these cyst are gelatinous. Hydronephrosis of one kidney 
 almost always produces hypertrophy of the opposite organ. 
 
 Symptoms. — During the early stage of development of a unilateral 
 hydronephrosis, no symptoms are developed by which this condition 
 can be diagnosticated. The unaffected kidney accomplishes the work 
 formerly performed by the two, and consequently no change in the 
 quantity or quality of the urine can be discovered, and suspicion is 
 seldom excited, sometimes not until a tumor is found in the lumbar 
 region, and even then there is often great difficulty in making the 
 diagnosis. Should the tumor suddenly disappear, and its disappear- 
 ance be accompanied by the discharge of a large quantity of turbid 
 urine, the diagnosis is no longer in doubt. 
 
 There is usually a gradual loss of flesh and strength. Pressure by 
 the tumor when large may cause embarrassed respiration, especially 
 during recumbency and after eating, together with distention of the 
 subcutaneous veins. 
 
 These or similar symptoms can occur with any abdominal tumor, 
 but an examination of the fluid drawn from the cyst by an exploring 
 needle removes all doubt as to diagnosis. 
 
 Rupture of the cyst is followed by collapse and death, while double 
 hydronephrosis is soon followed by a fatal result with symptoms of 
 nraemic poisoning. 
 
 Diagnosis. — This condition has to be differentiated from ascites, 
 from hydatids, ovarian cysts, pyelo-nephritis, and pyonephrosis. 
 
 From ascites it is sometimes quite difficult to distinguish, especially 
 if both kidneys are involved; an examination of the fluid is the only 
 means for settling the question. That from the hydronephrotic cyst 
 will contain the urinary salts, while that from ascites will not. It is 
 often impossible to distinguish it from an hydatid cyst of the kidney 
 unless the hooklets of the ecchinoccocus are found. If double, how- 
 ever, it is not likely to be due to a hydatid cyst. From the ovarian 
 tumor it is diagnosticated by the history, its location, vaginal exami- 
 nation, and the character of the contained fluid. 
 
 It is distinguished from pyelo-nephrosis and pyonephrosis, by the 
 presence or absence of pus in the contained fluid. 
 
 Prognosis. — So long as hydronephrosis is unilateral and the other 
 kidney remains healthy, the prognosis is favorable so far as duration 
 of life is concerned, but should any disease attack the other kidney, 
 
RENAL CALCULI. 12!) 
 
 the prognosis will be most serious. Rapture of the cyst-wall seldom 
 occurs, and little inconvenience is experienced by the patient from 
 the presence of the tumor. Bilateral hydronephrosis is of necessity 
 fatal, unless the obstruction to the free escape of urine is quickly re- 
 moved. 
 
 Treatment. — Absorption of the fluid cannot be produced by any 
 medicinal means known at the present day. Manipulation of the 
 tumor and abdomen along the course of the ureter may remove the 
 obstruction, but great care should be exercised not to use sufficient 
 force to rupture the sac of the cyst. Tapping with a small trocar 
 and can nl a, or aspiration may be employed with good results, though 
 the return of the tumor is almost certain. Nephrectomy or nephrot- 
 omy might be performed, should the symptoms be sufficiently 
 urgent. 
 
 EENAL CALCULI. 
 
 Definition. — A renal calculus is a concretion formed in the tubules 
 of the kidneys or in the renal pelves, by a deposition of one or more 
 of the solid constituents of the urine. Calculi may occur at any time 
 during intra- or extra-uterine life. 
 
 Etiology. — The precise cause of renal calculus is unknown, and al- 
 though many theories have been advanced to account for its devel- 
 opment, none are entirely satisfactory. 
 
 It is known, however, that every calculus has a nucleus of some 
 foreign substance, such as pus, inspissated mucus, blood, pigment 
 granules, or crystals of some sort, often uric acid. Eenal calculi 
 are usually composed of uric acid, but other kinds often occur, such 
 as those composed of oxalate of lime, phosphates of lime, carbo- 
 nate of lime, cystin, xanthin, and still others composed of several of 
 these ingredients. 
 
 Pathological Anatomy. — In cases where there has been a deposition 
 of crystals without the formation of large calculi, the kidneys upon 
 postmortem section have a streaked appearance, usually of brick-red 
 color, owing to the presence of the uric acid in the tubules. If the 
 concretion be large and yet retained in the substance of the kidney, 
 it becomes the source of much irritation; congestion and inflamma- 
 tion are excited and often followed by suppuration and abscess; in 
 fact, it acts as a foreign body would elsewhere. If, on the other hand, 
 it passes from the kidney and remains in the pelvis of the organ, it 
 becomes a fruitful source of pyelitis. By blocking up the opening to 
 the ureter, it may produce hydronephrosis. In case the calculus be- 
 comes large, it may of itself press upon the renal substance, and in 
 
130 RENAL CALCULI. 
 
 this way cause marked atrophy of the kidney. Passing from the 
 renal pelvis down to the bladder through the ureter, it may there 
 become the nucleus for the formation of a vesical calculus. 
 
 Sywiptorhs, — Renal calculi which are retained in the pelvis of the 
 kidney may increase to a very large size and even completely destroy 
 the renal substance without having given rise to any sign of its pres- 
 ence during the life of the patient. 
 
 But usually there is pain in the lumbar region, which shoots down 
 the groin and is aggravated by exercise or any jolting of the body. 
 In the urine, blood, pus, epithelial cells, and often crystals, usually 
 uric acid or oxalate of lime, are discovered. Sometimes a calculus 
 may pass from the pelvis through the ureter to the bladder, and so 
 out through the urethra without the patient's knowledge, but as a 
 rule the symptoms are painfully severe. 
 
 When attacked by a renal calculus, the patient complains of intense 
 shooting pains in the loins, radiating over the hypogastrium and 
 down the inner side of the thighs. The testicle and the scrotum of 
 the affected side are often retracted, and there is sharp pain there, as 
 well as in the head of the penis. In the female, the labia are affected 
 in like manner, but the female sex seldom suffer from renal calculi. 
 
 There is often nausea and vomiting, the patient is covered with a 
 cold perspiration, the respirations are rapid and shallow, the pulse 
 small, hard, and rapid, with great anxiety of countenance. 
 
 An attack may last for a few minutes only, or there may be remis- 
 sions followed by recurrences, each one appearing to the patient to be 
 more severe and serious than the one which preceded; but if the cal- 
 culus remains lodged in the ureter, the symptoms gradually subside 
 and hydronephrosis is developed. 
 
 Prognosis. — From the presence of a renal calculus in the pelvis of 
 the kidney, no danger is to be feared so long as complications are not 
 developed. Where they occur the prognosis rests upon the com- 
 plication and not upon the presence of the calculus. A fatal result 
 from renal calculi rarely occurs, unless by the induced suppression of 
 urine, secondary to nervous exhaustion. 
 
 Treatment. — Many different ways have been proposed with the view 
 to dissolving the calculus in situ, but none of them have been found 
 reliable. Perhaps a hygienic mode of life is as sure a safeguard as 
 anything in the way of a prophylactic. In the renal colic, baths as hot 
 as the patient can bear, or hot applications over the abdomen and 
 loins, relax the tissues and lessen the pain, but they do not arrest 
 the muscular contraction on the part of the ureters as much as the 
 administration of ether and chloroform. In conjunction with the 
 
RENAL CALCULI. \ ?,\ 
 
 heat, the internal administration of full doses of belladonna and 
 strychnia will diminish the irregular and spasmodic contraction of the 
 muscular coat of the ureter, while the normal and even peristaltic 
 action will be increased. By this method of treatment the rapidity 
 of transit is increased. 
 
 Opium and anaesthetics are to be avoided, if possible. The anaes- 
 thetics tend to diminish the peristaltic action of non-striated muscle: 
 fibres, and hence prevent the movements of the calculus along the 
 ureter. They will, of course, relieve the pain, but when the patient, 
 recovers from their influence, they are no better, and the stone has: 
 made little or no progress in its descent. They are of service in relax- 
 ing the tissues and giving the patient a rest. 
 
 The opium is equally inefficient, for the same reason as the anaesthet- 
 ics, and besides it has a dangerous element. To completely alleviate 
 the suffering, enormous doses of the drug may be required. If now 
 for any reason the calculus should slip through into the bladder, the 
 necessity for the opium at once disappears, and the patient may be- 
 come suddenly narcotized, which might prove both a troublesome and 
 serious, if not a fatal complication. For this reason, great care should 
 be exercised in reference to the quantity of opium administered either 
 by the mouth or hypodermatically. 
 
 In cases where a calculus is retained in the pelvis, and complications 
 make their appearance, nephrotomy is the only treatment that will 
 afford relief. 
 
 The recurring attacks of renal colic may be caused to disappear by 
 giving the patient one minim of glacial carbolic acid three times a 
 day. But a more satisfactory plan of treatment is to place the 
 individual upon a limited nitrogenous diet, as for instance, one com- 
 posed of skim-milk or butter-milk. At the same time giving the bile 
 pill and the damiana mixture (see pages 26 and 125). 
 
CHAPTER XL 
 
 ACUTE AND CHRONIC ATROPHY OF THE KIDNEYS. HYPER- 
 TROPHY OF THE KIDNEYS. CYSTS OF THE KIDNEYS. 
 
 ACUTE ATROPHY OF THE KIDNEYS. 
 
 Definition. — This is a disease that has been described as one in 
 which the kidneys rapidly diminish in size, owing to a rapid exuda- 
 tion into the cells of the organs, followed by fatty degeneration and 
 disintegration. The cause is unknown: it is characterized by a copi- 
 ous albuminuria and casts, and frequently with marked uraemic symp- 
 toms, terminating in death. 
 
 Etiology.- — The causes of this disease are unknown, but they appear 
 to be dependent upon blood poisoning, and acute hepatic diseases. 
 It has been described as associated with acute yellow atrophy of the 
 liver, when it usually follows, but may precede the hepatic lesion. It 
 is said to be more frequent in the female than in the male. It has 
 been met with during pregnancy and after confinement. 
 
 Pathological Anatomy. — In many respects this lesion closely resem- 
 bles acute atrophy of the liver. 
 
 The disease has been described as having two stages. In the first, 
 or that of exudation, infiltration, and enlargement, the organs are 
 not markedly congested, their capsules are not adherent, and the un- 
 derlying renal surface remains smooth, but soft and flabby. The cor- 
 tical substance is swollen, and the tubules enlarged and white. 
 
 Upon microscopic examination, the vessels are usually found empty, 
 and compressed by the swollen epithelium of the tubules. 
 
 The tubes are occupied by a dense opaque material, the individual 
 cells are swollen and granular, their nuclei being hidden by the mo- 
 lecular cell contents. Both medullary and cortical portions are 
 involved. Some of the cells are in a state of fatty degeneration, or 
 even broken down. 
 
 In the second stage, the organs are still paler and their capsules 
 wrinkled. 
 
 Where examined microscopically , the stroma is found to be intact, 
 
CHRONIC ATROPHY OK THE KlhXKVK. L33 
 
 the blood-vessels empty, and the tubules in various stages of retro- 
 grade metamorphosis; some being more advanced than others. The e 
 changes are identical with those found in the hepatic cells in acute 
 yellow atrophy. 
 
 Symptoms. — Little seems to be known of the symptoms, but they 
 are, so far as studied, a diminution in the quantity of water, abundant 
 albuminuria, and a large number of casts. 
 
 There is also a tendency to jaundice, hemorrhagic extravasations, 
 and uraemia — in fact, all the symptoms are those of the latter 
 condition. 
 
 Diagnosis. — Bather than place this condition under a special classi- 
 fication, it should be considered as a very severe type of the acute 
 parenchymatous metamorphosis of the kidneys, as its etiology, 
 pathological anatomy, and symptoms are precisely like those of a 
 severe acute parenchymatous metamorphosis. 
 
 Prognosis. — This is unfavorable. 
 
 Treatment. — The preventive measures applicable to acute paren- 
 chymatous metamorphosis of the kidneys are doubly applicable here. 
 But no therapeutic agent or other means have been found by which 
 this rapidly progressing cellular transformation can be arrested or 
 modified and the renal organs enabled to regain their former func- 
 tional activity. 
 
 CHRONIC ATROPHY OF THE KIDNEYS. 
 
 Definition. — Here, as in the acute form, the term applies to the 
 diminution in size which is usually associated with several forms of 
 renal lesions. The term is more a synonym than a specific lesion. 
 That form associated with hydronephrosis approaches closely to a true 
 atrophy of the renal substance, but all the other forms are a stage of 
 some other disease. 
 
 , Etiology. — The causes are hydronephrosis, the pressure of a. 
 tumor external to or within the gland, enlarging calculi within the 
 renal pelvis, or pressure upon the vessels entering the kidneys. 
 
 Pathological Anatomy. — Following the dilatation of the renal pelvis> 
 the kidney is replaced by a large, lobulated mass or series of c\ T sts y 
 containing a watery fluid. At first the Malpighian pyramids are 
 flattened, but later the cortical layer also disappears. This form of 
 atrophy occurs on one side, associated with a compensatory hypertro- 
 phy of the opposite kidney. There are no special symptoms and the 
 lesion is only a part of other diseases. 
 
134 EENAL CYSTS. 
 
 HYPERTROPHY OF THE KIDNEYS. 
 
 Definition. — Hypertrophy of the kidneys is that condition in which 
 all the elements of the organs are increased in size, and possibly in 
 number or both. 
 
 Etiology. — This condition is usually caused by long-continued con- 
 gestion, from which every element of inflammation has always 
 been absent, and hence occurs from congenital absence of one 
 kidney. It is also the result of hydronephrosis or pyelo-nephrosis on 
 one side, or a tumor, or any disease by which one kidney is diminished 
 or destroyed and the other left intact, to do the work previously ac- 
 complished by the two. The term hypertrophy is loosely applied to 
 almost every enlargement of one or both organs from any cause, but 
 this is not a correct usage. True hypertrophy is limited to a physio- 
 logical increase in size, with the production of normal, and not con- 
 gestive and inflammatory material. Its weight may reach eight or 
 ten ounces (226.796 or 283.496 grams) or more. The renal artery 
 and vein will be found proportionately enlarged. 
 
 Symptoms. — There are no symptoms connected with this condition. 
 
 Physical examination may in some few cases enable the physician 
 to make out the existence of an enlarged kidney, but the diagnosis is un- 
 certain and in most instances unsatisfactory. Should such a condition 
 be discovered or even suspected, the prognosis is always favorable and 
 no treatment is called for. This change is, strictly speaking, a post- 
 mortem revelation. 
 
 RENAL CYSTS. 
 
 Definition. — Cysts of the kidneys are so called when one or more 
 thin fibrillated connective-tissue sacs, containing a clear, faintly yel- 
 low serous fluid, are found in or protruding from the substance of the 
 glands. 
 
 Etiology. — The precise cause for these formations is not known, 
 excepting when they are congenital. 
 
 Pathological Anatomy. — There are four distinct varieties : 
 
 The first or congenital, are developed in the kidneys of the child 
 in utero. This is caused by the obliteration of some part of the urinary 
 tract, and is said to be due to the formation of connective tissue 
 between the calices and the papilla?. 
 
 Both organs are usually involved and converted into cystic masses, 
 which in some cases become very large, rendering evacuation neces- 
 sary before the child can be delivered. 
 
 This form of cystic transformation seems to have originated princi- 
 
RENAL CYSTS. 135 
 
 pally in the Malpighian tufts, the capsules of which are enormously 
 distended and the vascular supply atrophied. 
 
 In the second variety, we fiud one or more cysts in otherwise perfectly 
 normal kidneys. The cysts may be small, or of considerable size. In 
 either case the wall of the sac is composed of a very thin layer of dense 
 fibrillated connective tissue, lined by a thin layer of flat cells. 
 
 Their fluid contents are composed of a perfectly clear, light, straw- 
 colored serum which does not contain albumin nor any of the urinary 
 solids. 
 
 The third variety occurs with the various chronic renal lesions, 
 especially with the sclerotic and atrophic form of the chronic diffuse 
 nephritis. The formations are, more strictly speaking, retention 
 cysts, being formed either by the plugging of a uriniferous tubule or 
 by a strangulation produced by the contraction of the newly formed 
 connective tissue. The wall of these cysts not infrequently retains an 
 internal coating of the original cells of the uriniferous tubule from 
 which they have been developed. 
 
 The fourth variety is a cystic degeneration of the kidneys proper. 
 Both glands, as a rule, are implicated. Both become enlarged, and are 
 now composed of cysts of all sizes and colors. 
 
 These sacs contain serum, fibrin, colloid material, and may and do 
 go on to suppuration, when they also contain pus. 
 
 Hemorrhage into these cysts also occurs. 
 
 The surface of the kidneys will be nodular, and very little true or 
 normal renal substance will-be found. The little which is left may be 
 perfectly normal, compressed, atrophied, or in a suppurating condition. 
 
 This lesion is supposed to be due to a new growth originating be- 
 tween the lobules, and is usually a post-mortem discovery. 
 
 Symptoms. — In all four varieties the symptoms are obscure, and the 
 formation of a large tumor in the region of one or the other kidney is 
 the only prominent one, and even this is not diagnostic. 
 
 Diagnosis. — This is most frequently made at the necropsy. 
 
 Prognosis. — In the second form it is good. In the first and fourth 
 forms it is always fatal. The third depends wholly upon the disease 
 with which it is associated. 
 
 Treatment. — The first, second, and fourth forms require none. In 
 the third, it is that of the chronic renal disease. 
 
CHAPTER XII. 
 
 TUBERCULOSIS OF THE KIDNEYS. 
 
 SCROFULOUS KIDNEYS. RENAL PHTHISIS. 
 
 Definition. — Renal tuberculosis is that condition in which the kid- 
 neys, renal pelves, and the ureters are the seat of a tubercular inflam- 
 matory infiltration. It ma}* develop in the form of miliary tubercles 
 along the course of the vessels of the cortical substance and pyramids 
 of Ferrein, but more frequently it occurs in the form of large caseous 
 masses, which may be located in any portion of the kidneys, the renal 
 pelves, or ureters. 
 
 Etiology. — The precise origin here, as in other portions of the body, 
 is not known, except by those who accept the Bacillus tuberculosis 
 as the causative agent. Renal tuberculosis is developed in connection 
 with an inherited or acquired scrofulosis or tubercular diathesis, and 
 may be either primary or secondary to a similar condition in the lungs 
 or other parts of the body. It is more frequent in childhood and 
 youth than in advancing years. But when found late in life, it is 
 usually in the form of cheesy masses of secondary origin. It is more 
 frequent in males than females, and does not always attack both organs, 
 but when both are involved, the disease is always more advanced in 
 one than in the other. The right kidney is the gland most frequently 
 implicated, and when the two are invaded, the greatest damage is usu- 
 ally done to the right. Occasionally one kidney may be completely 
 destroyed by the tubercular process, while the opposite gland remains 
 absolutely free from disease. 
 
 Pathological Anatomy. — The microscopic appearances will differ in 
 the two forms. If miliary tubercles only be present, the organs will not 
 be much enlarged. The external and the cut surfaces will be dotted 
 with small white glistening bodies, which are scattered throughout the 
 cortical substance, but are rarely found in the pyramids of Malpighi. 
 As the disease advances, these miliary tubercles coalesce, their centres 
 undergo retrograde metamorphosis and caseation, and in this way form 
 
SCROFULOUS KIDNEYS. 137 
 
 large cheesy nodules. These larger masses are in all probability de- 
 veloped in some cases without the intervention of the miliary form. 
 
 In another variety, this peculiar inflammation commences in the 
 calices of the pelvis, which, with the apices of the pyramids, are '■on- 
 verted into a caseous mass of yellowish color, identical with tubercular 
 or scrofulous masses in other parts of the body. The process pro- 
 gressively extends to the Malpighian pyramids and the surrounding 
 cortical substance. In this way the kidneys become enlarged, the 
 renal tissue destroyed and replaced by tubercular new-formations, 
 either tubercular tissue or cheesy masses. 
 
 In some extreme cases where both the renal pelves and kidneys are 
 involved, the neoplasm, having but little vitality, readily dies, un- 
 dergoes liquefaction, and forms cavities containing thin pus and cheesy 
 debris. It is by this process that the kidneys are converted into a 
 bag of pus, sometimes as large as a child's head. 
 
 Microscopical Examination. — The small miliary bodies, when studied 
 in thin sections, are found to be composed of zones of altered renal 
 tissue. At these points the intertuhular tissue is infiltrated with 
 small round corpuscles. The epithelial cells of the involved tubules 
 degenerate, and the basement walls of the tubes collapse, or are ob- 
 literated by the abundant cell-formation. In some sections, the retic- 
 ulated or adenoid tubercular tissue, round, oval, and giant cells will be 
 found. But more frequently the central portion of the small granu- 
 lation has undergone a caseous transformation, while the periphery is 
 still composed of this aggregation of small round and oval corpus- 
 cles. The larger tubercular masses are either formed by the coales- 
 cence of smaller masses or are of independent development. The 
 microscopic appearances are the same in either case. 
 
 The principal differences between the miliary and cheesy masses is 
 the preponderance of the caseous disintegration in the latter. 
 
 Symptoms. — These are usually quite obscure. When the tuber- 
 cles occur in small quantities in the kidneys, or when the tubercular 
 inflammation is not extensive, all tangible symptoms of the disease 
 are absent. But as the process develops and involves larger areas, a 
 rise of temperature will be developed with some pain and tenderness 
 over the region of the kidneys. On percussion, increased dulness 
 may be discovered, and if the walls of the abdomen are thin, a tumor 
 may be made out by palpation. Hectic fever and progressive emacia- 
 tion rapidly ensue, together with chills, night-sweats, and the other 
 usual accompaniments of pulmonary tuberculosis. Frequently we 
 have all the rational signs of pulmonary phthisis, the cough excepted, 
 
138 SCROFULOUS KIDXKYS. 
 
 but with an absolute absence of all the physical signs; in such in- 
 stances renal tuberculosis should be suspected. 
 
 In some cases, the testicle is first attacked, and followed by the 
 renal lesion. 
 
 If there is an associated cystic tuberculosis, micturition is often 
 frequent and painful. 
 
 The urine is not often altered early in the disease, but later it may 
 become alkaline and filled with debris of the renal substance. The 
 bacillus tuberculosis is said to be diagnostic of the disease if found in 
 the urine. 
 
 
 \* 
 
 .-.--••Kv'^.-v 
 
 3 m 
 
 y/ 
 
 \ 
 
 N 
 
 ^^7 
 
 Fig. 28.— Bacillus Tuberculosis, x About 850. 
 Dalafleld and Prudden, " Hindbook of Pathological Anatomy and Histology." 
 
 Method for Staining the Bacillus Tuberculosis.— The method for 
 staining the Bacillus tuberculosis is as follows: 
 
 First, make a saturated solution of aniline oil in water, 1 to 15, 
 shake for five or ten minutes and then filter. 
 
 Second, make a saturated alcoholic solution of Gentian violet. 
 
 The urinary debris is drawn up with a pipette and a drop deposited 
 upon a clean cover glass and allowed to dry on the surface, or two 
 covers are rubbed together, thus producing an even film. 
 
 From 5 to 10 m (0.32 to 0.64 cc), of solution No. 2 is added to 
 one ounce (31.1 cc.) of solution No. 1 until the top assumes a metal- 
 lic lustre. 
 
 The prepared cover or covers are floated in this mixed fluid for 
 
SCROFULOUS KIDNEYS. 
 
 1 M 
 
 twelve hours, the side containing the specimen facing the staining 
 fluid. 
 
 The cover containing the specimen is next immersed in a 25$ aque- 
 ous solution of nitric acid for half a minute. 
 
 It is then soaked in a 60$ solution of alcohol for half an hour. 
 
 It is then dried either with or without the use of an alcoholic or 
 gas flame. 
 
 When dry, it is stained in a solution of vesuvin or Bismarck brown 
 for two minutes, then washed in ordinary alcohol, dried, and mounted 
 in Canada balsam or dammar varnish. 
 
 Sections made from the kidney may he stained in the same solutions. 
 
 In either case, if the bacilli are present, they will appear under the 
 microscope as blue rod-like bodies, varying in length from one-fourth 
 to one-half the diameter of a red blood-cell. They may have a beaded 
 appearance or may be slight] y curved. 
 
 A number of other methods have been recommended, but this one 
 will usually secure the desired result. 
 
 Upon microscopic examination, the urine will be found to contain 
 epithelial cells, pus, blood, granular matter, and shreds of broken- 
 down tubercular tissue. If the latter are distinctly made out, the 
 diagnosis is fairly certain. Albumin and casts and many of the evi- 
 dences of ordinary renal lesions may also be present. 
 
 The relative merits of the bacillus tuberulosis as a diagnostic aid 
 has not as yet been fully established. In the majority of cases of 
 genito-urinary tuberculosis in which they have been sought for, they 
 were found to be absent. 
 
 The urine is occasionally suppressed and the symptoms of urasmic 
 poisoning are developed and followed by a fatal result. 
 
 Diagnosis. — It is exceedingly difficult to diagnosticate this lesion 
 with any degree of certainty. But when a patient presents all the 
 rational signs of phthisis and the physical examination of the chest is 
 negative, without any evidence of cerebral, laryngeal, or peritoneal 
 tuberculosis, it is well to suspect a renal form and to examine care- 
 fully the lumbar region and the urine for some evidence of disease in 
 the kidneys or genito-urinary tract. Even this is very unsatisfactory, 
 as the urine contains no positive evidence, except tubercular tissue, 
 which in itself is difficult to recognize. 
 
 If the bacilli were positively diagnostic and readily found, the 
 diagnosis would be easy and certain. 
 
 If, however, the urine contains pus, blood, and fragments of cheesy 
 material, and one chances to find the bacilli with the above clinical 
 history, the diagnosis is tolerably correct. 
 
1 10 SCROFULOUS KIDNEYS. 
 
 The disease usually runs a very slow course, and the patient may 
 die of some intercurrent disease. 
 
 Scrofulous or tubercular nephritis is frequently a microscopic reve- 
 lation. One. of the most perfect examples observed occurred in an 
 accidenl ease. In that instance, it was found at the necropsy that 
 both kidneys, ureters, bladder, and prostate gland were a mass of 
 tubercular tissue. The patient, however, had died as the result of a 
 broken neck. 
 
 Treatment. — When discovered during life, the same treatment that 
 is proper for general tuberculosis is to he instituted: pure air, nutri- 
 tious food, and tonics, a ad particularly the syrup of the iodide of iron. 
 Cod-liver oil is usually detrimental in this as in all tubercular pro- 
 cesses, from the fact that in the majority of instances it upsets the 
 digestive apparatus, and prevents the assimilation of other substances. 
 Fats also are non-nutritious substances — that is to say, they do not re- 
 produce in the system albuminoid substances or tissues, their function 
 being that of heat-producing agents, lubricators, and energy-yielding 
 elements. 
 
 Change in climate may be found the most useful of all agents. 
 The change should not be for a few weeks or mouths, but for a life- 
 time, if it is expected to give the best result. The patient should 
 travel from place to place until that climate is reached which suits 
 the individual constitution, and there remain. 
 
 As soon as the testicle gives evidenca of tubercular inflammation, 
 it will not be of any use if allowed to remain, and for this reason and 
 the possibility that it precedes and sometimes excites the renal tuber- 
 culosis, it should be extirpated. 
 
CHAPTER XIII. 
 
 INFARCTION OF THE KIDNEYS. FAT EMBOLISMS OF THE KID- 
 NEYS. PYEMIC EMBOLI OF THE KIDNEYS. 
 
 IlsTFAECTIOlSr OF THE KlDNEYS. 
 EEN"AL EMBOLISM. 
 
 Definition. — Renal embolism or infarction is that condition in 
 which a terminal artery of the kidney substance has become occluded 
 by a non-irritating embolus. 
 
 Etiology. — The chief cause of this lesion is valvular disease of the 
 heart. The emboli may come from the cardiac valves in the form of 
 detached fibrin or atheromatous material. They may also originate 
 from arterial thrombi, aneurisms, or atheromatous patches. This 
 condition has been called " rheumatismal nephritis." Infarctions 
 may be single or multiple. 
 
 Pathological Anatomy.— As the result of the lodgment of the em- 
 bolus, we have the circulation cut off from a conical or wedge-shaped 
 area, which first becomes anaemic. 
 
 The anaemia lasts only a short time, when the blood returns into 
 this pyramidal space from the venous side, and a permanent conges- 
 tion is established. 
 
 The embolus, with the surrounding stasis, acts as a foreign body, 
 and may terminate in a number of ways. 
 
 When small and non-infective, they rarely cause suppuration. 
 If small, the coagulated blood of the infarction becomes gradually 
 decolorized, changing from dark red to brown and finally to a yellow 
 int; it is ultimately absorbed. A moderate degree of inflamma- 
 tion ensues, which results in the formation of new tissue; and finally 
 all that remains to mark the seat of the infarction is a cicatricial pit 
 or depression. 
 
 In other cases, especially when the territory involved is large, there 
 is, following the decoloration, a molecular disintegration and partial 
 softening which excites an active peripheral inflammation. This 
 
142 
 
 INFARCTION OF TIIF KIDNEYS. 
 
 zone is rapidly encapsulated by a band of newly formed connective 
 tissue, thus preventing a complete fatty degeneration and absorption; 
 but the watery constituents of this granular mass are absorbed, and a 
 gray semi-solid or solid substance remains. Its surrounding capsule 
 becomes firmer and continually contracts upon this conical mass until 
 a dry granular and prominent wedge is formed. The apex is 
 imbedded in the cortical substance of the kidneys, but the base often 
 protrudes beyond the free surface of the glands. Immediately around 
 the infarction there is usually found a zone of hypersemic tissue. 
 In still other instances, this dry and granular infarction may be 
 
 Fig. 23. — Acute Congestion of the Kidney, with Multiple Infarctions. 
 A, Medullary portion. B, Cortical portion, o, Infarctions. 6, Congested Malpighian corpuscle. 
 
 found to contain an abundance of inorganic salts, when it is spoken of 
 as a chalky or calcareous nodule. This change, however, is exceed- 
 ingly rare. 
 
 Symptoms. — As a rule, the lodgment of an embolus in the renal 
 tissue does not produce symptoms active enough to attract attention. 
 But occasionally during the course of a severe lesion of the cardiac 
 valves, or with extensive atheroma of the large vessels, the individual 
 will be attacked suddenly with albuminuria, renal hemorrhage, or 
 both, associated with a marked rise in temperature and great pain in 
 the back. 
 
FAT EMBOLISM OF TIIK KIDNEYS. 
 
 143 
 
 With such a history, the symptoms would justify the diagnosis of 
 infarction of the kidneys, tod in all such cases its probability will be 
 confirmed by a necropsy. 
 
 Diagnosis. — As a rule, none is made at the time of occurrence, nor 
 during the life of the patient. Infarctions of the kidneys are usually 
 necropsy discoveries. 
 
 Prognosis. — The prognosis is favorable. 
 
 Treatment. — None need be instituted. 
 
 FAT EMBOLISM OF THE KIDNEYS. 
 
 Definition.— Fat embolism of the kidneys is a condition in which 
 one of the terminal arterioles becomes occluded with an embolus 
 composed of fat globules. 
 
 Etiology.— Occlusion of the small vessels by fat (fat embolism) 
 appears to have been first observed by H. Miiller, in I860. 1 He 
 • found some of the choroidal vessels filled with fat, but did not at that 
 time attach much importance to the condition. 
 
 The discovery, however, of fat embolism is credited to Zinker, in 
 1862. Since that time, numerous cases have been reported as occur- 
 ring in the lungs, kidneys, and other organs of the body. They are 
 more frequently found in the lungs than in the kidneys. 
 
 When they do occur in the renal tissue, they are frequently 
 secondary to those deposited in the lungs, and are found two or three 
 days later. 
 
 Fat emboli occur in connection with simple and compound frac- 
 tures, especially the latter, and in those in which the cranial bones 
 are implicated, also in connection with pyaemia and after surgical 
 operations. In some cases of diabetic coma, similar formations have 
 been described. In all cases, fat embolism appears to be associated 
 with some form of blood taint which allows the fat to circulate in the 
 blood in an undigested or free state, and consequently it is arrested and 
 occludes some of the small arterial or capillary vessels in the various 
 organs. 
 
 Pathological Anatomy.— The microscopic appearances are variable; 
 the principal change is pallor of the whole organ, or marked zones of 
 paleness. There is also some increase in the size, with a flabby condi- 
 tion of the organ. In some instances, minute hemorrhages will be 
 found under the capsule. 
 
 Microscojjic examination shows that certain portions of the kidneys 
 are congested, while the remainder is normal. Near the congested 
 
 1 Wiirzburger Medic. Zeitschrift. 
 
14i 
 
 FAT EMBOLISM OF TIIK KIDNEYS. 
 
 arras, zones of fatty masses are found which, if the section has been 
 stained with osmic acid, appear under the microscope as little black 
 masses, some of which are located in the small capillary vessels of the 
 glomeruli, or they may he in the small vessels just outside the tuft. 
 
 In the immediate vicinity of the congestion, small extravasations of 
 blood will be noticed in which numerous fat droplets are found. 
 
 As a rule, fat is not present in the lumen of the uriniferous tubules. 
 but the epithelial cells lining the tubules often contain fat droplets of 
 large size. 
 
 Symptoms. — From the experimental researches of Scriba, the symp- 
 toms produced by fat emboli are as follows: The presence of fat in the 
 urine at intervals; transient attacks of dyspnoea; loweVing of tempera- 
 
 Fig. 30.— Fat Embolism of the Kidney. X 350. Section Stained with Osmic Acid. 
 A, Capillary vessel in Malpighian tuft occluded by fat embolism, which is stained black by the 
 acid ; B, portion of tuft not occluded by the fat embolism. 
 
 ture; temporary and slight haemoptysis, without fever, and generally 
 without dulnessor rales; irregular action of the heart; collapse, with 
 marked paiior of the skin and mucous membranes; at first shallow 
 respiration, at times interrupted by deep sighing inspiration, later 
 Cheyne-StoJces respiration; spasm of various kinds or paralysis, gen- 
 erally bilateral; and diminution of reflex irritability. 
 
 Diagnosis. — A case presenting the above symptoms, in conjunction 
 with one of the known causes, would be strong evidence in favor of 
 fat embolism. 
 
 Prognosis. — This is usually, if not always, unfavorable. Scriba be- 
 lieves from his experience that death occurs when the fat emboli reach 
 or attack the cerebro-spinal centres. 
 
PYEMIC EMBOLI. 145 
 
 Treatment. — Little can be done, except to treat the pre-existing dis- 
 ease. 
 
 PYiEMIC EMBOLI. 
 
 Definition. — This is a condition of the kidneys in which an embolus 
 charged with pyaemic poison has become impacted in a terminal artery, 
 resulting either in the formation of a secondary metastatic abscess or a 
 localized gangrenous patch of renal tissue. This condition, as a rule, 
 does not give rise to any special symptoms during the life of the 
 patient. 
 
 Etiology. — This form of abscess is always developed by the lodg- 
 ment of some of the infectious or pyaemia poison at a given point. 
 
 Pathological Anatomy. — The kidneys may be the seat of one large 
 suppurating mass, but usually they are dotted by numerous white 
 points or small abscesses. 
 
 If the kidneys are removed early in the disease, the intermediate 
 stage may be obtained, viz., wedge-shaped zones of red consolidation, 
 or a little later the dusky gray masses of inflammatory exudation. In 
 this form of infarction, the occluding embolus is not found at the 
 apex and near the periphery of the organ, but is now central and com- 
 pletely surrounded by the diseased process. 
 
 In rare cases, instead of a suppurating focus being developed, the 
 renal tissue becomes gangrenous in patches, with more or less sur- 
 rounding suppuration. 
 
 Symptoms and Diagnosis. — Pyaemic suppuration of the kidneys is 
 suspected if, during the course of a pyaemia, the urine suddenly be- 
 comes albuminous or bloody. 
 
 Prognosis and Treatment. — It is always a fatal disease and little 
 can be done in the way of treating the general symptoms; they are 
 usually, if not always, fatal. 
 10 
 
CHAPTER XIV. 
 
 TUMORS OF THE KIDNEYS : SARCOMA ; CARCINOMA ; ADENOMA ; 
 FIBROMA ; CONGENITAL RHABDO-SARCOMA ; ANGIOMA ; LI- 
 POMA ; LYMPHOMA ; OSTEOMA ; ANGIOMA OR CAVERNOUS 
 NEOPLASMS. 
 
 SARCOMA OF TIIE KIDNEYS. 
 
 Definition. — This is a condition in which the kidneys are the seat of 
 a new growth of the embryonic connective-tissue type. 
 
 Etiology. — The absolute causation of sarcomata in the kidneys, as 
 elsewhere, is unknown. This condition lias been met with both in 
 children and in adults,, but it is more common in children. There 
 appears to be considerable ground for believing that many of the cases 
 published as primary carcinoma of the kidneys have in reality been 
 sarcomata. 
 
 Only once has the opportunity presented for holding a necropsy in 
 a typical case of primary sarcoma in an adult. 
 
 Pathological Anatomy. — The kidneys become very much enlarged, 
 but they retain the general outline of the glands. The weight of the 
 tumor may be as high as 50 or 60 ounces (1,417.488 or 1,700.972 
 grams). 
 
 In one case, previously recorded, the left kidney weighed 48 ounces 
 (1,360.780 grams). When bisected, it measured in its long diameter, 
 from the superior to the inferior border, 5 inches (13 centimetres); 
 from the peripheral surface of the cortex to the pelvis at the apex 
 of a pyramid, 3^- inches (almost 9 centimetres). 
 
 In this case the capsule was very much thickened; the pelvis was 
 obliterated, the space being filled with a grumous material; the ureter 
 was dilated and very much hypertrophied. 
 
 Upon microscopic examination, very little renal tissue was found, 
 but the mass of the neoplasm was composed of medium-sized, round 
 connective-tissue corpuscles imbedded in a homogeneous matrix. 
 
 In this particular case, the right kidney also contained a similar 
 new growth ; but on this side about one-half the renal tissue was 
 plainly visible, and in a fairly normal condition. 
 
SARCOMA OF Til TO KIDNKVS. 
 
 147 
 
 The retroperitoneal glands were not implicated. A portion of the 
 stomach, duodenum, and colon, lying against the large tumor, had be- 
 come adherent to it, and were becoming invaded by the sarcomatous 
 growth. The diaphragm was also involved in the morbid process. 
 
 There was no way in which the new development in one kidney 
 could be traced to the opposite organ, except through the medium 
 of the vascular channels. A similar primary sarcoma of the kidney 
 was once found in a cow. This case was presented at the New York 
 Pathological Society, 1880. 
 
 Symptoms. — The symptoms of sarcoma and carcinoma of the kid- 
 neys appear to be about the same ; namely, a rapidly growing tumor 
 in the region of the kidneys, with recurring attacks of hematuria. 
 
 Fig. 31.— Round-Cell Sarcoma of the Kidney. X 350. 
 a, Sarcomatous tissue ; c, Malpighian corpuscles in partially uninvaded tissue ; b, urinif erous; 
 tubuli; d, renal tissue adjacent to the sarcomatous tumor, slightly infiltrated with sarcomatous, 
 cells. 
 
 So far as can be learned from the literature upon the subject, the 
 sarcomata are attended with much less pain than the carcinomata. 
 The sarcomata being the more vascular of the two, will in all 
 probability give rise to more copious and frequent attacks of haema- 
 turia. 
 
 Few cases have been recorded. Dr. Abraham Jacobi, in presenting- 
 a sarcoma of the kidney in a child at the Obstetrical Society, 1874, 
 remarked that he had not been able to find a recorded case either in 
 in a child or an adult. 
 
 At one of the meetings of the New York Pathological Society in 
 
14$ SARCOMA OF THE KIDNEYS. 
 
 1885. Dr. Jacobi, in presenting a similar case in behalf of a candi- 
 date, remarked that "there were only sixteen or eighteen cases of 
 unquestioned primary sarcoma of the kidneys on record." 
 
 Secondary sarcoma, or those developing near the renal glands and 
 growing into their substance, are not uncommon. 
 
 In sarcoma of whatever variety, there is not as characteristic a 
 cachexia as there is with carcinoma. 
 
 Diagnosis. — The rapidly growing tumor in the region of the kid- 
 neys, without much pain and the frequent renal hemorrhages, would 
 indicate a sarcoma rather than a carcinoma. 
 
 Prognosis. — Here, as in carcinoma, it in all probability will prove 
 fatal. 
 
 Treatment. — The only method of treatment which offers any pros- 
 pect of recovery would be that of nephrectomy. In the table of one 
 hundred cases collected by Harris, 1 there were twelve which were 
 either pure sarcoma, adeno- or angio-sarcoma; in 41.66$ of these 
 twelve, there was a complete recovery from this operation; in 33.33 
 per cent, death resulted; in the remaining 25 per cent, the diagnosis 
 was doubtful, or the authenticity of recovery was uncertain. 
 
 Dividing the cases into two classes and making the best showing 
 possible, 58.33 per cent recovered from, and 41.66 per cent died from 
 the operation. 
 
 Dr. Weir records in all thirty-two cases, 2 in which this operation 
 has been performed for various kinds of tumors of the kidneys, and 
 finds the mortality to be 68.75 per cent. 
 
 From this high mortality he argues that the operation cannot be 
 considered a surgical success, and remarks: "I think that the prin- 
 cipal, if not the sole condition in a diseased kidney that justifies a 
 nephrectomy is a suppurative process." 
 
 In Dr. Gross' paper upon nephrectomy, the following is found : 
 "The kidney has been removed for sarcoma thirty-three times, with 
 fourteen recoveries and nineteen deaths, or a mortality of 57.57 per 
 cent. In other words, 57.57 per cent died as the direct result of the 
 operation, while of the survivors 42.85 per cent died subsequently, 
 
 1 Harris, R. P., "An Analytical Examination of One Hundred Cases; with a 
 tabular record arranged chronologically." American Journal of the Medical 
 Sciences, July, 1882, p. 109. 
 
 a Weir, Robert F., " Remarks on Extirpation of the Kidney, with Cases of 
 Nephrectomy for Pyonephrosis, and Nephrotomy for Rupture of the Kidney." 
 Medical News, Philadelphia, December 27th, 1884, p. 709. 
 
CARCINOMA OF THE KIDNEYS. 
 
 140 
 
 and 35.71 per cent remained well for thirty-one and a half months on 
 
 an average." ' 
 
 CARCINOMA OF THE KIDNEYS. 
 
 Definition. — This is a condition in which the kidneys are the seat 
 of an epithelial growth having the characteristic appearances of car- 
 cinoma. 
 
 Etiology. — The cause of this disease is not known. Primary cancer 
 is said to be more frequent in the kidneys of children than adults. 
 
 Pathological Anatomy. — In primary carcinoma of the kidneys, the 
 
 m 
 
 Fig. 33. — Medullary Carcinoma. 
 ( " Handbook of Pathological Anatomy and Histology," Delafleld and Prudden.) 
 
 organs often become very large. The neoplasm may be twelve 
 inches long by six inches broad (30.4x15.2 centimetres). It will 
 weigh five or six times as much as a normal kidney. The shape of 
 the gland is usually retained, but the newly formed tissue is most 
 abundant in the cortical substance. The neoplasm may be evenly 
 diffused throughout the organ, or it may be in localized nodules 
 
 1 Gross, S. W., "Nephrectomy, its Indications and Con tra-indications." 
 American Journal of the Medical Sciences, Philadelphia, July, 1885, pp. 79, 85. 
 
150 . Ak< 1V>MA OF THE KIPXEYS. 
 
 which are separated from each other by altered renal tissue. The 
 calices and the pelvis are also invaded. 
 
 The renal substance immediately adjacent to these nodules will be 
 found either in a state of atrophy or hypertrophy, with the formation of 
 new connective tissue, depending upon the amount of pressure or 
 irritation. 
 
 The renal epithelial cells undergo more or less of a fatty disintegra- 
 tion. 
 
 The blood-vessels are usually congested. 
 
 The exact method by which this neoplasm is developed in the kid- 
 neys has not been satisfactorily demonstrated. 
 
 Microscopic examination, as a rule, reveals the evidence of medullary 
 carcinoma, in theshapeof very thin and delicate alveolar walls, form- 
 ing spaces the contents of which are composed of irregularly shaped 
 nucleated epithelial corpuscles. These cells are packed into these 
 alveolar cavities without reference to order of arrangement and with- 
 out intercellular tissue. 
 
 The eucephaloid is the variety most commonly found in the kidneys, 
 but the colloid and other forms have been described. 
 
 Symptoms. — The leading symptoms are pain, localized in the region 
 of the kidneys, associated with a rapidly growing tumor at the same 
 point. The neoplasm may be smooth or nodular. The growth of a 
 carcinoma at this point is more rapid than at any other portion of the 
 body. This form of abdominal tumor is said to be the most frequent 
 in children, and consequently the first to be thought of in case of 
 abdominal distention. In adults the growth is also rapid. 
 
 There are usually recurring attacks of hematuria, with a variable 
 interval between. After a short time, there is marked emaciation, 
 with the characteristic cachexia. 
 
 Diagnosis.— The recurring attacks of hematuria have been con- 
 sidered diagnostic. Certainly, with the clinical history, and the 
 rapidly growing and painful tumor, there ought not to be much 
 doubt as to the nature of the disease. 
 Prognosis. — This is always fatal. 
 
 Treatment.— This also is palliative and not curative. Operative 
 interference has been and may be resorted to, but as it offers so little 
 prospect of relief, it is hardly warranted. 
 
 Gross, in speaking of the results of removal of the kidney for car- 
 cinomatous and sarcomatous growths together, says: " In 49 cases, 
 61.22 per cent die as a direct result of the procedure; that 16.32 per 
 cent perish subsequently; that 12.24 per cent appear to make a per- 
 manent recovery." Subtracting the more favorable results obtained 
 
ADENOMA. OF THE KIDNEYS. 15L 
 
 in sarcoma alone, the success of carcinoma alone would be even more 
 infrequent than the above figures would indicate. The lumbar opera*- 
 tion appears to be less dangerous than the ventral. 
 
 ADENOMA OF THE KIDNEYS. 
 
 Definition.— Adenoma of the kidneys is that condition in which a 
 neoplasm is developed in the substance of these organs, which offers 
 the same structure as the racemose gland type. 
 
 Two varieties have been described, the papillary and the alveolar 
 adenoma. 
 
 Etiology.— Oi this little is known; probably the misplaced germ 
 theory offers as satisfactory an explanation as any. 
 
 Pathological Anatomy.— Adenoma is equally frequent in both kid- 
 neys. Tliey are most frequently located at one or the other extremity, 
 rarely in the centre. They are commonly found in the cortical sub- 
 stance near the periphery; seldom in or near the pelvis. When close to 
 the surface, the capsule also is involved. As a rule, they are single, but 
 two or more have been recorded. Both kidneys are invaded in about 
 twenty percent of the cases; the size varies between that of a millet- 
 seed and a hen's egg, or even larger; the more frequent size, how- 
 ever, being equal to a walnut or hazelnut. Their consistency is almost 
 the same as the renal substance, unless they have undergone metamor- 
 photic changes. 
 
 Papillary Adenoma.— When a papillary adenoma is completely 
 developed in the kidneys, it is separated from the surrounding renal 
 tissue by a capsule which varies in thickness. Within this capsule, 
 there may be a single growth, or it may be divided into several com- 
 partments, each filled with papillary neoplasms. These grow out 
 from one or more centres of the cavity wall, with a vascular network, 
 sometimes abundant, and again deficient in round and spindle cells. 
 When one or several growths are examined, they somewhat resemble 
 a tree. The walls of the cavity are lined with a layer of epithelium, 
 the cells of which have various forms and sizes, though the cylindrical 
 epithelium is the type most frequently found. Not unfrequently the 
 .epithelial cells have undergone a fatty degeneration, and in some cases 
 pigment granules are also found. In every case in which the tumor 
 has several cavities, there is found between them a fibrous web of 
 kidney substance. In the latter case, the uriniferous tubules are 
 easily seen, variously compressed, or distended with colloid matter, 
 while the Malpighian capsules have undergone fibrous degeneration, 
 or are transformed into cysts. When more recent stages of papillary 
 
152 ADENOMA OF THE KIDNEYS. 
 
 adenoma are observed, however, it is seen that it is not limited by the 
 surrounding renal tissue. It is made up of numerous cavities con- 
 taining gland iobules which increase from the periphery toward the 
 centre; the cells bearing a striking resemblance to the epithelium of 
 the collecting tubes of the cortex. The lobules lie so close together 
 that there is scarcely room between them for a firm connective-tissue 
 stroma, though in some places there is qnite a wide separation. 
 
 Alveolar Adenoma. — This is shown, as its name indicates, by an 
 exquisite alveolar structure. The alveoli are of various sizes and 
 shapes, the smallest being less than the cross section of a convoluted 
 tubule. They are round, oval, cylindrical or irregular in shape, and 
 contain epithelial-like cells, or there may be a central fissure or even 
 a complete lumen. The cells have a peculiar character, being generally 
 large, polyhedral, prismatic, or wedge-shaped, still free from retro- 
 grade metamorphosis, and lying in a homogeneous or granular proto- 
 plasm. Between the alveoli there is a very slight connective-tissue 
 stroma which is structureless, or contains spindle-shaped cells, and in 
 which the blood-vessels ramify. When the alveolar adenoma attains 
 a certain size, like papillary adenoma, it becomes invested by a cap- 
 sule. Whilst both the papillary and alveolar adenoma have clearly 
 defined forms, and are easily recognized during their genesis, they so 
 closely resemble each other in their latter stages that they can scarcely 
 be distinguished. 
 
 These tumors are said frequently to undergo metamorphotic 
 changes: 1, fatty; 2, fibroid; 3, fibrous; 4, cavernous and pigment 
 metamorphosis; 5, cystic degeneration; and 6, colloid degeneration, 
 with the formation of concretions in the stroma. 1 
 
 Symptoms. — During life, when small, it is hardly to be expected 
 that they would produce any symptoms that would attract special 
 attention. There is, however, one case reported by Czerny, in which 
 the left kidney was extirpated for a large adenoma of that organ in 
 a child eleven months old. 
 
 Differential Diagnosis.— -The diagnosis between adenoma and car- 
 cinoma is most important. Alveolar adenoma may easily be con- 
 founded with carcinoma, as not only the alveolar structure, but the 
 cells resemble those of a carcinomatous tumor, the adenoma cells being 
 scarcely less polymorphous than cancer cells. But after an adeno- 
 matous tumor has attained a certain size, it possesses a capsule, in 
 which respect it differs from carcinoma. A careful microscopic ex- 
 amination, however, will decide the diagnosis. 
 
 Adenoma is diagnosed from fibro-sarcoma by the fact that the 
 1 Medizin. Jahrbiicher, 1883, Hft. ii. 
 
LIPOMA OF THE KIDNEYS. 
 
 1 53 
 
 latter occurs in old age, and only in the medullary substance 
 of the kidneys, and by the well-known miscroscopic appearance 
 of sarcoma. Adenoma is easily diagnosticated from hsematangioma 
 cavernosa, and from cystic disease of the kidneys, by the macroscopic 
 and microscopic appearances. 
 
 FIBROMA OF THE KIDNEYS. 
 
 Localized and dense masses of white flbrillated connective tissue 
 have been found in the outer portion of the medullary substance. 
 They are usually considered as localized patches of interstitial neph- 
 ritis. This appears to be the nearest approach that occurs to a 
 fibrous neoplasm in the kidneys. 
 
 CONGENITAL RHABDO-SARCOMA OF THE KIDNEYS. 
 
 A congenital striped -muscle sarcoma has been described in Vir- 
 chow's Archives, Bd. LXV. The kidneys were removed from a child 
 who had been healthy during the first year after birth. At this time 
 it sickened, and three months later died. 
 
 Both renal organs were invaded by tumors, which were found, on 
 microscopic examination, to be composed of striped muscle fibres. 
 The fibrillar were small, long, and interwoven. A sarcolemmawasnot 
 discovered. In other parts, but not so plentifully, the typical struc- 
 ture of sarcoma was found. It was explained, according to Cohn- 
 heim, by an original faulty growth, and not as a result of metastasis. 
 
 ANGIOMA OR CAYERNOUS TUMORS OF THE KIDNEYS. 
 
 In rare instances, a neoplasm has been found in the kidneys, com- 
 posed of a bunch of dilated capillaries, and closely resembling erectile 
 tissue. They are analogous to the cavernous tumors so frequently 
 found in the liver. In size they vary from a small pea to that of a 
 hickory nut. These formations are pathological curiosities only, 
 having no clinical significance. 
 
 LIPOMA OF THE KIDNEYS. 
 
 Lipoma of the kidneys is another rare form of neoplasm. Two 
 tumors of this character have been found in making about one thou- 
 sand necropsies. This would make its frequency one in five hundred. 
 
 In the first case, the neoplasm was located in the medullary portion 
 of the kidney; it was about one inch (2.5 centimetres) in diameter. 
 The new growth was surrounded by a distinct capsule, and from its 
 
154 
 
 LYMPHOMATA OF THE KIDXKYS. 
 
 macroscopic appearances might easily be mistaken for a medullary 
 carcinoma or a round-celled sarcoma. But an examination by the 
 microscope proved conclusively that it was composed of adipose 
 tissue. In the second case, the neoplasm had its origin in the cor- 
 Hw. about one-fourth being imbedded in the renal tissue, the remain- 
 ing three-fourths protruding beyond the free surface of the gland. 
 In this instance, the new growth was distinctly encapsulated 
 and lobulated : upon microscopic examination, it was found to be 
 composed exclusively of adipose tissue. 
 
 Fig. 33.— Lipoma of Kidney. X 350. 
 
 a, Straight collecting uriniferous tubules ; b, lipoma imbedded in the kidney tissue ; c, fibril- 
 lated connective-tissue capsule of the lipoma ; e, commencing parenchymatous metamorphosis 
 of the renal epithelium. 
 
 This second tumor was about one and one-half inch (7 centimetres) 
 long by one-half inch (2.3 centimetres) in thickness. 
 
 LYMPHOMATA OK LEUKEMIC TUMORS. 
 
 Lymphomata or leuka?mic formations have been found in the 
 kidneys. This is a condition in which one or more small neo- 
 plasms, var} r ing in size from a small dot to that of a cherry, are 
 found. In shape they are round, pyramidal, or oval, and composed 
 chiefly of lymphoid corpuscles in a delicate adenoid reticulum. 
 From the frequency with which Virchow and Eindfleisch found a 
 collection of red blood-discs in their centre, they were led to believe 
 that these neoplasms had origin in an extravasation. 
 
 Such neoplasms are of pathological rather than of clinical interest. 
 
GUMMATA OF THE KIDNEYS. J DO 
 
 OSSEOUS TUMORS. 
 
 Bony transformation of a fibrous thickening has been recorded in 
 a few instances. 
 
 GUMMATA OF THE KIDNEYS. 
 
 Syphilitic disease of the kidneys in the shape of gummy forma- 
 tions, although not common, is more frequent than has heretofore 
 been supposed. Gummata of the kidneys are usually small and 
 multiple, and are most frequently located in the cortical portion. 
 Here, as in other parts of the body, they are pale, granular-looking 
 deposits, often having a cheesy centre. But the periphery is a little 
 more distinct, and frequently is formed of concentric layers of incom- 
 pletely fibrillated connective tissue, containing small blood-vessels, 
 thickened by a hyaline metamorphosis. By this tendency to encap- 
 sulation and the peculiar thickening of the blood-vessels, their nature 
 can be determined. 
 
 A special syphilitic disease of the kidneys, without gummata, in 
 which there is an interstitial thickening and amyloid transformation, 
 characterized by albuminuria, etc., has been described. 
 
 Such a disease is here omitted, as the various forms already de- 
 scribed are believed to completely cover the question, and also 
 from the fact that syphilis per se seldom excites an acute renal 
 lesion. It is very uncommon to meet a case of acute renal disease 
 during the active symptoms of syphilis, and when it does occur, it 
 is a question as to the excitant, whether it is the syphilis, the 
 medicines used, or some extraneous cause. On the other hand, from 
 an extended clinical macroscopic and microscopic study in well au- 
 thenticated cases of syphilis, the firm conviction has been developed 
 that the syphilitic vice determines in a large measure whether the 
 force of the renal disease is to be spent upon the interstitial tissue, 
 blood-vessels, or epithelial cells. 
 
 In patients suffering with a specific taint, a peculiar hyaline trans- 
 formation and thickeniug of the blood-vessels is found, which appears 
 to be diagnostic of the syphilitic disease, and which does not exist 
 where syphilis is not present. 
 
 When a renal lesion is developed in a person with a specific 
 taint, unless directly referable to the causes for the parenchymatous 
 group, it is most likely to be of the chronic diffuse variety with vas- 
 cular changes; or of a cirrhotic or an amyloid form. Observation 
 in several necropsies where there had been long-continued suppura- 
 tion of the bones with an absence of a syphilitic vice and of the 
 amyloid or hyaline changes in any part of the body, has developed 
 
156 GUMMATA OF THE KIDNEYS. 
 
 the belief that the syphilis is always the essential factor in producing 
 this hyaline vascular change; it was always marked in those cases 
 in which a decided specific taint was certain. 
 
 The oft reiterated remark that small and repeated doses of the 
 bichloride of mercury and iodide of potassium do as much, if not 
 more good than all other medicinal agents in Blight's, certainly aids 
 in substantiating the above view. Why not say, as syphilis is a fre- 
 quent etiological factor in producing, not only renal diseases, but many 
 other visceral lesions, that it should always be sought after and treated ? 
 The almost universal occurrence of syphilis is not a pleasant topic 
 from the moral side of the question, but from the medicinal it is, for 
 if the cause of the disease can be traced to a latent syphilis, and is 
 early recognized as such and properly treated, recovery will result, 
 where otherwise death would ensue. Who would not grasp at life, 
 even with a syphilitic taint, against a certain death warrant ? 
 
CHAPTER XV. 
 
 PARASITES: ECHINOCOCCUS, BILHARZIA H^MATOBIA, 
 STRONGYLUS SEU ESTRONGYLUS GIGAS, 
 ASCARIS RENALIS. 
 
 Hydatids of the Kidneys. 
 
 echinococcus cysts. 
 
 Definition. — The hydatid or echinococcus cyst is that form of dis- 
 ease in which an immature embryo of the Taenia echinococcus finds 
 its way into the kidney, and becomes fixed and swollen to a large 
 vesicle, on the inner wall of which a colony of young and immature 
 scolices is developed. 
 
 Etiology. — Hydatids are always due to the ingestion of the eggs of 
 the Taenia echinococcus, which may be taken in either with the water 
 or food. 
 
 Fig. 34. — Taenia Echinococcus Complete, x about 16. 
 
 The formation of the hydatid cyst is almost always a slow process. 
 
 Their frequency depends upon the abundance of dogs and the 
 habits of the people. They are quite common in Iceland, Egypt, and 
 in South Australia. In other countries they are exceedingly rare. 
 
 Pathological Anatomy. — The hydatid may be one of three varieties: 
 exogenous, endogenous, or multilocular. The first is rare in man; 
 the second and last, especially the endogenous, are found in the 
 human subject. 
 
 The essential character of the growth is the formation around the 
 parasite of a tough and well-developed capsule, composed of fibrillated 
 
i:»s 
 
 ECHINOCOCCUS CYSTS. 
 
 connective tissue, from which other bands of connective tissue pass 
 into and across the cyst cavity in every direction, thus forming small 
 interstices. 
 
 The alveoli are of various sizes and shapes, lined with vesicles and 
 filled with gelatiniform plasma, and occasionally with the so-called 
 echinococcus heads. A few blood-vessels may be found ramifying 
 through the mass, but no glandular tissue. 
 
 Fig. 35. — Cuticula of Echinococcus Cyst. X 250. 
 (" Handbook of Pathological Anatomy and Histology." Delafield and Prudden.) 
 
 From without inward we find first an investing capsule, formed 
 from the surrounding tissue. Within this there is a thick, homo- 
 geneous laminated elastic membrane which, when withdrawn, displays 
 a peculiar tremulous motion and coils upon itself when cut. This is 
 the so-called cuticular structureless layer, or entocyst of Huxley. Within 
 and closely applied to it, lies the endocyst, of the same author. This 
 
 Fig. 36. — Endocyst of Huxley, showing Buds and < ;kmmjk. 
 
 is a thin, soft, comparatively non-elastic, granulated membrane and 
 forms the essentially vital part of the bladder-worm. From this 
 inner membrane buds are produced and these gemma? become trans- 
 formed into echinococcus heads, both directly and indirectly. The 
 brood capsules often contain many heads, and by a process of 
 eversion project into the general cavity of the mother hydatids. By 
 
KOIIINOCOOCITM CYSTS. 
 
 159 
 
 a process of proliferation, daughter and grand-daughter hydatids are 
 developed within the maternal cyst, and these smaller cysts also pro- 
 duce the heads. Beyond this point, their method of development is 
 uncertain, and just how the heads are formed is unknown. 
 
 When located in the kidney, the organ becomes enlarged, sometimes 
 to an enormous extent. The cyst may connect itself to neighboring 
 organs by inflammatory adhesion. A globular tumor projects from 
 the surface and is imbedded in the kidney. By its pressure it often in- 
 duces atrophy of the renal tissue. The cyst has for an outer covering 
 a fibrous capsule of its own. The hydatid may be barren, that is, free 
 from daughter cysts, or it may be made up of many smaller cysts, and 
 processes growing inward and containing scolices, which may give 
 origin, if taken into the proper system, to the corresponding tape- 
 worm in that animal. In either case, the cyst-wall is tensely expanded 
 by a clear liquid, rich in the chloride of sodium. 
 
 Fig. 37. — Scolices of T-sjnia Ehinococcus. X 60. 
 In one the rostellum is projected, in the others it is withdrawn. (Delafleld and Prudden, 
 " Handbook of Pathological Anatomy and Histology.") 
 
 The cysts enlarge gradually and burst in various directions, either 
 into the pelvis of the kidney, lung, bronchi, peritoneum, etc., but 
 most frequently into the renal pelvis. 
 
 The hydatid may suppurate and the necropsy will show the remains 
 only of a shrunken and shrivelled cyst, with its cheesy contents, in 
 which are imbedded the remains of the daughter-cyst and hooklets. 
 
 Symptoms. — The course of hydatids in the kidneys is slow and 
 chronic, often lasting for many years. The first evidence of their 
 existence may be the discovery of a tumor, or rupture may be the first 
 indication. This may occur with or without a previous discovery of 
 the tumor. 
 
 If the sac ruptures into the renal pelvis, the passage of the daughter- 
 
160 
 
 BILHARZIA ELEMATOBIA. 
 
 cysi through the ureter may give rise to all the symptoms of renal colic. 
 
 The finding of the remains of the cyst or the hooklets in the urine 
 will complete the diagnosis. 
 
 The ruptured cyst may collapse and atrophy. Two or more dis- 
 charges may occur from the same cyst at varying intervals. 
 
 If they open and discharge by the respiratory tract, thoracic pain 
 and cough will be the prominent symptoms. Remnants or hooklets 
 will be found in the sputum. Such cases terminate quite favorably. 
 
 The globular form and elastic nature of the tumor strongly favor 
 the presence of hydatids. If the cyst suppurates, local pain and 
 fever are the additional and prominent symptoms. 
 
 Diagnosis. — The peculiar form and elasticity of the tumor is strongly 
 indicative of its being of hydatid formation. Finding cysts and 
 hooklets in the urine, or in the fluid withdrawn by aspiration, con- 
 firms the diagnosis. 
 
 Prognosis. — This is very uncertain; nothing positive can be given. 
 
 Fig. 38.— Hooklets from Scolex of Taenia Echinococcus. X 750. 
 (Delafield and Pradden, " Handbook of Pathological Anatomy and Histology.") 
 
 Treatment. — Medical agents are useless. The fluid may be removed 
 by aspiration, when the parasite will frequently die and the cyst 
 shrivel and become obliterated. Oil of turpentine has been adminis- 
 tered, also male fern, but their utility is doubtful. 
 
 The radical treatment is surgical. Both electrolysis and nephrec- 
 tomy have been employed with good success. 
 
 BILHARZIA HJEMATOBIA. 
 
 Definition. — This is a peculiar parasite, found in certain localities 
 in Africa and Europe, which, when taken into the system, becomes 
 lodged in the urina'ry apparatus and gives rise to an epidemic hasma- 
 turia. 
 
 Etiology. —This name was given to this special entozoon by Profes- 
 sor Cobbold in 1851, from the fact that Dr. Bilharz was the first to 
 
BILHAKZIA H/KMATOHIA. 
 
 61 
 
 discover the parasite. The worm was first found in the portal vein 
 of a man, next in the same vein of a monkey. At first it was sup- 
 posed to be aDistoma, but it is now generally known as the Bilharzia 
 hcematobia. Later, the same parasite was found in the mesenteric 
 and vesical veins, and also in other parts of the body, producing 
 symptoms of a formidable disease. Finally, it was found in the 
 urine. 
 
 Dr. John Harley next discovered that a form of epidemic hema- 
 turia at the Cape of Good Hope was due to a parasite which he con- 
 sidered a new species. Further research, however, proved that it 
 was the same Bilharzia, and this latter conclusion is now pretty gen- 
 erally accepted. The researches of Dr. Harley were very important, 
 
 Fig. 39.— Bilharzia Hcematobia. x about 15 times. 
 
 a, b and c, The female, partly placed in the gynaecophorous canal of the male; a, anterior 
 extremity; c, posterior extremity; d, body seen within the canal; e, /, gr, h and i, the male; 
 2, f, gynsecophorous canal, from which the female has been partly extracted; i, buccal sucker; 
 fc, ventral sucker; between i and fc, the trunk; after k, the tail. After Bilharz. 
 
 however, as they showed a much greater geographical range for this 
 parasitic disease. 
 
 Pathological Anatomy. — These worms differ from all the other 
 varieties of flukes in having separate sexes. 
 
 The female is a very slender worm, resembling filaria-form nema- 
 toids. During copulation, the female is lodged in a long slit-like 
 groove or gyngecophoric canal with which the male is furnished. 
 
 of an inch (1.4110 mm. to 4.233 mm.), 
 11 
 
 The ova measure from y^-g-to ^ 
 
162 BILIIAK/.IA lLKMATOHIA. 
 
 and are sharply pointed at one end. They are a form of ciliated 
 embryo, a complete and extended description of which will be found 
 by Dr. Cobbold in the British MedicalJournal, 1872. 
 
 Both the male and the female are found lodged in the walls of the 
 human bladder. 
 
 Symptoms. — There are no characteristic manifestations at first, and, 
 as a rule, there is no evidence of the entozoon*having become lodged 
 in the human system, until it has matured and commenced the dis- 
 charge of ova. The first symptom is pain on passing water, and at 
 the end of micturition there is a discharge of a few drops or more of 
 hlood . 
 
 Microscopic examination of this bloody urine will reveal the pres- 
 ence of the fertilized ova, and this will render the diagnosis positive. 
 
 There is little or no general distress: but in some cases there may 
 be a dull aching sensation in the lumbar region. But in the more 
 aggravated cases the bleeding increases until the quantity of blood 
 lost at each micturition is considerable, not alone mixed with the 
 urine, but in some instances clots are also expelled. Xow there is 
 severe perineal and lumbar pain, and a vesical catarrh is developed 
 which is not easily relieved, as its cause cannot be removed. 
 
 Diagnosis. — Persistent inematuria, in those sections of country 
 where the entozoon is known to exist, and the finding of the ova in 
 the bloody urine, settle the question beyond a doubt. 
 
 Prognosis. — It is usually good. Dr. Vasy Lyle makes the follow- 
 ing statements: " Grave as the picture is, I must, however, state that 
 I have not met with a fatal case of Bilharzia hcematobia, whether aris- 
 ing directly or indirectly from the presence of that entozoon." But 
 in the severe cases it may be several years before a complete cure is 
 effected. 
 
 Treatment. — Dr. Cobbold considers it unwise to employ active 
 drugs with the view of expulsion, or vermicides with a view to destroy- 
 ing the parasite, as both do more injury than good. 
 
 The system, on the contrary, needs to be supported and given 
 strength to withstaud and arrest the hemorrhages, and eventually rid 
 itself of the worms. 
 
 The arctostajdiylos uva ursi, either alone or combined with hyos- 
 cyamus, has been found the most serviceable in formiug a barrier 
 around the entozoon and in preventing the hemorrhages. At the 
 same time the patient should be ordered tonics, cold bathing, and the 
 most nutritious diet, and if possible be removed from the locality 
 where he is supposed to have contracted the disease. 
 
ASCARIS RENALI8. L63 
 
 Diuretics and vesical irritants of all kinds are contra-indicated, the 
 
 reverse being more efficacious. 
 
 Strongylus seu Estroxgyus gig as. 
 ascaris renal] s. 
 
 Definition. — This parasite is a round worm of the genus Ascaris. 
 
 Etiology. — This entozoon has been found in man, horses, oxen, 
 hogs, mules, wolves, and fish-eating carnivora. 
 
 It is much more common in the lower animals than in man; only 
 a few cases having been recorded in the human subject. 
 
 Pathological Anatomy. — In a necropsy made upon a horse which 
 had been infected by this parasite, the following conditions were 
 found, and are given in detail : 
 
 The peritoneal cavity contained a large amount of blood and 
 coagulum, also about twenty of these round worms, varying in length 
 from 2>\ to 8 inches (9.989 to 20.319 centimetres). 
 
 Fie. 40.— Strongylus seu Estrongylus Gigas. 
 
 The genito-urinary tract up to the kidneys appeared to be normal, 
 but both these glands were the seat of very interesting changes, and 
 presented a very peculiar appearance. They were full of small round 
 holes, about one centimetre (two-fifths of an inch) in diameter. These 
 canals were very numerous, and gave the kidneys a worm-eaten 
 appearance. 
 
 For two reasons this change was supposed to be due to the passage 
 of these round worms through the tissue of the glands. First, the 
 holes passed through the renal capsule, as well as the kidney tissue ; 
 and, second, a worm was found in one of the kidneys, and protruded 
 from one of the holes at the time of the necropsy. 
 
 Microscopic examination of the organs showed the renal epithelial 
 corpuscles to be slightly granular, but otherwise quite normal in 
 appearance. Transverse sections of the openings gave them the ap- 
 pearance of pretty clear-cut holes, at the expense of the renal sub- 
 stance. 
 
10-i ASCARIS Kl'.NAl.ls. 
 
 Each canal was surrounded by a thin layer of inflammatory exuda- 
 tion, but this action was limited to a very thin area, and evidently 
 had not irritated the gland tissue to any marked degree. 
 
 A similar, if not the same, form of strongylus has been reported 
 as occurring in the kidneys of the mule by Dr. Ballinger, of Cin- 
 cinnati. In his cases, some of the kidneys were entirely destroyed 
 and replaced by a ball of these worms. 
 
 The parasite itself has been described as a slender, cylindrical 
 worm, from two to six inches in length, and of a light gray color. 
 In some they have made their way into the parenchyma of the organs, 
 and caused suppuration, atrophy, and other mischief. 
 
 The male strongylus is smaller than the female, and tapers slightly 
 Towards each extremity. The head is obtuse, and furnished with an 
 orbicular mouth, encircled by six hemispherical papilla?; the body, 
 transversely striated, is marked by two longitudinal impressions; and 
 the tail, which is incurvated, ends in a dilated pouch, from the base 
 of which a penis projects. In the female, the tail is less pointed 
 than in the male, with the anus just below the apex; the vulva is 
 situated a short distance from the head, and communicates with a 
 slender cylindrical vagina ; the uterus in the large individuals is 
 about three inches long, and leads to a simple ovary, nearly four 
 times the length of the body. The nervous system of the body con- 
 sists of two delicate rings, one encircling the oesophagus, and the 
 other the anus, and connected by a single cord extending along the 
 middle line of the belly. 
 
 Symptoms. — Too few cases have been recorded to yield any trust- 
 worthy data. They are, when found in the human kidneys, rare curi- 
 osities. "When present, they are said to cause much distress. A 
 clinic patient once related the passage of a number of worms with the 
 urine, corresponding to this description, but at the time little atten- 
 tion was paid to the narrative, as none of the parasites were preserved. 
 The story may, however, have been true, and and may have been a 
 case of this kind. 
 
 Treatment. — For the expulsion of these worms, turpentine, cubebs, 
 and copaiba have been advised. 
 
CHAPTER XVI. 
 
 GLYCOSURIA OR DIABETES MELL1TUS. 
 ITS ETIOLOGY, PATHOLOGY, CLINICAL HISTORY, AND TREATMENT. 
 
 Definition. — This is a disease in which no uniform lesion has here- 
 tofore been described, but in which there is a constant and primary 
 parenchymatous metamorphosis of the hepatic cells, followed by a 
 similar metamorphotic change in the epithelial corpuscles of the kid- 
 neys. Careful study of the microscopic changes in several cases 
 where the patients died of this malady, lead to this decision, and 
 the detailed account of three necropsies will constitute the pathology 
 of this chapter. 
 
 The clinical features are drawn from a large number of cases which 
 have come under observation, and which are characterized by the void- 
 ing of large quantities of urine, usually of a high specific gravity and 
 more or less heavily loaded with glucose. There is also an abnormal 
 craving for starches and sugars; great thirst, and, usually, progressive 
 emaciation and weakness, all of which are characteristic of the dis- 
 ease. Numerous other symptoms due to secondary and complicating 
 lesions are developed. 
 
 Etiology. — An inherited tendency to diabetes mellitus seems to be 
 pretty clearly established in about twenty-five per cent of the cases. 
 By some observers it is believed to be still more frequent, but, owing 
 to the incomplete knowledge of the patient in regard to the disease 
 of which their ancestry died, it is impossible to arrive at any positive 
 conclusion. 
 
 Age. — The period of life is also important. The recorded observa- 
 tions show that it may develop at any time from birth to very ad- 
 vanced years. By dividing life into decades, commencing at birth, 
 the combined results, as computed from the tables of Griesinger, See- 
 gen, Schwartz, Andral and Mayer, show a progressive increase in fre- 
 quency up to the decade included between forty-one and fifty, where 
 it attains its maximum of frequency and continues stationary during 
 the succeeding decade of fifty-one to sixty. The largest number, 
 
166 GLYCOSURIA OE DIABETES MELLITUS. 
 
 therefore, may be said to occur between the ages of forty-one and 
 sixty. The neSt frequent period is between thirty-one and forty; 
 then between twenty-one and thirty; about an equal number occur 
 between eleven and twenty, and sixty-one and seventy. 
 
 Mme recent observation and an earlier recognition of the malady is 
 tending to increase the frequency of its occurrence in children and 
 early adult life. 
 
 Sex. — The disease is generally spoken of as being more frequent in 
 adult males; the proportion being about two to one. \n children, the 
 preponderance is in favor of the female sex. 
 
 The preponderance, among cases personally observed, in hospital 
 and private practice, was. even among adults, in favor of the females, 
 but, when the same number of each was taken as the standard of com- 
 parison, it was found to be of about equal frequency in both sexes. 
 Of the forty cases, however, recorded by Prof . Satterthwaite, 1 twenty- 
 seven were males, and thirteen were females. 
 
 Frequency. — This has been variously stated as ranging from one in 
 six thousand to three in ten thousand, but if all the cases were de- 
 tected and accurately recorded, it would probably be found as fre- 
 quently as two in three thousand. 
 
 Ascribed Causes. — Under this division may be mentioned: alcohol 
 iu excess, mental anxiety, concussion of the spine, sexual abuse, opium, 
 syphilis, mechanical injury, a variety of diseases and lesions of the 
 nervous centres, especially in and around the medulla oblongata, 
 physical impressions, pregnancy, tape-worm, etc., but the very di- 
 versity of these theories proves that no very definite idea exists of 
 the real causation. 
 
 The most frequent predisposing and exciting cause, however, ap- 
 pears to be a super-nutrition of the portal system, which, with a 
 jmrenchymatous metamorphotic change in the hepatic cells, is the 
 primary lesion; the nervous involvement being peripheral, reflex, 
 and secondary. It may be that over-mental activity, by weakening 
 the nervous mechanism of the liver, allows that organ to give way 
 under the increased pressure. This view is in a measure substan- 
 tiated by physiological experiments which point toward increased 
 nutrition as the essential to traumatic glycosuria. 
 
 Clinical experience teaches the same thing, namely, a greater fre- 
 quency of this disease among the well-to-do classes, and in a large 
 proportion of cases a careful inquiry into the habits of the individual 
 shows an inordinate use of the starches, fats, and nutritive materials 
 in general. 
 
 ] New York Medical Record, April 11th, 1885, p. 396. 
 
GLYCOSURIA OR DIABETES MKUJTUS. 107 
 
 Pathologically the only positive lesions, as far as known, are to be 
 found in the liver and kidneys. 
 
 Treatment also aids in sustaining the super-nutrition theory, for it 
 is a well-known clinical fact that a nitrogenous diet, aided by such 
 medicinal agents as steady both the nervous and circulatory systems, 
 especially the latter, affords the greatest relief. 
 
 Physiological and Pathological Considerations. — Diabetes mellitus 
 is said to be most frequent in the higher stations of life or among the 
 well-to-do class of people. It is a noticeable fact that diabetes is 
 especially frequent among the Jewish race, and strikingly so in wealthy 
 Jewesses. Consequently it would appear that excesses — and by this is 
 meant a physiological increase in nutritive material, which tends to 
 keep the liver or hepatic cells continually overworked — should be con- 
 sidered the starting-point. This condition may result from eating too 
 freely of hydro-carbonaceous substances, either alone or in conjunc- 
 tion with the proteids, both of which materially impair the physiolo- 
 gical activity of the hepatic cells, and thus excite a condition which 
 renders them incapable of performing their normal work. Overcharg- 
 ing the portal blood with glucose or cane-sugar has been found, by 
 actual experiment, to be followed by glycosuria. 
 
 • The experiments of Pavy show that oxygenated blood injected into 
 the portal circulation produces a super-oxygenation which apparently 
 increases the amount of work on the part of the liver, and which is 
 followed by glucose in the urine. A number of similar experiments 
 could be cited, besides those of Schiff, who excited glycosuria by 
 direct galvanization of the hepatic substance, as a proof that the pri- 
 mary trouble was located in the liver; but Pavy's experiment and the 
 introduction of sugar into the portal blood appear to point more 
 directly to the solution of the mystery. 
 
 From these observations it seems reasonable to suppose that an 
 excessive imbibition of nutritive elements into the portal circulation 
 must, of necessity, call for a super-oxygenation of the portal blood; 
 thus throwing additional work upon the hepatic cells; in consequence 
 of which the capillaries are dilated to furnish the necessary material 
 to carry on the excessive metabolism, and this peculiar disease is 
 developed by natural as well as experimental processes. It may be 
 that this increased demand which is made upon the liver is trans- 
 mitted through the sensory filaments of the sympathetic system, to 
 the hepatic medullary centre, producing either deficient or exces- 
 sive stimulation as the case may be, which, when it is transmitted 
 back to the liver, leads to an incomplete function, or an undue activ- 
 
168 GLYCOSURIA OR DIABETES MELLITUS. 
 
 ity on its part, instead of the exact equilibrium which should be sus- 
 tained. 
 
 This theory is quite as much in keeping with physiological laws as 
 the attempts to trace its source to indefinite and varying cerebral 
 lesions, which, in many cases, are wholly absent. Not that cerebral 
 lesions may not interfere with the nervous mechanism of the liver, 
 bring about this change in the capillaries and hepatic cells, and result 
 in incomplete or excessive transformation. In traumatic diabetes the 
 tendency is to recovery, which, as in experimental diabetes, proves 
 the necessity of a surcharging of the portal system with nutritive 
 materials to produce the permanent disease. In proof of this view 
 may be cited limitation, if not absolute restriction, of the diet, with 
 a regulation of the vascular system, which, in many cases, causes a 
 marked diminution of the glucose in the urine, and in some its total 
 disappearance, while a neglect to observe these laws almost invariably 
 increases the quantity. 
 
 The case recorded by Brunton serves as a proof of these statements, 
 since here, the glycosuria was directly traceable to the irritation 
 caused by a tape-worm. Undoubtedly the primary disturbance of the 
 nervous system, in this instance, was produced by the irritation of the 
 peripheral sensory fibres of the sympathetics, which conveyed the im- 
 pression to the medulla, whence it was transmitted to the liver. The 
 removal of the parasite was almost immediately followed by a per- 
 manent disappearance of the sugar. 
 
 It might be, however, that the enormous appetite which is some- 
 times produced by a taenia was the cause of surcharging the portal 
 system with nutritive material, and of thus producing the disease. In 
 either case, the nervous irritation was peripheral and not central. 
 
 The frequent occurrence of temporary glycosuria in pregnancy is 
 explained by the utero-gestation causing the well-known peripheral 
 irritation of the sympathetic system, and throwing more work upon 
 the liver; the same irritation exists during lactation, but is especially 
 marked when, for any reason, the flow of milk is suddenly arrested, 
 causing increased peripheral irritability of the nervous system, and at 
 the same time throwing more work upon the liver. This explains 
 the glycosuria which occurs in both these instances, and helps to sus- 
 tain the present theory of increased nutrition, an hepatic lesion, and 
 peripheral nerve-irritation. 
 
 The weight of evidence, deduced from the large number of experi- 
 mental and pathological lesions of the nervous system, points decid- 
 edly in one direction — namely, that to produce glycosuria, even tern- 
 
GLYCOSURIA OR DIABETES MELLITU8. 169 
 
 porary in nature, there must be an increased amount of nutritive 
 material in the blood of the portal vein. 
 
 The frequency of the renal lesion in diabetes, which is an epithelial 
 metamorphosis of a peculiar and severe type, and the finding of no 
 evidence of sugar in the blood, in many cases, as was practically 
 proven by a recent necropsy, suggest the probability that glucose is not 
 produced by the liver, or discharged as such into the blood. The liver, 
 however, does produce the sugar-forming elements which circulate in 
 the blood until they are conveyed to the kidneys, where they are seized 
 upon by the renal epithelial cells as foreign substances, drawn from the 
 circulation, changed into glucose, and discharged into the uriniferous 
 tubules. Admitting that all forms of parenchymatous metamorphoses 
 of the kidneys are due to an increased amount of work on the part of 
 the renal cells, this explanation offers a tangible reason for the very 
 general if not constant renal lesion found in these cases. It also helps 
 to explain the final termination of so many by a kidney lesion, which 
 is usually indicated by albumin and casts. The small amount of al- 
 bumin may be explained upon the theory that some, if not a con- 
 siderable quantity, of the glucose is produced from the albuminoids, 
 and that the sugar represents what otherwise would be eliminated as 
 albumin, urea, carbon dioxide, and water. 
 
 Exception may be taken to this view from the fact that sugar has 
 been said to have been found in the blood of a diabetic patient during 
 life; but both urea and sugar are said to be found in normal blood; 
 yet there does not appear to be a sufficient quantity of sugar present 
 to account for the large amounts discharged in the urine. In regard 
 to urea, this statement is known to be the fact. 
 
 The close relationship existing between the sympathetic nerves of 
 the liver and those of the kidneys explains the primary dilatations of 
 the renal vessels. The marked increase in the lumen is maintained 
 by the hyaline transformation, which causes a permanent thickening 
 of the vascular wall and completely destroys its elasticity. The result 
 of this is that all power to regulate the pressure upon the glomeruli is 
 removed, and the increased hydrostatic pressure forces a very large 
 quantity of water through, which explains the copious quantity of 
 urine voided. 
 
 The pathological anatomy of diabetes as here given is based upon a 
 number of necropsies, in all of which a marked parenchymatous 
 metamorphosis of the liver and kidneys was the chief lesion. Three 
 are given in full to illustrate the characteristic, as well as come of the 
 accessory changes. Usually after wasting diseases of any duration, 
 the cadaver is found much emaciated, but in some instances, when 
 
170 GLYCOSURIA OB DIABETES MKLLITUS. 
 
 they die early, the body may retain its rotundity. In two of the cases 
 cited, there was marked emaciation; one. however, died in what might 
 be called full flesh, even though the disease had lasted for more than 
 a year. 
 
 The following is the result of the necropsy in full, with two others 
 appended, together with all the various lesions that have been described 
 as being found by different observers. 
 
 Eigor mortis was absent, the lower extremities were covered by an 
 eruption which did not disappear upon pressure. This was syphilitic in 
 all probability. The skin was unusually pale and blanched. The pan- 
 nieulus adiposus was nearly absent. The muscles were thin and dry. 
 The pericardial sac contained about half an ounce (15.5 c.c.) of clear 
 
 Fig. 41.— Miliary Gumma. 
 Showing cheesy centre, fibrillated capsule, and hyaline thickening of capillary vessels, a, Sur- 
 rounding pulmonary substance: b, c, fibrillated connective-tissue capsule walling in cheesy 
 centre; rf, hyaline metamorphotic thickening of the capillary blood-vessels. 
 
 serous fluid. The heart cavities contained a small quantity of blood 
 and coagulum. The muscular tunic was very soft and flabby, so that 
 the cavities collapsed and the organ became flattened when it was laid 
 upon the table. Microscopic examination showed granular and fatty 
 degeneration of the cardiac muscles. All the valves were free and 
 sufficient, but, owing to the relaxed condition of the organ, could not 
 be made to close perfectly to the water-test. The heart weighed eleven 
 ounces (311.844 grams). 
 
 In the other two, the heart was slightly enlarged, in the third case 
 weighing nineteen ounces (538.642 grams). In the second case, there 
 
 \ 
 
GLYCOSURIA OK DIAHKTKS MKLLITIIS. 
 
 171 
 
 was some fatty infiltration. The muscular elements in it and the third 
 case were similar to those described in the first. There was marked 
 fatty infiltration of the valves on the left side of the heart in all, and 
 of the aorta in the second and third cases. 
 
 The left lung was perfectly free in the pleural cavity. It presented 
 nothing especially abnormal. There was, however, a slight amount 
 of interstial thickening of the apex and the superior portion of the 
 upper lobe. It weighed twenty-one ounces (595.340 grams). 
 
 The right lung was quite adherent at the apex, at which point the 
 pulmonary tissue was indurated and presented the gross appearance 
 
 Fig. 42. — Large Gumma. 
 Showing the outer portion and cellular infiltration ; the.open spaces representing spots of soft- 
 ening. 
 
 of consolidation, with a tendency to the formation of cavities. The 
 remaining portions were free in the pleural cavity. When the in- 
 durated apex was bisected, a large, cheesy-looking nodule was divided, 
 also numerous smaller zones of like material. Two small cavities 
 were developing. The intervening pulmonary tissue was indurated. 
 The contents of the cheesy nodule were examined for the bacilli of 
 tuberculosis by Dr. G. E. Elliott, but none were found. The larger 
 of the two distinct cheesy masses had the sticky feeling so common to 
 gummy tumors. On microscopic examination, it appeared to be 
 
172 
 
 GLYCOSURIA OR DIABETKS MELLITUS. 
 
 partially encapsulated or blended with the adjacent pulmonary tissue 
 by a fibrous band, which was lined by concentric rings of fibri Hated 
 connective tissue. The centre of this neoplasm was more decidedly 
 granular and. cheesy. The surrounding pulmonary substance showed 
 to the unaided eye a distinct increase in connective tissue studded 
 with numerous granular spots or bodies somewhat resembling miliary 
 tubercles, but which proved to be miliary gummata, see Fig. 41. 
 Sections were made which included the capsule of this large mass and 
 
 Fig. 43.— Syphilitic Pneumonia. 
 a, Thickened vesicular walls; v, an air-space showing red hepatization; c, an air-spac" show- 
 ing gray hepatization; d, an air-space showing catarrhal desquamation of epithelial cells; e, an 
 air-space showing the degenerative pneumonia of syphilis; x, a blood-vessel between two thick 
 bands of flbrillated vesicular wall. 
 
 the adjacent tissues on both sides. This apparent flbrillated capsule, 
 when examined under the microscope, was found to be composed of 
 numerous layers of flbrillated connective tissue which were irregularly 
 interpersed with blood-vessels. 
 
 Some of the tissue appeared to be of recent formation, in a state of 
 
GLYCOSURIA OR DIABETES MELLITU8. 173 
 
 activity, and took the stain deeply, while other portions were older, 
 granular and degenerated, and did not stain. On the inner side of 
 this band, going toward the centre of the focus, the granular and 
 degenerated condition became more and more decided. The structure 
 closely adjacent to the outer portion was the vesicular tissue, but this 
 was markedly altered. The walls of the air vessels were enormously 
 thickened, being in some instances five or six times greater than nor- 
 mal, Fig. 43, a. Sections from various portions of this indurated 
 nodule showed numerous broad bands of fibrillated connective tissue 
 in various stages of formation. In some places they presented the 
 lively and deeply stained appearance of newly formed connective 
 tissue; at other points they appeared to be in a state of active inflam- 
 mation, being dotted with deeply stained leucocytes; in still others 
 they were almost obliterated by an abundance of deeply stained, round 
 connective-tissue corpuscles, with positive nuclei, and of about twice 
 the size of the lymphoid corpuscles. The last-described, if viewed 
 alone, could not be distinguished from a round-cell sarcoma. See 
 Fig. 42. Some of the fibrillated bands showed a slight disposition or 
 carbon pigmentation. The yellow elastic fibres were very distinct and 
 abundant. 
 
 In all the sections there was an unusual and marked thickening of 
 the alveolar walls, which in many places were congested and in many 
 others quite granular. See Fig. 43, a. 
 
 Numerous spots were found which somewhat resembled tubercle 
 granulation, but close inspection failed to reveal any distinct tubercle 
 tissue or giant cells with multiple nuclei. These zones were composed 
 of this thickened tissue, and showed various changes in the alveoli, 
 some of which were simply filled with red blood-corpuscles, some with 
 fibrillated fibrin, red blood-corpuscles, and large and small desquamated 
 epithelial or lining cells of the air-vescicles, Fig. 43, 0. Some were 
 simply packed full of these desquamated corpuscles, Fig. 43, d; others 
 were filled with a granular substance which would not take the stain, 
 Fig. 43, e. All these conditions were interspersed without any refer- 
 ence to a uniform' progressive development of pneumonic inflamma- 
 tions. The walls of the capillary vessels were thickened, Fig. 43, x. 
 
 The interstitial induration diminished progressively from the apex 
 to the base. The weight of the right lung was twenty-eight ounces 
 (793. 787 grams). Both lungs were slightly congested and cedematous, 
 but no more than would be expected in connection with a death with- 
 out special pulmonary symptoms. 
 
 This condition undoubtedty was that of a gummatous formation, 
 rapidly approaching liquefaction and the formation of cavities. (See 
 
174 GLYCOSURIA OK DIABETES MELLITUS. 
 
 Fig. 4'2.) The numerous smaller foci were probably smaller gum- 
 mata. or the nuclei of larger ones. The interstitial thickening was 
 of syphilitic origin (Fig. 43, a), which condition is quite frequent and 
 often mistaken, clinically, for tubercular phthisis. This certainly 
 was not a tubercular process. 
 
 In the second case, the lungs were normal, a slight amount of em- 
 physema excepted. 
 
 In the third case, there was a marked destruction of the pulmonary 
 substance, with the formation of large cavities. Their gross appear- 
 ance was not that of a tubercular or syphilitic lesion, but was more 
 that of an inflammatory and necrotic condition. Various portions of 
 both lungs were subjected to both Erlach's method for staining the 
 bacilli of tuberculosis and to Lustgarten's method for staining the ba- 
 cilli of syphilis. In the former case, no blue bacilli were found, but 
 with the latter they were quite numerous. If this be a differential 
 test which can be relied upon, the lesion of the lungs in the third case 
 was. like the first, syphilitic. These conditions of the lungs were 
 of great importance. They established positively in the first case, 
 and probably in the third, that the pulmonary affection was not 
 tubercular, but syphilitic in origin. 
 
 It certainly suggests the inference that many reputed tubercular 
 processes in the lung may have been due to a similar or independent 
 condition. 
 
 Various lesions have been described as affecting the lungs in dia- 
 betic cases, particularly chronic inflammatory conditions leading to 
 the formation of cavities; also all forms of pneumonia and tubercle 
 with cavities; pleuritic exudations, and even gangrene. 
 
 The first thing noticed when the abdomen was opened was an un- 
 usual pallor of its contents. The colon was over-distended with gas, 
 and contained only a slight amount of soft faecal matter. The lower 
 portion of the ileum, and several coils of the small intestine were bound 
 together and adherent to the lower border of the pelvic cavity on the 
 right side by firm and old fibrous bands. This binding down, how- 
 ever, had not to any marked degree occluded the lumen of the gut. 
 Both the ileum and the jejunum were nearly empty, and at places so 
 markedly contracted that at first it gave rise to the supposition that 
 there was a stricture; but, on displacing what little gas remained in 
 the lumen of the small intestine, the apparent stricture disappeared, 
 and a similar appearance was produced at a distant point. The stom- 
 ach and duodenum were distended by considerable gas. The whole 
 alimentary tract and all the abdominal viscera, the liver excepted, 
 were very pale. 
 
GLYCOSURIA OR DIABETES MELLITTJ8. 175 
 
 The lesions which have heen described in connection with the ali- 
 mentary tract are chronic catarrh, hyperemia, thickening and tume- 
 faction of the mucous membrane, slaty pigmentation, liiijiiiorrhn^ic 
 erosions of the stomach, and hypertrophy and muscular thickening 
 of the stomach and the upper portion of the intestine. 
 
 The spleen was pale, soft, and larger than normal. Microscopic 
 examination failed to show anything abnormal. It weighed 8 ounces 
 (22G.796 grams). 
 
 Little or no mention is made of the spleen in histories of autopsiee 
 in diabetic cases, but Andral speaks of a singular induration of this 
 organ, its parenchyma being so dried up that not a drop of liquid fol- 
 lowed incision and pressure. 
 
 The sexual organs were not specially examined, as there, was 710 
 gross change which attracted attention. 
 
 The change which has been recorded is atrophy of the testicle in 
 some of the younger subjects. 
 
 Both kidneys were very much enlarged. The left one weighed 
 10-J ounces (297.070 grams); the right, 10 ounces (283.495 grams). 
 Their capsules were normal in thickness and non- adherent, excepting 
 at one or two points where a large vessel connected the capsule with 
 the underlying parenchyma. The renal surface, after enucleation of 
 the kidney from its capsule, was perfectly smooth. Both the free and 
 cut surfaces were very pale, and the latter looked quite granular to 
 the unaided eye. The cortex was very much thickened, being about 
 four times as deep as in a normal organ. The markings of the corti- 
 cal arches were distinct and straight, and, by their deep color, gave 
 evidence of apparent congestion. No cysts were found. 
 
 The microscopic examination gave no evidence of a diffuse lesion, 
 but all those which are so common to a chronic parenchymatous meta- 
 morphosis of the kidneys were present. The lesion was found to be 
 located in the epithelial cells of the uriniferous tubules, and in the 
 walls of the smaller arteries and vessels entering the Malpighian tufts. 
 The epithelial corpuscles in every portion of the organ were in a state 
 of advanced and extensive granular metamorphosis, each individual 
 cell being enormously enlarged, and in most instances all evidence of 
 a nucleus obliterated. 
 
 The destructive process in this instance differs from the ordinary 
 parenchymatous metamorphosis, and has been described as a necrosis 
 of the epithelial elements. Regarding this lesion in the light of a 
 necrotic process, and that of ordinary parenchymatous transformation 
 in the light of a carious process, we have a good comparison for the two 
 conditions. Pig. 44 shows the ordinary, and Fig. 45 the diabetic form.. 
 
176 
 
 (JI.YCOSI/IUA OK IHABKTKS MKLLITUS. 
 
 This peculiar process caused the tubules to become larger than 
 normal, ami in some of them all evidences of a lumen had been ob- 
 literated, so that all that remained to represent the original urini- 
 ferons tubule was a space filled with necrotic epithelial cells. At 
 other points, the basement membrane of the tubule was entirely 
 stripped of its epithelial lining. 
 
 The intertubular tissue was rendered more apparent and thickened 
 by an cedematous swelling which, taken together with the denuded 
 tubules, would at first lead to the supposition that the lesion was that 
 of chronic diffuse nephritis. (See Figs. 44 and 45.) In fact, this lesion 
 
 Fig. 44. — Chronic Parenchymatous Metamorphosis of the Kidney. X 350. 
 a, Uriniferous tubules showing the epithelial cells in a state of granular metamorphosis and 
 desquamation; 6, tubules showing a less marked change; d, cedematous intertubular tissue. 
 
 has been, and by many would be, called a diffuse nephritis. But a 
 closer study readily shows that the intertubular tissue is free from any 
 inflammatory exudation or recent formation in the shape of new con- 
 nective-tissue and lymphoid corpuscles. The true lesion, therefore, is 
 a metamorphotic process of the cells, brought about by an excessive 
 amount of work; while that of the interstitial trouble is secondary, 
 cedematous, and not inflammatory in character. None of the sections 
 showed any granular casts in the tubules, but an occasional hyaline 
 cast was found. 
 
GLYCOSURIA OK DIABETKS MELLJTUS. 
 
 177 
 
 The walls of the small vessels were very much thickened by a process, 
 the exact nature of which has not been satisfactorily ascertained, but 
 ■one that may properly be called a hyaline metamorphosis. (S<;f: 
 Fig. 46.) This hyaline metamorphosis causes a permanent thicken- 
 ing of the dilated arterioles, so that they ultimately become converted 
 into non-elastic tubes opening directly into the tuft, as seen in 
 Fig. 46, a. 
 
 The intimate connection between the liver and kidney, by the sym- 
 pathetic system, is offered as a solution of the primary dilatation of 
 the renal vessels, which finally become thickened and wholly unable 
 to contract, and, consequently, remain open after death, as seen in 
 the sections and in the drawing (Fig. 46, a). It was also found that 
 
 co b a 
 
 Fig. 45.— Diabetic Parenchymatous Metamorphosis of the Kidneys, Medullary Portion, 
 
 X 350. 
 a, Uriniferous tubules distended and occluded with necrotic epithelium; 6, swollen cedema- 
 tous, and non-inflammatory intertubular tissue, with an occasional epithelial cell. 
 
 the lumen was of more than twice the normal size, and that this 
 condition extended up to and even through the capsule of Bowman, 
 until the coil of vessels was reached. This lesion was not so advanced 
 in every vessel, but all of them were more or less involved. 
 
 This enormous thickening and loss of contractility easily explains 
 the abundant flow of urine. The pressure exerted upon the tuft of 
 vessels within the Malpighian capsule, or upon the dilated or ex- 
 panded extremity of the uriniferous tubule, is governed by the con- 
 12 
 
ITS 
 
 ..I.Y OsriMA on DIABKTKS MKLLITTJS. 
 
 tractility ol the arteriole just anterior to it. If, for any reason, 
 this is constantly dilated, and its walls are thickened, it loses its- 
 normal contractility, and a great volume of blood is constantly poured 
 into the tuft, of vessels. This, with the unequal strain upon these 
 vessels, from the constantly varying blood-pressure, weakens their 
 walls and permits of a more abundant escape of water from the blood, 
 and, consequently, a more copious volume of urine. This view is 
 substantiated by pathological and clinical data, for there are three 
 other lesions of the kidneys in which this or a similar transformation of 
 the vessels is met with; and in every instance the lumen is increased 
 and the walls are thickened, a copious discharge of urine being the in- 
 
 Fig. 46.— Diabetic Parenchymatocs]Metamorphosis of the Kidneys, Cortical Portion, X 350. 
 a, Hyaline transformation of an afferent vessel; 6, a Malpighian tuft; c, basement tubes 
 stripped of their epithelium; tl, tubules filled with necrotic epithelium; e, cedematous inter- 
 tubular tissue. 
 
 variable rule. The three conditions referred to are the well-known 
 cirrhotic or red atrophy of the kidneys, the waxy kidneys, and one 
 form of chronic diffuse nephritis. 
 
 The capillaries of the glomeruli had a peculiar waxy and trans- 
 lucent appearance, but did not respond to the ordinary test for amy- 
 loid material. 
 
 The nuclei of the cells covering the vessels of the tuft were very 
 
GLYCOSURIA OK DIABKTES MELLITTTS. 17'.> 
 
 indistinct and often imperceptible. The capsule of Miiller was also 
 the seat of the same oedemafcous thickening as was noted in the inter- 
 tubular tissue. There was an absence of blood in the kidneys, which 
 may have accounted for the suppression of urine which existed before 
 death. 
 
 In the second case, the renal lesion was identically the same as in 
 the first. In the third, the lesion was practically the same, but the 
 destruction of the epithelial corpuscles was more marked, many of the 
 tubules being entirely stripped of their epithelial coating. The epi- 
 thelial cells in situ and the vascular changes were the same in all three. 
 
 In all, the kidneys ranged in weight between 8 and 11 ounces. 
 (226.796 and 311.844 grams). 
 
 In the majority of the recorded necropsies, a lesion of the kidneys 
 lias been noted, apparently from gross appearances. The organs are 
 spoken of as being enlarged, hyperEemic, and with a hypertrophic 
 swelling of the epithelium. The more recent writers speak of the 
 change in the cells as a necrotic transformation, similar to that al- 
 ready described. 
 
 The hilum of the kidneys and the ureters presented nothing spe- 
 cially abnormal. The bladder was empty and contracted down to a 
 hard ball. 
 
 Catarrh of the pelves of the kidneys and of the ureters has been spoken 
 of as a common ocurrence. Abscesses, amyloid degeneration, and 
 nephritic tuberculosis have been described as being found after death. 
 
 The liver was considerably enlarged and dark in color, contrasting 
 strongly with the pallor of all the other viscera. Its weight was 
 90 ounces (2,551.458 grams). It was tested for amyloid transforma- 
 tion, but none was detected. When cut into, it offered rather more- 
 resistance than is usually the case in a normal organ. No further 
 macroscopic evidence of cirrhosis could be detected. The external 
 surface was perfectly smooth, with a few spots of chronic perihepati- 
 tis. Throughout the entire cut surface, there were found numerous 
 disseminated, dark-red, degenerated-looking spots or zones of hepatic 
 tissue, which were surrounded by what appeared to be perfectly 
 normal liver-tissue. On microscopic examination, these red zones 
 were found to be composed of hepatic cells in various stages of 
 retrograde metamorphosis. In some instances, the nuclei, the proto- 
 plasm, and. even the outlines of the corpuscles were obliterated by 
 the granular metamorphosis and swelling of the epithelial cells. 
 The central portion of these zones showed the most marked de- 
 generative changes. The destructive metamorphosis grew less and 
 less marked as the periphery was approached, and finally blended. 
 
L80 GLYCOSURIA OH DIABETES MKLLITUS. 
 
 with the surronnding liver tissue, in which the hepatic cells were 
 found to be perfectly normal. None of the epithelial corpuscles 
 showed the fatty degeneration, with the formation of fat droplets, so 
 common in the acute and disseminated hepatic metamorphoses of 
 acute blood diseases. The intervening normal hepatic tissue will 
 account for the long duration of the lesion and the reason for im- 
 provement under proper treatment. The duration of the disease may 
 have depended, therefore, upon the rapidity of the hejoatic metamor- 
 phosis. On account of the difficulty of localizing a central vessel with, 
 certainty, it was impossible to determine positively at just what point 
 of the circulation the centres of these degenerated foci were located. 
 
 Another interesting lesion was a marked dilatation of the hepatic 
 capillaries, with a thickening of their walls and the development of a 
 slight amount of interstitial tissue. 
 
 The peculiarity of this interstitial nevv formation was that it sur- 
 rounded each individual cell, or a cluster of two or three, and ran 
 along the walls of the intralobular plexuses, instead of the walls of the 
 interlobular vessels, as is commonly the case in ordinary cirrhosis. 
 In this respect, the lesion bore a very strong resemblance to, if it was 
 not, a true syphilitic sclerosis of the liver. 
 
 This general formation of new tissue undoubtedly accounted for the 
 resistance to the knife so noticeable when the organ was first cut. 
 
 Fig. 47 very accurately represents the changes in the liver, as seen 
 "under the microscope. The same can be said of those showing the 
 ai^pearances in the lungs and kidneys. 
 
 The thickening of the walls of the hepatic capillaries, already 
 alluded to, was due to a hyaline transformation similar to that 
 found in the renal vessels. 
 
 In the second case, the hepatic lesion was similar to, but more ex- 
 tensive than that of the first. There was not a single epithelial cor- 
 jrascle found in any of the sections that did not show this marked 
 metamorphotic change, the protoplasm being packed by minute gran- 
 ular and fatty particles. Here and there a cell was found with a 
 large fat droplet or globule similar to the condition found in fatty 
 infiltration. There was also a marked congestion of the intralobular 
 capillaries, many of them being distinctly distended with red blood- 
 cells. There was also a marked intralobular sclerosis and thickening 
 of the walls of the portal capillaries. The liver was decidedly en- 
 larged. 
 
 In the third case, the patient had been a heavy drinker prior 
 to his glycosuria. In his case there was marked interlobular sclerosis, 
 but aside from this, the lesion of the liver was the same. There was 
 
GLYCOSURIA OK DIABETES MELLITT78. 
 
 181 
 
 the marked parenchymatous metamorphosis of the hepatic cells, also 
 the marked intralobular sclerosis and thickening of the portal capil- 
 laries. 
 
 There was a very striking similarity in the change in the hepatic 
 cells, and, in each, the intralobular sclerosis, with thickening and 
 dilatation of the intralobular capillaries, was a decided lesion. There 
 was some congestion in all, but it was particularly marked in the 
 
 Fig. 47. — Diabetic Metamorphosis op the Liver. 
 aa, A zone showing normal hepatic cells ; ba, a zone showing parenchymatous metamorpho- 
 sis of the hepatic cells ; c, portal systems and intralobular cirrhosis. 
 
 second case. The weight of the liver in the last case was ninety-four 
 ounces (2,644.850 grams). 
 
 Finding such a close correspondence in the changes in the hepatic 
 and renal epithelial elements and in their vascular walls, has led to 
 the firm conviction that the theory here advanced is the correct one. 
 
 Different stations of life were represented by each, and in all there 
 was a clear history of the imbibition of more nutritive material than 
 
182 GLYCOSURIA OR DIABETES MELLITl s. 
 
 was absolutely demanded by the system. In none were there any 
 nerve Bymptoms or lesions. 
 
 The descriptions which have been given of the changes occurring 
 in the liver are numerous and contradictory. The major part of them 
 appear to be based upon gross appearances instead of minute micro- 
 scopic details. The various conditions which have been found are 
 hyperamiia, hypertrophy, congestion, increase in volume from changes 
 in the glandular cells, cirrhosis, atrophy, amyloid degeneration, the 
 formation of abscesses, and obliteration of the portal vein. Marks of 
 hepatic degeneration, similar to those already described, have been 
 quite frequently met with, together with a diminution of fat in the 
 liver, etc. 
 
 In the first case, no special change, either macroscopic or micro- 
 scopic, could be made out in the pancreas. The same was true of the 
 third case. In many of the recorded cases, however, various lesions 
 have been found. The numerous lesions which have been recorded 
 as found in this organ are atrophy, or atrophy with degeneration (on 
 the other hand, it has been found small and hard), primary fatty de- 
 struction of the gland-cells, cancer, calculi, and obstruction to the 
 duct, with cystic degeneration of the gland. In other instances, it 
 has been found very soft and anaemic. 
 
 Including all these lesions, some form of abnormality has been 
 detected in nearly fifty per cent of the cases. On the strength of 
 this, some have gone so far as to locate the cause of diabetes in the 
 pancreas. 
 
 In the first case, the only gross abnormal appearance in the nervous 
 system was an extreme pallor of the cerebral substance. Microscopic 
 examination of the medulla failed to reveal anything abnormal. The 
 sections apparently represented a normal medulla, save for a little 
 thickening of the vascular walls. 
 
 The almost innumerable experimental lesions which have been in- 
 stituted for the production of glycosuria, either permanent or tem- 
 porary, have not been cited; neither have the many cerebral and 
 upper spinal lesions which have now and then been found in connec- 
 tion with diabetes. The reason for omitting them in detail is that 
 they only prove one thing: that no constant or certain lesion has been 
 shown to be pathognomonic of this disease. The majority of them 
 sustain the theory that overloading and overworking of the liver are 
 necessary for the establishment of a permanent diabetes. For, unless 
 the super-nutritious condition of the portal blood, with a possible 
 hepatic lesion, is present, the removal of the nervous injury is invari- 
 ably followed by a disappearance of the glycosuria, while in the in- 
 
GLYCOSURIA OR DIABETES MELLITUH. L83 
 
 -curable forms of diabetes death occurs and no nervous lesion is detected, 
 but marked lesions are found in the liver and kidneys. But, as be- 
 fore stated, an injury, or irritation, or undue mental depressions, may 
 be the spark which kindles the fire, and only in this way can these 
 numerous lesions act; for all of them are frequently met with in cases 
 in which there has been no appearance of glucose in the urine. 
 
 In this case, the pericardial fluid, blood, and hepatic tissue were ex- 
 amined for glucose by Dr. Henry Eolando, house physician at the 
 Presbyterian Hospital, who did not find it in any of the samples. 
 
 The fact that no sugar was found in the blood appears to be strong 
 proof that the glucose does not pass out of the liver as such, but 
 rather in the form of sugar-producing elements, the nature of which 
 is unknown, and that the renal cells complete the formation. This 
 hypothesis has its analogy in the formation of urea, uric acid, etc. 
 
 The practical points of interest derived from this study are, that 
 diabetes mellitus has for its primary cause a change in the portal 
 blood and in the hepatic tissue and vessels; that the influence of the 
 nervous system is secondary and not primary. 
 
 Clinical History. — Glycosuria from a clinical aspect is divisible 
 into three sets of cases: the temporary, the mild, and the severe. 
 
 The first, as the word indicates, is of short duration and soon 
 passes away. In some incidental cases, as after pertussis, asthma, 
 chloroform, carbon dioxide (COJ, and other drugs, the glycosuria is 
 almost too transient to be classed as a distinct disease. But the follow- 
 ing is a typical example of this class. A rather obese medical student, 
 while preparing for his examination, became suddenly straitened 
 in his finances, and took to drinking largely of lager beer and living 
 upon German bread. Glycosuria set in quite actively, no less than 
 four gallons (15.924 litres) of urine being voided in twenty-four hours. 
 Diabetic treatment was instituted, and bromides with opium admin- 
 istered, which caused the disease to disappear in eight weeks. Here 
 the nervous element and supernutrition seem to go hand in hand, al- 
 though the former may appear to predominate. The fact, however, 
 that many students have the same anxiety, but do not indulge so 
 freely in carbonaceous substances and stand the mental strain without 
 suffering from glycosuria, tends to support the theory that there 
 must be an increased quantity of work demanded of the liver with 
 primary changes in the hepatic cells before the nervous system can 
 come into play and excite the disease. 
 
 The mild form is occasionally met with in elderly and obese people, 
 who have been in the habit of " living well and enjoying life/' and 
 may last for a number of years. At first they void an increased 
 
l s 4 GLYCOSURIA OK DIABETfcS MELLITU8. 
 
 amount of urine which contains glucose, at the same time there 
 is some thirst, a good appetite, a little wasting, muscular weakness 
 and mental lassitude. But upon a modified diet and appropriate 
 therapeutic agents the symptoms all abate, and the person appears as 
 well as ever both mentally and physically, but the urine still contains 
 glucose, the quantity voided being nearly normal. 
 
 The severe form is the most common. In this the individual voids 
 abnormally large quantities of light-yellow urine, which has a high 
 specific gravity, and contains large amounts of grape sugar. Thirst 
 is troublesome, the mouth is dry and parched, the tongue red or 
 coated, and the appetite acute with a craving for carbonaceous sub- 
 stances. The countenance becomes pale, and the patients progressive- 
 ly emaciate, and are both physically and mentally weak. Upon appro- 
 priate treatment they may temporarily improve, but, as a rule, the 
 disease is progressive, and a steady decline in all the vital forces 
 marks its course until complications are developed and death ensues. 
 
 The symptoms of all forms of glycosuria are divisible into different 
 sets. Those common to all forms are failure in strength and mental 
 activity, with pallor of the countenance, and gradual or progressively 
 rapid emaciation. There will be increased or unbearable thirst, with 
 copious as well as frequent micturition. The thirst and urinary 
 symptoms finally cause the individual to consult the physician. 
 
 The symptoms of the digestive tract are the increasing thirst, which 
 soon compels the sufferer to rise at night to satisfy it. A dry red or 
 heavily coated tongue, with an accumulation upoii the lips, gums, 
 and teeth of a saccharine substance resembling sordes. The gums are- 
 red, swollen, flabby, and recede from the teeth, which may become 
 carious. 
 
 The salivary secretion is sometimes acid in reaction. 
 
 The sense of taste becomes more acute with a strong jjartiality or 
 desire for saccharine and starchy substances. Later in the disease, 
 it may be perverted for certain things, as for instance pepper. 
 
 The appetite and gastric digestion, as a rule, remain good or are 
 abnormally increased, but, like the thirst, it is not satisfied even if 
 the things most desired are taken. 
 
 As the disease advances and approaches towards the end, the diges- 
 tion may become impaired. This has been attributed to the increased 
 digestive strain, and to the limited nitrogenous diet. But from our 
 present pathological and physiological knowledge, this loss in appetite 
 and giving way of the digestive powers is better explained by the failure 
 on the part of the kidneys to eliminate the effete material from the sys- 
 tem; the alimentary tract then attempts to eliminate what the renal 
 
GLYCOSURIA OK, DIABETES MELLITU8. 185 
 
 organs are unable to accomplish. The digestive trouble now becomes 
 a prominent symptom and is due to precisely the same ursemic cause 
 so frequently witnessed in renal lesions in which the epithelial cells of 
 the kidneys fail to effectually perform their work. 
 
 It is a well-known clinical fact, in cases closely watched, that the 
 failure in digestion is preceded by or is associated with a diminution 
 in the quantity of urine and sugar excreted, and a simultaneous ap- 
 pearance of, or increase in, albumin and casts. If the kidney lesion 
 can be improved and more sugar eliminated with less albumin and 
 casts, and more of the effete materials thrown off, tbe digestive symp- 
 toms will improve and the appetite return. 
 
 The progressive transition and interchange from a glycosuria to an 
 albuminuria is not uncommon. In fact, many cases, if not a large 
 proportion, show a gradual or rapid disappearance of the glucose, with 
 a diminution in the quantity of the uric acid and the appearance of 
 albumin and casts as the fatal issue approaches. 
 
 Diarrhoea or constipation may occur. The former is more fre- 
 quently met with daring the course of the disease. Toward the end, 
 constipation and flatulence are developed which are ursemic in nature 
 and often exceedingly obstinate. 
 
 Respiratory Symptoms. — The breath has been described as emitting 
 a peculiar apple-like odor. It, like the coma, has been ascribed to 
 acetonemia, but it is probably of the same origin as that in connection 
 with uraemia. 
 
 A number of pathological conditions are met with in the lungs, 
 each one giving its special rational and physical signs. They are both 
 lobar and lobular pneumonia, phthisis, tuberculosis, pulmonary syphi- 
 lis, gangrene, hemorrhage, etc. 
 
 In one case observed, death was due to a pulmonary hemorrhage; 
 in another, marked syphilitic changes were found; in other in- 
 stances, no special change was found. 
 
 Each of the above lesions will give its special and diagnostic rational 
 and physical signs. The pneumonococcus, the bacillus tuberculosis, 
 or that of syphilis, may also be detected. 
 
 Circulatory symptoms are specially confined to the heart, which is- 
 often weak and intermittent, and calls for special therapeutic atten- 
 tion. 
 
 Nervous Symptoms. — These are'muscular weaknesses and trembling, 
 and a dimunition in the sexual desire, perhaps no more than in any 
 wasting disease. Headaches, abdominal, gastric, and wandering pains 
 throughout the body, are not uncommon. 
 
 Diabetic Coma. — This condition, from the peculiar reaction given 
 
ISO GLYCOSURIA OR DIABETES BfELLITUS. 
 
 to the urine by the chloride of iron, is believed to be due to the devel- 
 opment of acetonemia or acetone in the blood. 
 
 The opinion advanced by Dr. Satterthwaite and others, that the 
 coma, and death which frequently ensues, is developed in precisely 
 the same way as that of renal lesions proper, seems to be established 
 by the more recent investigations. 
 
 The stupor or coma is insidious in its origin. There may be some 
 prostration, headache, restlessness, and anxiety, epigastric pain, nau- 
 sea, and vomiting, just what precedes any uremic coma. 
 
 The urine is diminished in amount, and the sugar is less abundant: 
 or total suppression is developed. The albumin and casts become 
 more plentiful. In one instance, the quantity of urine fell from 250 
 ounces, TTT5.874 cc, to 15 ounces, 466.552 cc. in twenty-four hours, 
 and during the twelve hours just prior to death, there was absolute 
 suppression: at the necropsy the bladder was empty and firmly 
 contracted. The pulse at first is high, small, and quick, but 
 soon becomes weak, often intermits, and is absent at the wrist; the 
 temperature at first is a little elevated, but it soon falls to normal or 
 below. The breathing is rapid, labored, and superficial. In some 
 instances, the mind is disturbed and delirium precedes the coma. 
 
 A decrease in the quantity of urine and sugar, and an increase in 
 albumin and casts, should always be looked upon with anxiety, and 
 a fatal coma suspected in the near future. 
 
 Ocular Symptom*. — A number of lesions have been narrated in 
 connection with this disease. Diabetic cataract, with a loss of vision, 
 is perhaps as frequently mentioned as any. 
 
 But all the lesions that occur in any form of chronic renal disease 
 may be met with, viz., retinal thrombosis, embolism, hemorrhage, or 
 atrophy, fatty embolisms of the retinae, and the various forms of 
 retinitis and neuro-retinitis. With these, there will be specks before 
 the eyes, dimness of vision, or blindness. An ophthalmoscopic exami- 
 nation only can decide the nature of the lesion. 
 
 The acuteness of hearing is, in some instances, diminished, but 
 more often tinnitus aurium is a troublesome symptom. 
 
 It appears from clinical observation that sugar, like urea, is occasion- 
 ally eliminated by all the excretory glands, and hence the finding of 
 glucose in the perspiration, tears, and other excretions and secretions 
 is explained. This, however, does not seem to be of frequent occur- 
 rence, and is somewhat doubtful. 
 
 Integumental Lesions and Symptoms. — Extreme dryness of the skin 
 is among the early symptoms. With the complicating lesions of the 
 
GLYCOSURIA OK DIABETES MELLITUS. 
 
 187 
 
 lungs, hectic sweats may become marked; unilateral sweating has been 
 noted in a few cases. 
 
 Itching of the skin, sometimes extending over the greater part of 
 the body. But this symptom is usually most marked in females and 
 is limited to the genital regions, and appears to be excited by the fre- 
 quent micturition and accumulation of the saccharine particles among 
 the hairs of the parts. The meatus urinarius in males becomes irritated 
 and inflamed. An eczematous erythema is occasionally developed. 
 Pruritus vulvae also occurs in some cases. Late in the disease, furuncles 
 and even carbuncles are developed, and the latter may act as a potent 
 cause in producing a fatal issue. 
 
 Spontaneous thrombosis and consecutive gangrene of the extremities 
 or other parts is also met with in five to six per cent of the cases. If 
 the lungs are included, it is much more frequent. Any slight injury 
 may be sufficient to excite a destructive inflammation. 
 
 Falling out of the nails has once been observed. 
 
 (Edema of the extremities may be developed, but this is rarely seen, 
 for, like all conditions when large quantities of water are constantly 
 expelled from the body, it is not likely that much will transude from 
 the blood-vessels and accumulate in the perivascular spaces. 
 
 Urinary Symptoms.— The quantity is abnormally large, sometimes 
 reaching as high as six or seven hundred ounces (18,662.097 c.c. or 
 21,772.447 c.c). It is usually transparent, but has a heavy appearance 
 and is acid in reaction. At first there is no sediment, but when vesi- 
 cal catarrh is excited, or much uric acid is excreted, a more marked 
 deposit will be found. The color is pale yellow, and its odor has been 
 compared, when fresh, to a faint whey-like fragrance, but when fer- 
 menting to that of sour milk. The specific gravity is abnormally high, 
 ranging from 1.030 to 1.060, the usual range being from 1.020 to 
 1.030. In this respect it differs from all the other conditions in which 
 there is an abnormally large quantity of urine voided. Sugar, how- 
 ever, may be found in urine having a specific gavity as low as 1.008 
 and perhaps lower, but this is exceptional. 
 
 The urea is increased in quantity, which would naturally be expected, 
 from the unusually large amount of nitrogenous elements ingested. 
 The uric acid is also increased for the same reason, the quantity of 
 the latter often being so large that it is spontaneously precipitated in 
 the crystalline form. 
 
 Albumin is rarely found early, but as the disease advances and the 
 metamorphotic changes in the kidneys become more marked, it often 
 makes its appearance. In all the cases under observation, this was 
 found to be true, and if every sample was examined for albumin, a 
 
18S GI.YCOSL'KIA OR DIABETES MELLITUS. 
 
 Large proportion of eases, if not all, would be found to contain more 
 or less toward the end of the disease. 
 
 Glucose is always present at some time and generally throughout 
 the whole course of the malady. In occasional cases, sugar may be 
 absent for a time and the urine may be heavily loaded with uric acid, 
 or the two may alternate. As the fatal end is approached, the 
 amount of sugar declines, while the amount of albumin steadily 
 increases. A partial or complete interchange between the glucose 
 and albumin may occasionally be witnessed. 
 
 On account of the constant danger from the renal lesion, the urine 
 of every diabetic subject should be carefully analyzed at least once a 
 week. By so doing the physician is best prepared to meet and ward 
 off the approaching danger, and to combat it when it does come. 
 
 There is no microscopic object typical of the diabetic state, but 
 when the renal lesion is fully established casts are found. After the 
 urine has stood and fermented, the finding of the thali of the saccha- 
 romyces cerevisias renders the presence of sugar positive. 
 
 A number of other substances have been described as occurring 
 in the urine, viz., hippuric acid, acetone, inosite, cholesterin, alcohol, 
 oxalate of lime crystals, etc. But up to the present time, no 
 really practical inference has been drawn from them. 
 
 Diagnosis. — This rests exclusively upon finding glucose in the urine. 
 The general history in a large proportion of the cases is characteristic. 
 If the urine of every new case be tested for the presence of sugar and 
 albumin independent of its specific gravity, as should be the universal 
 rule, no case will pass undetected. In those instances where the 
 interchange occurs between the sugar and uric acid, an error might 
 occur if only one examination was made, but repeated trials usually 
 reveal its presence. 
 
 Prognosis. — In the first or temporary form, it is good. In the 
 second class or mild variety, it is also good, the patient living for a 
 number of years, five, six, or seven, or even more. With the third or 
 severe type, the prognosis is always unfavorable. They may die within 
 a few hours or not for several years after the detection of the glyco- 
 suria. 
 
 When the disease apparently lasts but a few hours, some questions 
 may justly be entertained as to the actual duration. In the majority, 
 the average course is from one to two years after pronounced symptoms 
 have developed. 
 
 Treatment. — This is a disease which taxes the physician's skill as a 
 therapeutist to its utmost capacity. Having accepted the above 
 theory of diabetes, it plainly shows that no one drug or remedy can 
 
GLYCOSURIA OR DIABETES MELLITUS. 1 89 
 
 i 
 
 "be expected to combat the numerous physiological problems. No one 
 medicinal agent can be expected to diminish the super/nutrition, renal 
 and hepatic metamorphosis, nervous irritation, and circulatory abnor- 
 malities. The disease calls for a wide therapeutic range to combat it 
 successfully. 
 
 The excess of nutriment sent to the liver must be cut off or so 
 regulated that it will cause the least possible strain on an already 
 weakened hepatic digestion. In this way nutrition may be improved, 
 and the liver cells given a chance to recuperate their wasting powers. 
 To cut off all starchy and sugary substances at once is often too 
 great a change to the system and makes the patient absolutely 
 worse; sometimes exciting an albuminuria with alarming ursemic 
 ■symptoms. Many cases will do better to cut off the carbonaceous 
 articles of diet one by one, at the same time gradually increasing the 
 nitrogenous. Others appear to do equally well on a limited amount 
 of the mixed diet. It will require no little skill to decide this ques- 
 tion wisely. 
 
 The nervous system must not be neglected, as it plays no small 
 part in all the digestive processes, and especially in influencing the 
 hepatic functions. It must be stimulated or depressed, as each indi- 
 vidual case may seem to require, until its influence upon the functions 
 of the liver is brought as nearly to the normal as possible. 
 
 In many instances, there appears to be an over-excitability of the 
 nerves, which the bromides are just sufficient to regulate; in others, 
 opium and its alkaloids have to be employed; cocleia perhaps holding 
 the first place among the remedial agents. This action of opium and 
 its alkaloids is not simply upon the nervous system, but is almost as 
 complex as the disease itself. It acts as a sedative, not by its depress- 
 ing influence, but by its stimulating properties upon the nervous 
 centres, and upon the circulation by stimulating the heart and pro- 
 ducing an even tension of the blood pressure, and also by retarding 
 oxidation. 
 
 The vascular system also requires especial attention on account of 
 the changes in the vessels of the liver and the renal arterioles. All 
 remedies which regulate the heart's action and cause its movements 
 to remain steady will have a tendency to institute improvement. The 
 vascular tension should be kept as nearly even as possible, for, by so 
 doing, the hepatic congestion will be least marked, nutrition will be 
 most perfectly effected, and secretion and excretion will be raised to 
 the necessary standard. For this, ergot or ergotine may be said to 
 hold the first place. Stimulating as they do the vaso-motor system, 
 
190 GLYCOSURIA OR DIABETES MELLITCS. 
 
 and causing a steady contraction of the smaller arterial vessels, the 
 general circulation becomes more even. 
 
 By these combined remedies the nervous system works eventy, the 
 heart strongly, and the circulatory pressure is steady, and, as a result, 
 the hepatic circulation is rendered more uniform, its work is more 
 perfectly performed, and less straiu is brought to bear upon the renal 
 cells and the Malpighian tufts. The effete materials are more com- 
 pletely removed and nutrition is raised to the highest possible degree, 
 which gives Nature a chance to repair the primary hepatic damage, 
 and, consequently, all the secondary changes are benefited or re- 
 moved. 
 
 If the disease be fully appreciated in all its complex physiological 
 changes and abnormalities, its early recognition with appropriate 
 treatment suggests the possibility of a cure; this is indicated from the 
 rapid recovery in the temporary variety and the long-continued im- 
 provement in the mild form. The temporary case already cited, 
 page 183, would have become a confirmed diabetic had he con- 
 tinued the excessive use of the carbonaceous substances. 
 
 Early recognition, therefore, is absolutely essential, and especial 
 attention should be paid to the relief of the kidneys, for the sugar- 
 forming elements are picked up from the blood and thrown into the 
 uriniferous tubules by the action of the renal cells, causing them, 
 first, to hypertrophy, and then to undergo retrograde changes, until 
 finally there is developed a true metamorphotic lesion with albumin 
 or casts and urasmic symptoms to prove its presence. It, therefore, 
 appears that in the epithelial corpuscles of the uriniferous tubules lies 
 the turning point of the disease in a large measure. So long as we 
 can protect and preserve the renal ejrithelial cells, just so much longer 
 can the life of the individual be prolonged. But when they once 
 begin to fail, and albumin or casts appear in the urine, the duration of 
 life is placed in jeopardy. If syphilis has anything to do with excit- 
 ing or keeping in motion this fatal disease (not an improbable supjjo- 
 sition), the anti-syphilitic treatment should be instituted and persisted 
 in. 
 
 The general principles only of the diet treatment have been dealt 
 with in this chapter, as the minutiae must be regulated to the require- 
 ments of each case. 
 
 The diet table of Professor Austin Flint, Jr., is appended. From 
 this elaborate list any one can adjust the demands of individual cases* 
 
GLYCOSURIA OR DIABETES MELLITUS. I U] 
 
 Breakfast. 
 
 Oysters stewed, without milk or flour; clams stewed, also without 
 milk or flour; beefsteak, beefsteak with fried onions, broiled chicken, 
 mutton or lamb chops; kidneys, broiled, stewed, or devilled; tripe, 
 pig's feet, game, ham, bacon, devilled turkey or chicken, sausage, 
 corn beef hash without potatoes, minced beef, turkey, chicken, or 
 game, with poached eggs. All kinds of fish, fish roe, fish balls, with- 
 out potatoes or flour; eggs cooked in any way except with flour and 
 sugar; scrambled eggs with chipped smoked beef; picked salt codfish 
 with eggs; omelets plain or with ham; smoked beef; kidneys; aspa- 
 ragus points, fine herbs, parsley, truffles, or mushrooms. 
 
 Eadishes, cucumbers, water-cresses, butter, pot-cheese. 
 
 Tea or coffee with a little cream, but no sugar. (Glycerin may be 
 used instead of sugar, if desired.) 
 
 Eolls, pancakes, fritters, griddle cakes, etc., made of gluten bread 
 only and eaten with butter, no syrups or sugar. 
 
 Light red wines for those who are in the habit of taking wine for 
 breakfast. 
 
 Lunch. 
 
 Oysters or clams cooked in any way, except with flour or milk; 
 chicken, lobster, or any kind of salad except potato; fish of all kinds; 
 chops, steaks, ham, tongue, eggs, crabs, or any kinds of meat; head- 
 cheese. 
 
 Eed wines, dry sherry, or Bass' ale. 
 
 Dinner. 
 
 Eaw oysters, raw clams; consomme of beef, of veal, of chicken, or 
 of turtle; consomme with asparagus points; consomme with okra, 
 oxtail, turtle, terrapin, oyster or clam, all without flour or milk; 
 chowder, without milk or potatoes ; mock turtle, mullagatawny, 
 tomato, gumbo fillet. 
 
 Fish. 
 
 All kinds of fish, lobster, oysters, clams, terrapins, shrimps, craw 
 fish, hard-shell crabs, soft-shell crabs. No sauces containing flour, 
 unless gluten flour be used. 
 
 Relishes. 
 Pickles, radishes, celery, sardines, anchovies, olives. 
 
L92 GLYCOSURIA OR DIABETES MKLLITUS. 
 
 Meats. 
 
 All kinds of meats cooked in any way. except with flour; all kinds 
 of poultry without dressings., containing bread or flour: calves' head, 
 kidney, sweet breads, lamb fries, ham, tongue: all kinds of game; 
 veal, fowl, sweet breads, etc., with currie, but not thickened with 
 flour, and no liver. 
 
 Vegetables. 
 
 Truffles, lettuce, romaine, chickory, endives, cucumbers, spinach, 
 sorrel, beet tops, cauliflower, cabbage, Brussels sprouts, dandelions, 
 tomatoes, radishes, oyster plant, celery, onions, string beans, water 
 cresses, asparagus, artichokes, Jerusalem artichokes, parsley, mush- 
 rooms, all kinds of herbs. 
 
 Substihites for Siveets. 
 
 Peaches preserved in brandy without sugar; wine jelly without 
 sugar; gelee au kirsch without sugar; gelee au rhum without sugar; 
 omelette a la vanille without sugar. 
 
 Miscellaneous. 
 
 Butter, cheese of all kinds; eggs cooked in all ways except with 
 flour and sugar; sauce without flour or sugar, and thickened if de- 
 sired with gluten flour; almonds, hazelnuts, walnuts, cocoanuts; tea 
 or coffee with a little cream, and without sugar. (Glycerin may be 
 used instead of sugar, if desired.) 
 
 Bread made with gluten flour. 
 
 Alcoholic Beverages. 
 
 Clarets, Burgundy, dry sherry, Bass' ale, or bitter beer. No sweet 
 ■wines or malt lkjuors. 
 
 Proltibited. 
 
 Ordinary bread, cake, etc., made with flour and sugar; desserts 
 made with flour and sugar; vegetables, excejjt those mentioned above; 
 sweet fruits. 
 
 Gluten flour and diabetic bread may be obtained in New York 
 from the Health Food Co., 74 Fourth avenue. This bread and flour 
 should be used moderately, as it is not entirely free from starch and 
 sugar-producing elements. 
 
 The diet list of Professor Andrew H. Smith is also given- This is 
 
GLYCOSUKIA OK DIABETES MELL1TU8. 193 
 
 not strictly speaking a diabetic table, but one so arranged that, by 
 striking out certain articles of food or drink, it can be utilized in 
 regulating the diet of patients suffering from renal or hepatic diseases 
 .as well as diabetes. 
 
 Diet List. 
 
 patient may eat. 
 
 1. Oysters or Little Neck clams in season, in any form, except 
 ■when fried or served with sauces of hot butter, flour, etc. 
 
 2. Soups. Broths of ordinary meats, poultry, and game; soups not 
 thickened or mealy, and not containing any vegetables, save those men- 
 tioned in this diet list. 
 
 3. Bread. Stale or toasted; rye bread. 
 
 4. Fish of all kinds, with certain exceptions. No fried fish should 
 be eaten. 
 
 5. Meats. Lean mutton, beef, lamb, veal, tongue, and sweet 
 breads. 
 
 6. Poultry and game of all kinds, except duck and goose. 
 
 7. Eggs and milk, with or without cream. 
 
 8. Vegetables. Greens, spinach, lettuce, water-cress, chickory, 
 -dandelions, French beans, Lima beans, string beans, dried beans, 
 green peas, asparagus, Brussels sprouts, cabbage, cauliflower, cucum- 
 bers, celery, artichokes, radishes, onions, tomatoes, pickles, and 
 olives. 
 
 9. Dessert. Jellies, flavored but not sweetened; baked apples and 
 pears without sugar; peaches, oranges, lemons, and limes, without 
 milk or sugar. 
 
 10. Drinks. Tea and coffee without sugar, or with very little, and 
 with or without cream; dry wines, brandy, whiskey, only if necessary; 
 Apollinaris, Clysmic, St. Galmier, Bethesda, Poland, Buffalo Lithia, 
 or Bedford water. 
 
 AETICLES OF FOOD AND DKINKS TO BE AVOIDED BY THE PATIENT. 
 
 1. Soups. Thickened, mealy or sweet, or containing vegetables 
 specified in this list. 
 
 2. Fish. Salmon, herring, eels, sardines, and dried fish. 
 
 3. Meats. Fried meat, pork in any form; dried, preserved and 
 potted meats; the fat of meats, meat pies. 
 
 4. Sauces. Of hot butter, or containing flour, served usually with 
 fish, meat, or game; Mayonnaise, dressings of oil and vinegar on 
 
 13 
 
194 GLYCOSURIA OR DIABETES MELL1TUS. 
 
 salads, the use of spices, Worcestershire, Harvey's fish sauce, Tobasco 
 sauce, etc. 
 
 5. Butter. None, or the merest trifle. 
 
 6. Bread. No fresh or hot bread, biscuit, corn bread, griddle cakes,. 
 \va tiles, fritters, etc. 
 
 7. Vegetables. No saccharine or starchy vegetables, as potatoes, 
 rice, sago, tapioca, arrow-root, corn meal, hominy, oatmeal, wheaten 
 grits, macaroni, vermicelli, semolina, beets, carrots, parsnips, no 
 sugar, no fried vegetables, all canned vegetables in the preparation of 
 which sugar has been used, tomatoes, onions, and corn. 
 
 8. Cheese. None. 
 
 9. Dessert. Sweets of all kinds, custards, creams, ices, puddings,, 
 cakes, nuts, dates, and raisins, dried and candied fruit, and sweet 
 grapes. 
 
 10. Drinks. Ales, porter, stout, beer, especially heavy beer, sweet 
 and effervescent wines, and all alcoholic drinks, as brandies, whiskeys, 
 gin, rum, liqueurs and cordials, except when ordered. 
 
 A well authenticated case of cure of the severe forms of diabetes 
 has not yet been recorded, but life can be made quite endurable and 
 prolonged for months and years. From our present knowledge, it 
 appears that a well regulated diet offers quite as satisfactory results as 
 the former exclusive plan. If the limited diet is to be instituted, it 
 is far better to make a gradual and not a sudden change. 
 
URINARY ANALYSIS. 
 
 PART II. 
 
 CHAPTER I. 
 
 URINARY ANALYSIS. INTRODUCTORY REMARKS. 
 
 The urine lias long been recognized as affording valuable aid in the 
 diagnosis of disease, and as much is being added to our knowledge in 
 this field, it is quite important that these additions should be noted. 
 The purpose of the following sections is to elucidate the utility and 
 make plain the necessity of the microscope in its bearings upon prac- 
 tical medicine, and at the same time to simplify some of the methods 
 in vogue. 
 
 To every one conversant with the subject, it is well known that, 
 while much work has been done upon urinary analysis, it has been 
 chiefly from a chemical standpoint, the clinical features not receiving 
 the attention which they deserve. It is hoped, therefore, that these 
 chapters may commend themselves to the readers as a contribution to 
 clinical medicine. They are the result of much work, in the hos- 
 pital, in the mortuary, and in the laboratory, which, together with 
 several years' experience in teaching, encourages the belief that they 
 will satisfy the long-felt need of the busy and active practitioner. 
 
 An accurate understanding of urinary analysis in its relation to 
 clinical medicine is absolutely essential for a clear comprehension of 
 any disease. 
 
 This statement is especially true in typhoid fever, pneumonia, 
 scarlet fever, and in fact with all the acute blood diseases; and also 
 with acute surgical conditions. In all these instances, a careful study 
 of the urine frequently proves to be a more accurate index to the rise 
 and fall of the diseased process than any other single symptom, 
 enabling the physician to foretell with accuracy an approaching im- 
 
1:m; urinary analysis. 
 
 provement or a threatened exacerbation, which is to speedily termi- 
 nate in a fatal issue. It places him in a position to know what to 
 expect, and better prepares him for coming emergencies. 
 
 Accuracy in the application of urinary analysis is not to be confined 
 to acute diseases ami surgical conditions alone, but is largely applica- 
 ble in many of the chronic disorders. 
 
 The results obtained from urinary analysis and their application to 
 clinical symptoms, together with the effect of medicinal agents, are 
 unquestionably the only methods by which the mystery so long con- 
 nected with hepatic disorders can be made plain. In this way we 
 may be enabled to understand and diagnosticate hepatic diseases 
 almost as easily and accurately as we now do renal affections. The 
 recent studies which have been made in the long uncertain and mys- 
 terious disease, diabetes mellitus, show what can be accomplished, 
 and not only suggests the possibility, but strongly indicate an 
 approaching advance in all forms of hepatic lesions. 
 
 Chemical Compositioti. 
 
 The various substances which enter into the formation of the urine 
 have been differently stated by the numerous observers; they also 
 vary somewhat in reference to the relative quantities of each, but in 
 general there is a striking correspondence. Slight variations must be 
 •expected, from the very fact that the examinations cannot be made 
 under precisely the same circumstances. 
 
 The tables of Flint and Roberts are both quite complete. 
 
 » 
 
 Table of Composition from Flint. 
 
 Water, 967.47 to 940.36 
 
 Urea (in 24 hours, 355 to 463 grains, Robin), . . 15.00 to 213.00 
 
 Urate of soda, neutral f 
 and acid, 
 
 Urate of ammonia, I In 24 hours, 6 to 9 grains of uric 
 neutral and acid (in J acid — Becquerel — or 9 to 14 i 
 small quantity), 1 grains of urates, estimated as j ' ° 
 
 Urate of potassa (trace), neutral urate of soda. 
 
 Urate of lime (trace), 
 
 Urate of magnesia (trace), i 
 
 .-,. , n „„ •,„ f In 24 hours, about 7.5 grains of 1 
 
 Hippurate of soda, . . ' . , _,. f . , I 
 
 ... c . hippunc acid — Thudichum — i 1 nrt ,„ i An 
 
 Hippurate of potassa, ■{ . , , , , „ „ . , r I- 00 to 1-40 
 
 TT . . i: equivalent to about 8.7 grains of 
 
 Hippurate of lime. ? fe 
 
 ^ hippurate of soda. 
 
 Lactate soda, 
 
 Lactate potassa, < Daily quantity not estimated. > 1.50 to 1.60 
 
 Lactate lime. 
 
URINARY ANALYSIS. 
 
 197 
 
 Sulphate of soda, 
 Sulphate of potassa, -{ 
 Sulphate of lime (trace), I 
 
 Creatin, j In 24 hours, about 11.5 grains of / 
 
 Creatinine, 1 both — Thudichum. ) 
 
 Oxalate of lime (daily quantity not estimated), 
 Xanthin, ....... 
 
 Margarin, olein, and other fatty matters, 
 
 Chloride of sodium (in 24 hours, about 154 grains — Robin), 
 
 Chloride of potassium, ..... 
 
 Hydrochlorate of ammonium, ..... 
 
 f In 24 hours, 28 to 38 grains of 
 sulphuric acid — Thudichum. 
 About equal parts of sulphate 
 of soda and sulphate of potassa 
 — Robin — equivalent to from 
 j 22.5 to 37.5 grains each. 
 
 Phosphate of soda, neutral, c Dail quantity not estimated. I 
 Phosphate of soda, acid, ] ) 
 
 Phosphate of magnesia (in 24 hours, 7.7 to 11.8 grs. — Neubauer) 
 Phosphate of lime, acid, t In 24 hours, 4.7 to 5.7 grains — ) 
 Phosphate of lime, basic. ( Neubauer. ) 
 
 Ammonia-magnesian phosphate (daily quantity not estimated), 
 (Daily excretion of phosphoric acid, about 56 grs. — Thudichum. 
 Silicic acid, . ...... 
 
 Urosarcin, j 
 
 Mucus from the bladder, j 
 
 1.60 to '.',.00 
 
 trace to 1.10 
 
 not estimated. 
 
 0.10 to 0.20 
 
 3.00 to 8.00 
 
 trace. 
 1.50 to 2.20 
 
 3.00 to 7.00 
 
 2.50 to 4.30 
 
 .50 1.00 
 
 .20 to 1.30- 
 
 1.50 to 2.40- 
 
 0.03 to 0.04 
 
 0.01 to 0.50 
 
 1,000 1,000 
 
 Table of Composition from Roberts. 
 
 "Water, 
 Solid matters, 
 
 Urea, 
 Uric acid, 
 
 Extractives. ■{ 
 
 Creatin, creatinin, ammonia, hippuric "| 
 acid, xanthin, hypo-xanthin, sarcin | 
 
 pigments, unoxidized sulphur and phos 
 phorus, mucus, etc., etc. 
 
 Chlorine, .... 
 Sulphuric acid, 
 Phosphoric acid, 
 
 J 
 
 Fixed salts, i f°f sh > 
 Soda, 
 
 Lime, . 
 
 Magnesia, 
 
 21.57 
 .36 
 
 6.53 
 
 4.57 
 1.31 
 2.09 
 1.40 
 7.19 
 0.11 
 0.12 
 
 954.81 
 45.19 
 
 1,000.00 
 
 28.46. 
 
 16.79 
 
198 
 
 i kinary analysis. 
 Blank For Urinary Analysis in Full. 
 
 No 
 
 
 
 
 
 
 
 
 Dnilv Onunt.itv 
 
 
 Chem ical Examination . 
 
 Day and hour of exair 
 
 lination, 
 
 Daily quantity, 
 
 Color, 
 
 
 Odor, 
 
 Translucency, 
 
 
 Reaction, 
 
 Sediment, 
 
 
 Specific gravity, 
 
 Albumin. 
 
 
 Glucose, 
 
 Proteids, 
 
 
 Urea, 
 
 Uric acid, etc., 
 
 
 Urates, 
 
 Phosphates, 
 
 
 Chlorides, 
 
 Adventitious coloring 
 
 matter, 
 
 Fatty matters, 
 
 Mucus, 
 
 
 Blood, 
 
 Microscopic Examination . 
 
 Red blood-corpuscles, Leucocytes, 
 
 Mucus, Uric acid, 
 
 Oxalate of lime, 
 
 Urates, Pigments, 
 Amorphous, Blood, 
 
 Ammonium, Bile, 
 
 Soda, Miscellaneous, 
 
 Phosphates, Spermatozoa, 
 
 Amorphous, Vegetable Organisms, 
 Triple, Sphero bacteria, 
 
 Stellar, Simple bacteria, 
 
 Epithelium, Vibriones, 
 
 Squamous, Leptothrix, 
 
 Bladder, Desmo-bacteria (bacillus), 
 
 Vaginal, Fungi, 
 
 Buccal, Penicillium glaucum, 
 
 Renal, Torula cerevisiae, 
 
 Ciliated, Saccharomyces cerevisiae, 
 
 Tailed, 
 
 Casts. Small Variety. Large Variety. 
 
 Blood 
 
 Hyaline 
 
 Epithelial 
 
 Nucleated 
 
 Granular, finely 
 
 " coarsely. 
 
 Fatty 
 
 Tubular 
 
 Corkscrew 
 
UKINAEY ANALYSIS. 
 
 199 
 
 Sediments of Doubtful Importance. 
 
 Lime carbonate, 
 
 Cholesterin, 
 
 Leucin, 
 
 Xanthin, 
 
 Foreign matters, 
 
 Fatty matter, 
 
 Cystin, 
 
 Tyrosin, 
 
 Analysis of Case. 
 
 Animal Organisms. 
 Ecchinoccocus, 
 Filaria sanguinis hominis, 
 Bilharzia, 
 Strongylus gigas, 
 Miscellaneous, 
 
 Indications as to Diagnosis and Treatment. 
 
 A condensed blank for office work is also given, and its use is strongly 
 recommended as a great help in the study of clinical medicine. 
 
 Blank for Urinary Analysis. 
 
 No 
 
 
 
 
 Hour Voided 
 
 Daily Quantity 
 
 Day and hour of examination, 
 
 Color, 
 
 Odor, 
 
 Translucency, 
 
 Reaction, 
 
 Sediment, 
 
 Albumin, 
 
 Glucose, 
 
 Phosphates, 
 
 Urates, 
 
 Chlorides, 
 
 Bile pigments, 
 
 Microscopic Examination. 
 
 Red blood-corpuscles, 
 Uric acid, 
 Oxalate of lime, 
 Phosphates, 
 
 Amorphous, 
 
 Triple, 
 
 Stellar, 
 Epithelium, 
 
 Bladder, 
 
 Vaginal, 
 
 Buccal, 
 
 Renal, 
 
 Ciliated, 
 
 Tailed, 
 Spermatozoa, 
 
 Leucocytes, 
 
 Mucus, 
 
 Urates, 
 
 Amorphous, 
 
 Ammonia, 
 
 Soda, 
 Pigments, 
 
 Blood, 
 
 Bile, 
 
 Miscellaneous, 
 Bacteria, 
 
 Penicillium glaucum, 
 Saccharomyces cerevisiaa, 
 Fatty matters, 
 Foreign matter, 
 
200 urinary analysts. 
 
 Casts, Large. Small. 
 
 Blood 
 
 Hyaline 
 
 Epithelial 
 
 Nucleated 
 
 Granular, finely 
 
 " coarsely 
 
 Fatty ., 
 
 Tubular 
 
 Corkscrew 
 
 Analysis of Case. 
 
 Indications as to Diagnosis and Treatment. 
 BLANKS. 
 
 The first thing to he considered in studying the urine from a clini- 
 cal standpoint is a blank upon which to record the result. 
 
 Two forms are inserted, one as a guide for further elucidation in 
 this work, and a second as a guide in ordinary practice. 
 
 The latter only differs from the former in the omission of a number 
 of substances of rare occurrence, and two or three of doubtful authen- 
 ticity. 
 
 Blanks should always be used, numbered, and kept for future 
 reference, which many times will be found of great service. 
 
 The dale, name, and address should be carefully noted. The hour 
 of voiding, and the exact daily quantity, especially the latter, should 
 be rigidly enforced. 
 
 The hour when voided. This question is one of great importance, 
 for the reason that the normal composition varies greatly during the 
 twenty-four hours. Therefore, unless this fact is remembered, the 
 examiner may be misguided by the results and led into an error in 
 diagnosis, prognosis, and treatment. 
 
 There are three ways by which this source of error maybe obviated. 
 
 The most accurate method is to save the whole quantity voided 
 during the twenty-four hours, and examine a sample of this mixed 
 urine. But in some instances this may not be practicable, which is 
 especially true in walking cases and in men at business. In the very 
 warm weather of summer, it may not be wise to save the urine for 
 the whole twenty-four hours, on account of the changes resulting 
 from fermentation. 
 
 Under such circumstances, a very fair average sample can be ob- 
 tained by instructing the patient to collect that passed at night be- 
 fore retiring and that during the night, if any, and that voided in the 
 morning upon rising. Great care should be exercised in having all 
 
URINAKY ANALYSIS. 
 
 201 
 
 receptacles perfectly clean, as patients are apt to think moderately 
 clean vessels sufficiently good to collect urine. 
 
 The only difference now as compared with the total daily quantity 
 is a larger quantity of the solids, and consequently such a sample will 
 be of higher specific gravity, by two or three or more degrees. This 
 is specially true in larger cities, where the heaviest meal is taken late 
 in the day. 
 
 By taking that passed upon rising, a little lower specific gravity 
 will be obtained, and one which ap- 
 proaches more nearly to the daily 
 average. 
 
 By one or both of these methods 
 very nearly accurate results will be 
 obtained, and any gross error be 
 avoided. 
 
 In all important cases, the exact 
 quantity discharged during the twenty- 
 four hours must be collected and ac- 
 curately measured. This should be 
 insisted upon as absolutely indispen- 
 sable. 
 
 If only one of the daily passings is 
 to be examined, the hour of voiding 
 should be noted, and then by remem- 
 bering the daily variations, error may 
 be avoided. 
 
 In studying renal diseases, it is al- 
 ways well to note the number of times 
 the individual is compelled to empty 
 the bladder. 
 
 The kind of receptacle for collecting the total daily quantity is of 
 no practical importance, so long as the exact quantity is accurately 
 determined, and the receptacle is kept closed. Long graduated cylin- 
 ders, with or without stoppers, have been recommended; the latter are 
 preferable. Graduated bottles answer very well, or it may be collected 
 in a number of smaller receptacles, and then mixed and measured. 
 
 Fig. 48— Glass Cylinder Grad- 
 uated Either in Ounces or Cubic 
 Centimetres. 
 
CHAPTER II. 
 
 CHEMICAL EXAMINATION. 
 
 Having ascertained those facts which must be obtained from the 
 patient or nurse, the next step is to institute a thorough chemical 
 analysis, and then set aside a sample in a conical glass for the micro- 
 scopic examination. The reason for using a 
 conical receptacle is, that in many instances, 
 when a microscopic examination is most essen- 
 tial, the urine contains but little sediment, and 
 unless it is collected in this way, very valuable 
 information is easily overlooked. 
 
 Day and liour of examination. — It is of great 
 
 fig. 49.— conical Re- importance to note accurately not only the day, 
 
 ^^menuwitthausr ting ^ut ^ ne h° ur °^ examination of each sample 
 
 tested. In this way the number of hours that 
 
 have elapsed since the urine was passed can easily be computed. 
 
 The reason for laying so much stress upon this point is, the rapidity 
 with which urine undergoes decomposition, and the numerous new 
 products developed by its fermentation. By remembering this, due 
 allowance can be made, when the source of error cannot be otherwise 
 obviated. A calculation, however, should never be allowed to take 
 the place of a fresh sample and an early examination if it can possi- 
 bly be avoided. 
 
 For absolute and indisputable accuracy, all urine should be ana- 
 lyzed within twelve hours after its discharge from the bladder. 
 
 In case this is absolutely impossible, it may be filtered, for in this 
 way some of the mucus is removed, and for a time, at least, fermenta- 
 tion is retarded. Filtration will, of course, hold back casts and any 
 solid matter, and for this reason, in the majority of cases, it is im- 
 practicable. 
 
 The presence or absence of the mucus appears to influence to a con- 
 siderable degree the rapidity with which fermentation is established. 
 If the mucus could be dispensed with, without losing other impor- 
 tant ingredients, it would be of great aid in many instances. 
 
 When the urine is first expelled, it contains no free acid; its acidity 
 
CHEMICAL EXAMINATION. 203 
 
 :at this time being ascribed, to the biphosphate of soda. If then, as 
 soon as the urine is voided, we add a few grains of salicylic acid, 
 chloral hydrate, or some mild disinfecting agent, fermentation may 
 be delayed for days or hours. This is essential when the urine is to 
 be sent any distance for examination. By observing these rules, the 
 most accurate results will be obtained. 
 
 If casts are to be specially sought for, the patient should be in- 
 structed to collect separately the urine voided three or four hours 
 after the heaviest meal of the day, provided, of course, that there is a 
 fair quantity of urine discharged at that time. 
 
 A still more certain way for securing casts is to place the patient 
 upon hydragogue diuretics, with copious draughts of water, and have 
 the urine collected as soon as free diuresis is established. In this way 
 large quantities of casts are dislodged, and are found in abundance. 
 After a discharge of casts, lasting two or three days, the urine will 
 often be found free from them, and it may remain so for several days. 
 It not unfrequently happens, in some forms of renal lesions, that this 
 alternation between an abundance and scarcity or absence of casts be- 
 comes one of the characteristic symptoms of the disease. 
 
 DAILY QUANTITY. 
 
 The normal quantity of urine expelled from the bladder during 
 the twenty-four hours has been variously estimated by different ob- 
 servers. A good general average is from forty to fifty ounces. This 
 will be assumed as the normal standard for further comparison. 
 
 A temporary variation of ten, fifteen, or even twenty-five ounces 
 either way, does not in itself indicate an abnormal condition of the 
 kidneys, but if prolonged, it is a deviation from the normal standard, 
 but does not of necessity indicate disease. The differences in the 
 solidity of the food, the quantity of fluid taken, the activity of the 
 skin and alimentary tract, and the surrounding temperature will 
 often explain the change. 
 
 If, however, all these conditions remain about the same from day 
 to day, and. are then associated with a persistent increase or decrease 
 in the total quantity voided, a careful and complete examination 
 should at once be made. This positive change in quantity is fre- 
 quently the first symptom to attract the attention of the patient and. 
 cause him to seek medical advice. 
 
 A continued increase is indicative of chronic interstitial nephritis; 
 one form of chronic diffuse nephritis, in which there is a hyaline 
 metamorphosis and permanent dilatation of the afferent vessels of the 
 glomeruli; amyloid or waxy kidneys in which a similar condition 
 
20-i CHEMICAL EXAMINATION. 
 
 of the afferent vessels is present; polyuria, diabetes insipidus, or dia- 
 betes mellitus. 
 
 A continued decrease is indicative of a lesion of the kidneys involv- 
 ing the epithelial cells, and occurs in acute and chronic parenchyma- 
 tous metamorphosis of the kidneys; also in chronic congestion there 
 is a persistent diminution in quantity. 
 
 A close study of the clinical history, and a careful chemical analy- 
 .-is and microscopic examination of the urine will enable the exami- 
 ner to readily and accurately decide which of the above diseases is 
 the cause of the persistent increase or decrease in the urine voided daily. 
 
 In some forms of the chronic diffuse nephritis, there may be a con- 
 tinued decrease for several days, and then the quantity will increase 
 again. This fluctuation is often repeated, and consequently becomes 
 a diagnostic element in itself. 
 
 The relation existing between quantity and specific gravity is one 
 of the most important facts in connection with urinary analysis. It 
 will be fully considered when studying the specific gravity. 
 
 It is almost impossible to determine with absolute certainty the 
 quantity voided by a female, for the reason that some will unavoid- 
 ably be lost when at stool. In case there is no movement of the 
 bowels, not an uncommon occurrence, the exact quantity can be de- 
 termined. 
 
 COLOR. 
 
 It is almost impossible to determine with accuracy the varying 
 shades of color which may be met with in urine. For this reason 
 the four general headings, adopted by other writers upon urinary 
 analysis, will be retained, as they can be readily appreciated and 
 recognized by all; viz., pale, normal, golden or orange-yellow, high-col- 
 ored, and dark urine. In speaking of color, it should be applied to 
 a considerable quantity or to its appearance when in the chamber. 
 Viewed in a bottle or test-tube by transmitted light, it will be much 
 lighter than in the first receptacle. For this reason, what may appear 
 to be dark urine to the patient will be considered much lighter in color 
 by the examiner, and give rise to a variance of opinion. This should 
 be remembered in taking the patient's statements in regard to color. 
 
 (a) Pale urine varies from a clear liquid closely resembling pure 
 water to a light straw-yellow color, or to the normal, and is usually 
 abnormal. 
 
 (b) Normal colored urine ranges anywhere between a rich golden 
 yellow and a deep orange-yellow. 
 
 (c) High-colored urine ranges between a reddish-yellow and a de- 
 cided red. 
 
CHEMICAL EXAMINATION. 205 
 
 (d) Dark urine ranges from a reddish-brown to a blackish or deep 
 
 black. 
 
 Pale urine is duo to an increase in the watery constituents result- 
 ing either from copious draughts of water or liquids, a rapid excre- 
 tion, or to a diminished perspiration following exposure to cold. A 
 variation in the quantity of pigments excreted will also vary the color. 
 
 A thickening of the walls of the vessels, and especially of the arteri- 
 oles of the kidneys, by diminishing their power of contractility, al- 
 ways increases the quantity of water discharged from the body. These 
 vessels, and especially the afferent to the glomeruli, having lost their 
 power of contracting and expanding with the constantly varying blood 
 pressure, are no longer able to regulate the pressure in the capillary 
 tuft of the glomeruli and, as a result, the now increased hydrostatic 
 pressure brought to bear upon the tufts over-distends their capillaries, 
 weakens their walls, and forces the water of the blood into the urini- 
 ierous tubules more rapidly, thus greatly augmenting the flow of urine. 
 
 This fact is well borne out in the amyloid degeneration of the kid- 
 neys, in the sclerotic kidneys, and in that variety of chronic diffuse 
 nephritis where there is a hyaline transformation, with thickening 
 and dilatation of the afferent vascular walls. In all of these three 
 ■conditions, this change in the vessels is a noticeable feature of the 
 lesions, and in all an abnormally large quantity of urine is one of 
 the pronounced symptoms. 
 
 On the other hand, in all forms of renal disease in which the ves- 
 sels are not thickened and dilated, but retain their contractility, it is a 
 noticeable fact that the quantity of urine excreted is, as a rule, below 
 normal. 
 
 In every instance where an opportunity has presented for making a 
 necropsy in diabetic subjects, a careful study of the renal organs showed 
 a marked thickening and dilatation of the afferent vessels of the glo- 
 meruli, which easily explained the large flow of urine in this disease. 
 This inability on the part of the system to regulate the discharge of 
 water is undoubtedly the true explanation for the extreme thirst. 
 
 The quantity of urine is also increased in anaemia, diabetes insipi- 
 dus, after hysterical fits, asthmatic attacks, and all forms of marked 
 nervous excitement. In all of these, the urine is very pale 
 (urina spastica), and contains little else than water. It is quite 
 apparent that a relaxation of the vaso-motor system distributed to 
 the splanchnic arcade is the cause which dilates the afferent vessels, 
 increases the pressure brought to bear upon the tuft of vessels form- 
 ing the glomeruli, and explains the copious discharge of urine. 
 The urine is pale during convalescence from fevers. 
 
206 CHEMICAL EXAMINATION. 
 
 Chylous urine should be classed as pale, for it lacks the yellow color 
 of a normal sample. It is in some instances positively white, like 
 milk, from the emulsified fat which it contains. At other times it 
 has a muddy appearance. 
 
 High-colored urine occurs with increased perspiration, with a small 
 daily use of liquids, with disorders of the liver in which its function 
 is incompletely performed, and with all febrile diseases. After a. 
 hearty meal, it not infrequently happens that the urine of a perfectly 
 healthy individual is high-colored. 
 
 In connection with the acute febrile disorders, the color of the urine- 
 often serves as a sure index to the rise and fall of the diseased process, 
 and proves a safer guide than any other single symptom. For this 
 reason, the urine should be carefully recorded day by day, and in 
 some cases more frequently. 
 
 The causes of the increase in color in all acute and febrile diseases 
 which are associated with a blood poison* appear to be dependent upon 
 tbe diminution in quantity and also upon the hsematoglobinuria 
 theory (page 107), in which there is a destruction of the red blood- 
 corpuscles, brought about by the original poison and the increased 
 tissue metamorphosis, setting free the blood pigment which is dis- 
 charged by the kidneys. It certainly offers a reason for the high 
 color, and accounts for the changes in the shade, with the slightest 
 variation in the disease. 
 
 In acute yellow atrophy of the liver, and in various chronic affec- 
 tions of the hepatic gland, there often is an increase in the color of 
 the urine from changes in the biliary function, and a discharge of 
 the bile pigment or some of its derivatives. High-colored urine is 
 not inconsistent with health, and is found after a full meal, after ex- 
 ercise, and in samples that have stood some time. 
 
 Dark urine is due to bile, blood, and various forms of pigments- 
 and their derivatives. 
 
 When the urine is colored by bile pigments, the shade may vary 
 from brown to green. When colored by blood, haemoglobin, or other 
 pigments derived from blood, it is smoky, blood-red, coffee-colored, 
 or even blackish. 
 
 It has been stated that a smoky tint is absolutely diagnostic of 
 blood (Legg). This is thought to be an error, from the fact that, in 
 connection with carbolic-acid poisoning, the same appearance is 
 noticed. If the high-colored urine of carbolic-acid poisoning can be 
 traced to an induced haemoglobinuria by the acid, then the original 
 statement is not far from correct, otherwise it is inaccurate. 
 
 Various adventitious substances also change the color of the urine. 
 
CHEMICAL EXAMINATION. 207 
 
 Very strong coffee deepens the color. Large closes of rhubarb or senna 
 will often produce a deep-yellow or reddish hue. This condition can 
 be distinguished from urine colored by blood by the addition of a 
 mineral acid. If the color depends upon the first cause, the urine 
 will become brighter and of a light-yellow color; but if due to blood, 
 it will become muddy and darker in color. Haematoxylon gives the 
 urine a reddish hue; santonine in aikaline urine an orange-red, but 
 in an acid sample a golden-yellow color. If an acid be added to such 
 urine, it will become saffron-yellow or greenish, and resemble that- 
 containing bile pigment. Carbolic acid, creasote, and tar prepara- 
 tions occasionally give a blackish or even black color. With melanotic 
 tumors, the urine often turns black upon standing or after the addi- 
 tion of nitric acid. 
 
 Saffron, pareira brava, beet-root, indigo, camphilia, and cochineal 
 all tend to impart color to the urine. 
 
 All the causes of hemoglobinuria will increase the color, viz., 
 muscular fatigue, mental excitement, malaria, syphilis, rheumatism; 
 malignant, septic, putrid, and typhus fevers; purpura, scurvy, phthi- 
 sis; naphthol, pyrogallic acid, arseniurated hydrogen, carbon anhy- 
 dride, chlorate of potash, etc. 
 
 The above appears to cover all the points which are practical in 
 connection with the color of urine. At the same time, VogeFs standard 
 scales of colored plates are not to be ignored, for they will often be 
 found of service by way of comparison. Vogel divides the tints exhibited 
 by urines into three groups, each consisting of three members: yellow, 
 reddish, and brown or dark urines. (See plate.) The first grouj) he 
 subdivides into: 1st, pale-yellow; 2d, bright-yellow; 3d, yellow. The 
 second group into: 4th, reddish-yellow; 5th, yellowish-red; 6th, red 
 urines. The third group into: 7th, brownish-red; 8th, reddish- 
 brown; and 9th, brownish-black urines. 
 
 There are, however, several objections which may be raised against the 
 usefulness of VogeFs test-plates as a method by which reliable and prac- 
 tical information can be obtained. 1st, for those who are color-blind they 
 are useless; 2d, unless the sample be tested in the same vessel, each time 
 the information must be inaccurate as regards any definite quantity of 
 pigment; 3d, no value can be placed upon the study of these colors, 
 for the reason that any one of them may be produced by a variety of 
 different coloring matters and circumstances; 4th, the degree of light 
 transmitted through the fluid medium would in itself be a source of 
 error; 5th, few are sufficiently well trained in differentiating delicate 
 shades in color to judge accurately; 6th, it is a noticeable fact that 
 the different lithographers, in reproducing the test-plates, give a dif- 
 
_" s CHEMICAL EXAMINATION. 
 
 ference in the shades of color. This, of course, would make no dif- 
 ference if the same plate was constantly used, but two persons exam- 
 ining the same sample and using different plates, all other things 
 being equal, would not get the same result. 
 
 ODOR. 
 
 The odor of normal urine has been variously described, but it is a 
 noticeable fact that it corresponds to that of the fat of the animal 
 from which the urine comes. 
 
 "When alkaline from fixed alkalies, it is said to be aromatic. Dia- 
 betic urine often has a sweetish smell, and has been said to have a 
 whey-like fragrance when fresh, but on fermenting to have the odor 
 of sour milk. 
 
 Urine that contains decomposing blood has a foetid odor, while that 
 containing bile a peculiar and often offensive smell. 
 
 The normal odor may be changed by articles of food or by drugs, 
 viz., asparagus, onions, garlic, turnips, and by juniper berries, tur- 
 pentine, asafcetida, cubebs, copaiba, oil of sandal wood, carbolic 
 acid, alcohol, etc. 
 
 If the urine undergoes alkaline fermentation, it develops an ammo- 
 niacal odor, which often is decidedly perceptible. 
 
 It is rare that the sense of smell is of any diagnostic value. 
 
 TRANSLUCENCY. 
 
 In normal urine, when first expelled, its transparency is so nearly 
 perfect that no appearance of turbidity is perceptible by ordinary 
 diffused light. On account, however, of the trace of mucus obtained 
 from the walls of the urinary tract, a faint opalescence can be de- 
 tected when a sunbeam is made to pass through the sample in a 
 lateral direction. But at the end of a few hours the mucus will 
 subside, and ajtpear at the lower third of the bottle or receptacle as a 
 cloudy mass, and the supernatant fluid will now be perfectly trans- 
 ]Darent. 
 
 On cooling, if the urine be concentrated and acid, the urates will 
 be deposited. As the sample becomes more acid, an abundant deposit 
 of uric acid crystals may result. 
 
 Kormal urine, however, under all circumstances, should at first be 
 perfectly transparent. 
 
 REACTIOX. 
 
 The reaction, taking the whole quantity passed during the twenty- 
 four hours, is, as a rule, acid. Its acidity has been ascribed by 
 
CHEMICAL EXAMINATION. 209 
 
 different observers to a variety of substances, in part to free acids> 
 such as carbonic, acetic, lactic, oxalip, uric, and hippuric. Weight 
 of evidence, however, goes to prove that the above enumerated 
 acids play little or no part directly in causing the reaction. It ap- 
 pears rather to be due to a chemico-physiological combination between 
 the ordinary sodium phosphate of the blood and the organic acid de- 
 veloped in the system, by which the uric acid is united with a part of 
 the sodium phosphate to form a sodium urate, the remaining portion 
 being left as an acid sodium phosphate; and to this substance the 
 urine directly owes its acidity. 
 
 From this it is readily seen that, after all, it is the uric acid indi- 
 rectly which causes the reaction. This is also confirmed by the well- 
 known fact that in herbivora, where but little uric acid is produced, 
 the urine is normally alkaline, but when deprived of their vegetable 
 diet, and compelled to subsist upon their own flesh, the urates and 
 uric acid rapidly increase, and the urine becomes strongly acid. 
 
 The acidity also varies considerably during the twenty-four hours. 
 At times, it may be neutral or even alkaline. This change in acidity 
 was explained by Bence-Jones as -an off-setting action between the 
 acidity of the stomach and kidneys. His argument was that during 
 digestion the acid of the blood was poured into the stomach to form 
 the gastric juice, and consequently the urine became alkaline; but as 
 soon as the nutritive materials were taken up by the blood, it again 
 received this acid, and this in turn increased the acidity of the urine. 
 In herbivora, there is no such alternation, and we know that no 
 amount of acids administered by the mouth will change the reaction. 
 
 Eoberts, in opposition to Bence-Jones, holds that the alkalinity is 
 due to the absorption into the blood of the large quantity of nutritive 
 material ingested at each meal. But the explanations of both Bence- 
 Jones and Eoberts fall a little short of a complete elucidation of this 
 phenomenon. The latter theory is unquestionably more in keeping 
 with physiological laws, but it should have gone further, for the pro- 
 cess does not cease with the influx of the alkali; but the liver becomes 
 occupied in receiving and transforming the newly ingested nutritive 
 materials which are to be distributed to the various parts of the body. 
 Consequently while this part of the work is being accomplished, the 
 production of urea and uric acid is reduced to the minimum, and this 
 naturally diminishes the quantity of uric-acid forming elements in the 
 blood which can join with the sodium phosphate. As a result, the 
 quantity of acid biphosphate formed is diminished, and this, in con- 
 junction with the increased alkalinity of the blood, naturally tends to 
 decrease the acidity of the urine. But as soon as this portion of the. 
 14 
 
210 CHEMICAL EXAMINATION. 
 
 hepatic function is accomplished, it produces again an increasing quan- 
 tity of uric acid until the next period of absorption commences. This 
 would seem to offer a more complete explanation for the rise and fall 
 in the acidity of the urine. It also explains the increasing acidity 
 during the day and following the greatest amount of bodily and men- 
 tal metamorphosis, and shows why, after a night's rest, the first meal 
 is most likely to render the urine alkaline. 
 
 In some cases, the urine may remain alkaline for a whole day. It 
 need not be considered especially, but, according to the above theory, 
 would indicate a deficient production of uric acid; and, if the alka- 
 linity were prolonged, would indicate a serious abnormality either due 
 to a deficient absorption of the nutritive material from the intestinal 
 tract, or to a deficient production of uric acid, probably the latter. 
 
 Under perfectly normal circumstances, it is true that the urine 
 holds an inverse ratio to the amount of acid secreted by the stomach, 
 which, by being above or below normal, will interfere with intestinal 
 digestion, and consequently will, in a measure, alter the reaction of 
 the urine. The acidity, therefore, decreases after food is taken, but 
 increases as the gastric digestion advances, and is most decided at the 
 height of intestinal digestion or after the stomach has accomplished 
 its work. 
 
 Food and its contained elements will of necessity vary the reaction 
 of the urine; vegetables tend to diminish the acidity, and produce 
 positive alkalinit} 7 , while an animal diet intensifies the acidity. 
 
 After the urine has been expelled from the bladder, the acidity for 
 a time increases, which is caused by acid decomposition. The acid 
 fermentation is probably brought about by some specific ferment not 
 yet thoroughly understood, and the development of some acid, either 
 lactic or oxalic, or both together. As these changes take place most 
 rapidly when exposed to air, and in urine that contains considerable 
 mucus, the latter undoubtedly is one of the essential factors, as it has 
 already been proved that, by filtration and removing the mucus, this 
 fermentation is decidedly retarded. 
 
 Hofman and others, however, deny that there is any " acid fermen- 
 tation;" but there certainly is often an increased acidity after the 
 urine has been passed for a time, and this Scherer has said to be due 
 to the mucus of the bladder. 
 
 This increased acidity often causes a precipitation of the urates and 
 uric acid which previously were held in solution. 
 
 After a time, the acid is followed by alkaline fermentation. This 
 change is brought about by the splitting up of the urea into carbonate 
 of ammonia, probably by the influence of another ferment, which is 
 
CHEMICAL EXAMINATION. 
 
 211 
 
 thought to be due to a microscopic organism which acts as a ferment, 
 as the yeast fungus is supposed to do in producing alcohol. This 
 alkaline decomposition does not, as a rule, occur unless the urine is 
 exposed to air. But in some abnormal conditions it may occur 
 within the urinary tract, either in the bladder or, less frequently, in the 
 pelves of the kidneys. 
 
 In case the urine be alkaline when voided, alkaline fermentation 
 soon ensues; but if strongly acid when expelled, several days will often 
 elapse before any change can be detected. 
 
 The first product to follow the development of the carbonate of 
 ammonia is a deposit in the sample of the earthy phosphates, which 
 cause the urine to become cloudy, with the formation upon the surface 
 of an opaline scum. Still later a new salt is formed by the combining 
 of the free ammonia with the magnesium phosphate. This new salt 
 
 Fig. 50.— Crystals of Ammonia-Magnesium Phosphate. 
 
 is known as the triple phosphate or the ammonia-magnesium phos- 
 phate. 
 
 If the urine is constantly neutral when first passed or alkaline, it 
 indicates an abnormal condition, and calls for treatment by removal 
 of the cause. 
 
 This constant alkalinity may be due to the fixed salts (soda and 
 potassa) or to a volatile one, ammonia. The former are derived from 
 the blood, the latter from the decomposition of the urea. In both 
 instances the urine is turbid from the precipitation of the earthy 
 phosphates. 
 
 The fixed salts can be recognized by their property to turn red lit- 
 mus paper blue, which retains the color when dried; from the ab- 
 sence of any ammoniacal odor; and also from the presence of crystals 
 when examined microscopically. 
 
212 
 
 CHEMICAL KXAMIXATIOX. 
 
 The ammonia also turns red litmus paper blue, but the color here 
 does not remain after it lias dried: the ammoniacal odor is pro- 
 nounced, and triple phosphates are developed and found in the urine 
 in abundance. Both these conditions occur in the bladder and 
 upper urinary tract, and in some instances give rise to a vesical or 
 renal calculus. 
 
 The fixed salts are said to be the least likely to give rise to this con- 
 dition, as they are in an amorphous state, while the triple phosphates 
 are supposed to favor deposition. This is, however, somewhat ques- 
 tionable. 
 
 These two conditions should be accurately differentiated; the former 
 
 Fig. 51.— Uric Acid Crystals. 
 
 is due to changes in the blood, and needs to be treated by a change in 
 diet and internal medication; but in the latter the decomposition is 
 primarily external to the renal cells or somewhere in the urinary tract, 
 and the treatment is both local and systemic, but principally the 
 former. 
 
 Abnormally acid urine is occasionally met with, and often causes a 
 scalding sensation during the act of micturition. Outside of the body 
 this undue acidity produces an abundant deposit of uric acid crystals, 
 which may also be the case within the urinary tract, and it then 
 gives rise to the condition known as gravel and the formation of renal 
 and vesical calculi. In other cases, these uric acid crystals irritate 
 
CHEMICAL EXAMINATION. 213 
 
 the mucous membrane of the bladder, in this way inducing a cystitis, 
 which, in turn, is followed by alkaline fermentation, decomposition 
 of the urea, and the formation of the carbonate of ammonium with 
 the production of the earthy phosphates, which, being deposited in 
 successive layers upon a nucleus of uric acid, ultimately forms a phos- 
 phatic calculus. 
 
 From this it will readily be seen that undue acidity of the urine 
 when discharged from the kidneys may be followed by a discharge of 
 alkaline urine from the bladder. This point should always be care- 
 fully considered in making a diagnosis. 
 
 In both acid and alkaline urine due to increased primary acidity, 
 the trouble originates in a faulty action on the part of the liver, by 
 which there is an increased production of uric acid. 
 
 This condition can be temporarily modified by giving alkalies or 
 vegetable acids. But the most effectual and permanent treatment 
 consists in a regulation of the diet and plenty of open-air exercise. 
 Carbolic acid in one-minim doses, in water, three times a day, in some 
 instances appears to prevent the formation of uric acid calculi, and 
 relieves the symptoms of gravel. 
 
 The internal administration of fresh ox bile or the inspissated fel 
 bovis will often do more toward improving this condition than any 
 other form of medication. The fresh bile can be given in drachm 
 doses in capsules before each meal, or from three to five grains of the 
 inspissated in pill form (see page 26). 
 
 Urine occasionally is found to react both to red and blue litmus 
 paper, and is then said to be amphoterous, but has no clinical signifi- 
 cance. 
 
 SEDIMENT. 
 
 Normal urine, when first voided, is perfectly clear and transparent, 
 but after standing for a few hours the lower third often becomes 
 cloudy or opaque from the deposition of the contained mucus. 
 
 Chyle, spermatozoa, and epithelium often render the urine opaque 
 when first voided without any further precipitation. Pus, blood, and 
 the phosphates in concentrated and alkaline samples produce the 
 same result. The urates in concentrated and acid solutions, as soon 
 as cooled, produce a decided cloud, and often an abundant precipi- 
 tate. 
 
 All the crystalline substances are deposited, but usually being in 
 such small quantities they do not produce a precipitate which is per- 
 ceptible to the unaided eye. 
 
 Normal urine, when voided, may be transparent and, upon standing, 
 
214 CHEMICAL EXAMINATION. 
 
 become opaque. The same is true of abnormal urine. On the other 
 hand, abnormal samples may remain perfectly clear and transparent, 
 as for example, urine which contains glucose, albumin, or both at the 
 same time. Both substances being perfectly soluble in the urine, 
 it remains clear independent of its reaction. They are most per- 
 fectly soluble, however, in acid specimens. 
 
 The amount of sediment is roughly estimated by the eye. 
 
 The deposit which may form is composed of organic and inorganic 
 substances, some being normal to this fluid, others foreign to it;, 
 each will be considered separately. 
 
 SPECIFIC GRAVITY. 
 
 This question, like that of quantity, has been variously stated. The 
 normal specific gravity ranges between 1.017 and 1.023, and accord- 
 ing to some writers from 1.015 to 1.025. 
 
 This variation in density, associated with the changes in the daily 
 quantity of urine eliminated, is one of the most important points 
 to be observed in connection with urinary analysis. 
 
 The specific gravity, as well as the quantity, will vary naturally 
 with the amount of fluids taken and the quantity and solidity of the 
 food. 
 
 When there is no special excess or diminution in the fluids and food 
 taken, a close observation of the quantity and density will give the 
 most valuable information. By the quantity and specific gravity, but 
 especially the latter, a positive diagnosis is often to be determined. 
 
 If we have persistently a small quantity of urine with a high sj)ecific 
 gravity, say 1.020 to 1.025 or above, it is a strong indication, in fact 
 almost positive evidence, of parenchymatous metamorphosis of the 
 epithelial cells of the kidneys, or a derangement in the action of the 
 liver, which may be functional or due to some organic hepatic lesion. 
 In such a sample, further examination will reveal the presence of albu- 
 min and casts, or an increase in the uric acid and urates, and then 
 the diagnosis is positive. 
 
 This fact in reference to the specific gravity, so far as is known, was 
 first advanced by Professor Satterthwaite as a strong diagnostic point 
 in favor of parenchymatous metamorphosis of the kidneys. 
 
 A large quantity of urine and a specific gravity of 1.025 to 1.040 
 or LOGO indicates the probable presence of sugar. In all cases 
 where the quantity is above normal and the density above 1.025, 
 sugar should be suspected and tested for. Glucose, on the other 
 hand, may be found in urine of a low density. This, however, is the 
 exception. 
 
CHEMICAL EXAMINATION. 
 
 215 
 
 When the specific gravity fluctuates between 1.017 and 1.010 or 
 lower, with a varying quantity of pale urine, it is strongly indicative 
 of the existence of chronic diffuse nephritis. The finding of albumin 
 and casts will confirm the suspicion. 
 
 With a small quantity of urine of a dark, smoky hue, and a specific 
 gravity ranging between 1,020 and 1.012, acute diffuse nephritis is to- 
 be suspected. The finding of albumin and casts, especially blood- 
 casts and blood-corpuscles, completes the diagnosis. 
 
 In cases where the urine is abnormally increased, and continues at 
 sixty or one hundred ounces per day, 
 with a specific gravity constantly rang- 
 ing between 1. 010 and 1.005, a sclero- 
 sis of the kidneys is indicated. If al- 
 bumin and casts are absent, or seldom 
 found, the diagnosis is almost assured. 
 
 If the quantity of urine continues 
 very large, with a specific gravity rang- 
 ing from 1.005 to 1.001 persistently, 
 and there is a clinical history of long- 
 continued caries, suppuration, phthisis, 
 or syphilis, amyloid kidneys will usu- 
 ally be found at the necropsy. In the 
 urine excreted by waxy kidneys pure 
 and simple, albumin and casts are 
 rarely present. If, however, the amy- 
 loid transformation is secondary to 
 the other chronic forms, then albumin 
 and casts, one or both, will be found 
 in the urine. 
 
 There are a number of methods by 
 which the specific gravity can be determined — with the picnometeiv 
 Mohr-Westphal balance, or with a hydrometer, commonly designated 
 in connection with the urine a urinometer. 
 
 The first two are the most accurate, but least convenient. For a 
 further elucidation of the first two, the reader is referred to works on 
 physics. 
 
 The latter, however, deserves a word of attention, as it is the method 
 in common use and the most practical, although not quite so accurate 
 as the former. 
 
 The instrument should be carefully made to register densities from 
 1.000 to 1.060. All this can be indicated upon the stem of a single 
 instrument, but it is much better to use large instruments, covering 
 
 FlGr. 52. 
 
 C, Urinometer with full scale, to 
 60; D, glass for holding urine; 15, top 
 of fluid indicating a density of 15 or 
 1.015. 
 
216 I HEMICAl I \.\MI.\ ATlo\. 
 
 only a part of this stale: one covering the space from 1.000 to 1.030, a 
 second from 1.030 to LOGO, or better still, three, each covering twenty 
 degrees. 
 
 The accompanying cylinder, in which they are to be used, should 
 be sufficiently large to allow them to float easily and without adhering 
 to the sides. 
 
 The great objection to the small nrinometers with a short stem and 
 a scale of sixty degrees is that a large proportion of them are exceed- 
 ingly inaccurate, and the error has been found to be as great as thirty 
 degrees on a single scale. It is also difficult to read them with 
 accurat' v. 
 
 Some of the small instruments having a porcelain stem with the 
 scale cut upon it are quite accurate. 
 
 Pains should be taken to compare the whole scale with a urinometer 
 of known accuracy at the different densities, and if it is then found 
 correct, the smaller instruments may be used. 
 
 The nrinometers are very convenient many times when small quan- 
 tities of urine only are obtained. This difficulty, however, can be 
 obviated by diluting the urine with equal volumes of distilled water 
 until the larger instruments can be used. Multiply the specific 
 gravity above one thousand by the number of volumes of water added, 
 and then add 1,000. If three volumes are added and the specific gravity 
 of the mixture is 1.005, multiply the five by three, and add 1,000, 
 wdiich will equal 1.015 as the density of the urine. 
 
 On accouut of the difference in density of any fluid at different tem- 
 peratures, some of these instruments are furnished with a thermometer 
 irpon the float; by it the temperature can easily be determined and 
 brought to a proper standard, and a computation made from tables 
 constructed for that purpose. 
 
 With an instrument of this kind in which the scale of the thermom- 
 eter and the urinometer have been accurately made, very close esti- 
 mates can be determined. 
 
 Unless an accurate quantitative estimate is desired, this precaution 
 is not absolutely essential, and the ordinary urinometer, which is cor- 
 rectly graduated, answers every purpose. 
 
CHAPTER III. 
 ALBUMIN ; TESTS FOR ALBUMIN ; CLINICAL SIGNIFICANCE. 
 
 Albuminuria. — Albumin in the urine occurs under a number of 
 -different circumstances and is best divided into adventitious, some- 
 times called false, and intrinsic, or what has been termed true 
 albuminuria. 
 
 The various forms of albumin found in adventitious albuminuria 
 are haemoglobin, and egg-albumen, a peculiar form of albumin de- 
 scribed by Bence-Jones 1 as occurring in mollities ossium, which he 
 designated as hydrated deutoxide of albumin (par-albumin). It is 
 characterized by not being precipitated by heat, by nitric acid, nor 
 by adding nitric acid to boiling urine, but if it is boiled, and then al- 
 lowed to cool, a precipitate falls, and this is immediately redissolved 
 by heating it again. A similar substance has been found in the buff 
 coat of inflamed blood and in the albuminous fluid of pus. 
 
 Globulin or paraglobulin, acid-albumin and alkali-albuminate, 
 peptone, hemfcalbuminose of Kuhne, and fibrin should be included in 
 the list. They all have their origin in some condition outside of the 
 kidneys, either in an intestinal indigestion or in an incomplete hepatic 
 metabolism. 
 
 The first or haemoglobin is found in the urine when there has been 
 a haemorrhage into the urinary tract and the red blood-globules have 
 been liquefied; or in cases of haemoglobinuria. The presence of 
 haemoglobin can be ascertained by Almen's guaiac test or by Heller's 
 potassa test. (Part II., Chapter VII.) 
 
 The globulins are precipitated by heat and by passing carbon diox- 
 ide (C0 2 ) through a very dilute acidulated solution for one or two 
 hours, but this precipitate is soluble in very dilute solutions of chloride 
 of sodium, consequently the test is quite impracticable unless this 
 salt has first been removed or the urine diluted one or two thousand 
 times. 
 
 The alkaline albuminates are precipitated by neutralization with 
 
 1 Bence-Jones, "Animal Cliem.,'' p. 109. 
 
21 S ALBUMIN. 
 
 acetic acid, except in the presence of the alkaline phosphates. There- 
 fore, if this alkalinity be overcome, they may appear, but they are not 
 precipitated by heat. 
 
 The acid albumins are not precipitated by heat nor by the carbon 
 dioxide (COJ, but they are precipitated by neutralization, and the 
 presence of the alkaline phosphates does not interfere with this reac- 
 tion. 
 
 The peptones are not precipitated by heat, by carbon dioxide (CO,), 
 nor by neutralization, but they are precipitated by alcohol in excess,, 
 especially if absolute, and by nitric acid. 
 
 Before testing for the peptones, all other forms of albumin should 
 be eliminated by boiling, or better still, by dialyzation, and then the 
 tests for the proteids in general are applicable. 
 
 Egg-albumen is usually detected by the addition of ether, which, 
 causes it to be precipitated, but does not affect the serum-albumin. 
 
 Adventitious albuminuria has been considered of infrequent occur- 
 rence, but more recent observation naturally leads to the belief that 
 many times the small traces of albumin detected in urine by the more 
 delicate tests are in reality of the adventitious variety, and do not 
 indicate any renal disease. 
 
 The great difficulty in obtaining valuable information from these 
 different albumins is the inability to distinguish one form from the 
 other with ease and certainty. It can, of course, be accomplished, 
 but it requires a very careful and often extended analysis, and conse- 
 quently is not, as yet, practicable. There appears to be no doubt but 
 that the two forms of albuminuria have been confounded, and in this 
 way errors in diagnosis have arisen. 
 
 In the intrinsic form of albuminuria, there must be some change in 
 the renal circulation, or in the structure of the kidneys and their ves- 
 sels and epithelium, for serum albumin is not, as a rule, excreted by 
 the kidneys while perfectly normal. 
 
 Changes in the blood, however, may produce either the adventitious 
 or the intrinsic albuminuria. The abstinence from salt, too free use 
 of eggs or egg-albumen, certain forms of indigestion during the severe 
 fevers, and in connection with all conditions in which the alimentary 
 and hepatic digestion is incompletely performed, will give rise to ad- 
 ventitious albuminuria. This is especially true in the latter. The 
 albuminates now pass into the blood and remaining unchanged or not 
 being completely converted into serum-albumin, they pass on to the 
 kidneys and are forced out with the water, causing an adventitious 
 albuminuria. This may in a measure explain the not infrequent oc- 
 currence of albumin in the urine in connection with all severe febrile 
 
ALBUMIN. 219 
 
 diseases in which there are no marked structural lesions of the kidneys. 
 But more frequently the poisonous element which produces the primary 
 disease, together with the extra work to he accomplished hy the renal 
 epithelial corpuscles, causes a decided hepatic and renal lesion to be 
 developed, and now the albuminuria becomes both adventitious 
 and intrinsic. 
 
 The most common cause of intrinsic albuminuria is to be found in 
 changes in the blood, renal circulation, and structural changes in the 
 parenchyma. It occurs in connection with congestion of the kidneys 
 from certain forms of cardiac and pulmonary lesions, after cold bath- 
 ing, and varnishing the skin. 
 
 Increased pressure in the renal arteries was at one time thought to 
 produce intrinsic albuminuria, but later experiments are somewhat 
 opposed to this view. But increased pressure upon the venous side is 
 without doubt one of the great causes in producing this form of 
 albuminuria. 
 
 Even in connection with these vascular changes, albumin does 
 not appear in the urine until a marked metamorphotic transformation 
 has been developed in the epithelial cells. This tends to substantiate 
 the theory already advanced that abnormalities in the vascular pres- 
 sure alone are not sufficient to cause an intrinsic albuminuria, but to 
 this must be added metamorphotic changes in the renal epithelium and 
 a malnutrition of the vascular walls of the Malpighian tufts. Then 
 the albuminuria becomes intrinsic, persistent, and does not disappear 
 until the integrity of the epithelium is restored and the nutrition of 
 the vascular walls is raised to the normal standard. 
 
 The necessity of having retrograde changes in the renal epithelium 
 before an intrinsic albuminuria can be developed also suggests the 
 possibility of the discharged albumin being given off by the epithelial 
 cells in a similar manner to the excretion of glucose in diabetes. This 
 theory is also substantiated by the fact that the amount of albumin 
 discharged is in direct relation to the retrograde change in the renal 
 epithelium. If there is only a slight metamorphotic change in the 
 epithelium, the quantity of albumin in the urine is small; but, if exten- 
 sive, the amount of albumin will be large. 
 
 Cardiac and pulmonary lesions that obstruct the general venous 
 circulation, and secondarily interfere with the free escape of blood 
 from the kidneys, will increase the pressure in the renal veins and 
 produce an intrinsic albuminuria. Pressure upon the inferior vena 
 cava above the entrance of the renal veins will produce the same result. 
 Structural lesions of the kidneys which interfere with a free escape of 
 blood from the intertuhular plexus, increase the venous pressure, and 
 
220 ALBUMIN. 
 
 consequently the pressure upon the capillaries of the Malpighian tuft 
 and in this way act as a cause in producing an inherent albuminuria. 
 This condition appears to explain the abundance of albumin in the 
 parenchymatous group of renal lesions, the varying quantity in the 
 diffuse form, and its absence in the truly sclerotic variety. 
 
 In all the forms of renal lesions commonly classed as Bright's, there 
 is some change in the blood, as well as venous obstruction, and also a 
 change in the walls of the capillaries which form the Malpighian tuft. 
 All these changes are most marked in the parenchymatous group, 
 least marked in the sclerotic, and intermediate in the chronic diffuse 
 variety. In this way we have a pathological explanation for the 
 varying quantities of albumin. 
 
 In all the forms of structural change where the epithelial cells of 
 the tubules are primarily and principally involved, they swell and 
 compress the interlobular capillaries and veins, and in this way in- 
 crease the venous pressure, and with the blood changes, and especially 
 those of the walls of the vessels of the tuft, produce a constant and 
 often abundant discharge of albumin. But in structural changes in 
 which the lesion is confined principally to the interstitial tissue with a 
 thickening and loss of contractility on the part of the afferent vessel 
 entering the tuft of Malpighi, there is no obstruction to the venous 
 side, or changes in the capillaries of the tuft. Consequently there is 
 an increased arterial pressure, with a diminished venous pressure. As 
 a result, a greater mechanical pressure is brought to bear upon the 
 walls of the vessels composing the Malpighian tuft, and now a con- 
 stant and abundant discharge of water is the result. But the walls of 
 the vessels seem to retain their power to a degree sufficient to hold 
 back the albumin and consequently, as a rule, the urine does not 
 contain albumin. It appears, therefore, that the discharge of albumin 
 is principally due, first, to the integrity of the renal epithelium; 
 second, to the obstruction to the circulation through the intertubular 
 plexus of vessels, and third to the integrity of the walls of the vessels 
 constituting the Malpighian tuft. In like manner it appears that the 
 quantity of water discharged depends largely upon the condition of 
 the afferent vessels and the intertubular plexus, principally the former. 
 For in all instances where the intertubular plexus is free, and the 
 walls of the afferent vessels are thickened, their lumen is expanded, 
 and there is a loss in contractility, so that the quantity of water is in- 
 variably large. 
 
 By the above theories, based upon a large amount of clinical and 
 pathological data, any one can easily appreciate why in some varieties 
 
ALBUMIN. 221 
 
 of renal lesions there is an abundance 'and in others an absence of 
 albumin in the urine. 
 
 In like manner the irregularity in the quantity of urine voided can 
 be understood, as it varies with the nutritive changes in the epithe- 
 lium and the varying vascular pressure. In opposition to thechanj 
 in tension, it maybe said that quantity depends upon many things 
 besides pressure, but it appears that the other causes are only condi- 
 tions which aid in determining the amount of force brought to bear 
 upon the vessels of the Malpighian tuft, the condition of the inter- 
 tubular plexus, and the afferent vessels. It makes but little difference 
 whether this change be a direct or an indirect one; the ultimate result 
 is the same. 
 
 Albumin may occasionally be produced by the spontaneous decom- 
 position or liquefaction of the epithelial protoplasm of the urinary 
 tract. This assumption is made upon the strength of an experiment 
 performed by Prof. Satterthwaite, who removed the bladder from a 
 necropsy subject and immersed it in a water-bath which was kept at 
 the temperature of the body for a number of hours; the cavity of the 
 bladder being distended with non-albuminous urine. He found that 
 the fluid contained in the bladder rapidly became albuminous. To be 
 sure, this is not a parallel case v/ith the living subject, but it suggests 
 the possibility of a similar formation of albumin in connection with 
 retained urine and impaired nutrition of the mucous wall in contact 
 with the fluid. 
 
 Precautions to be observed before testing for albumin. 
 
 Before applying any test for albumin, the urine should be first 
 filtered to remove various substances which tend to make it cloudy 
 and which would obscure the albuminous precipitate. A very ready 
 method is to moisten a mass of absorbent cotten, wring it dry, and 
 pack it tightly into the bottom of a clean glass funnel. One thing 
 should, always be remembered, and that is, to add enough urine to 
 completely displace all the water required to moisten the cotton, other- 
 wise only water may come through, and no reaction for albumin will 
 occur. But if a sufficient quantity has passed through to completely 
 displace the water, albumin, if present, will always be found. 
 
 When the urine is supposed or known to contain pus, it should first 
 be boiled with a few drops of liquor potassse to the half test-tube of 
 urine (which will precipitate the albumin of the pus), and filtered. 
 After filtration, the fluid should be faintly acidulated with nitric 
 acid. Then the heat test, Heller's or any other test, can be employed 
 
222 ALBUMIN. 
 
 and the most positive information obtained in reference to the exact 
 quantity and source of the albumin contained in a given sample. 
 
 It requires considerable pus to produce anything more than a trace 
 of albumin, .but in some cases, when only a few pus-corpuscles are 
 found with the microscope, a large part of the albuminous precipitate 
 may be found to be due to pus. This is due to the sample having 
 been taken from the top of a vessel, the corpuscles having fallen to 
 the bottom. In all cases in which a renal lesion is suspected, this 
 question of doubt should be eliminated. 
 
 Tests for albumin. — A number of methods are in use for detecting 
 the albumin in the urine or in solution. Some are capable of de- 
 monstrating the presence of a very minute quantity. But as yet no 
 ready test or tests have been discovered by which an accurate diag- 
 nosis can be made between serum-albumin, egg-albumen, and many 
 of the forms resulting from incomplete digestion and transformation 
 of the peptones which not infrequently pass out of the body with the 
 urine. 
 
 Many of the tests are so delicate that all the varying forms of albumin 
 are precipitated along with the serum-albumin. Most of the albumi- 
 nates are soluble at a higher temperature than serum-albumin, but the 
 fact that the urates, oleo-resins, and some of the alkaloids are precipi- 
 tated and disappear by heat when these tests are used, renders it abso- 
 lutely impossible to say which substance is causing the reaction, with- 
 out resorting to an eliminating analysis, which takes time and skill. 
 
 It does not appear certain that boiling eliminates all the serum- 
 albumin; consequently, a response to some of the more delicate tests 
 for the proteids cannot be said to eliminate serum-albumin and indi- 
 cate only modified forms of the proteid substances. 
 
 The peptones, as already seen, can be detected by their precipitation 
 with absolute alcohol, but to obtain an accurate result, the urine 
 needs to be dialyzed. This naturally detracts from the practical value 
 of the test, and in every instance there is a chance for an error to 
 creep in while making the differential analysis. 
 
 Some observers are inclined to believe, and perhaps with good 
 reason, that even the minutest trace of albumin is indicative of an 
 approaching renal lesion which will very soon be easily recognized by 
 other symptoms, as a confirmed and serious disease of the kidneys. Such 
 a conclusion seems hardly warrantable, however, until we can differen- 
 tiate between the adventitious and intrinsic albuminuria more readily 
 and accurately. For it is well known that few, if any, are able to 
 secure and maintain an absolutely perfect digestion and assimilation 
 even under the most favorable circumstances. It is quite consistent 
 
ALBUMIN. 223 
 
 with physiological laws to have a few of the albuminates slip into 
 the blood, on through the circulation, and out with the urine as albu- 
 min, peptones, hemi-albuminose, or some of the many other forms. 
 
 Such circumstances as these easily account for the presence of the 
 minute traces of albumin, and in the absence of all the other urinary 
 symptoms, argue strongly against the existence of any organic renal 
 lesion ; it does not in itself prove the approach of an organic renal 
 disease. 
 
 In proof of these statements, there are now a fair number of re- 
 corded cases of prolonged albuminuria, with no further renal symp- 
 toms, which have not terminated in an organic lesion of the kidneys, 
 but on the contrary, in complete recovery. This certainly is strong 
 proof that the simple escape of albumin from the blood through the 
 kidneys does not in itself damage their structure. 
 
 The presence of albumin, with the absence of all other renal symp- 
 toms, tends to prove that the patient is taking too much albumin, or 
 is unable to completely digest and assimilate the peptones, and com- 
 pletely form serum-albumin. Now if this condition be allowed to 
 pass unnoticed, and without proper treatment, it may become more 
 and more pronounced, nutrition may become decidedly impaired, dis- 
 ease may be developed, and it may be followed ultimately by a giving 
 way of the renal glands. Under such circumstances, the organic 
 lesion of the kidneys is simply the last of a long chain of maladies. 
 A combined study of the physiological and pathological changes in 
 the kidneys tends to substantiate this view. Clinical studies added 
 to these also show how increased work ultimately destroys the normal 
 functions of the renal organs, and finally causes death by the devel- 
 ment of an organic kidney lesion. 
 
 On the other hand, there are organic lesions of the kidneys which 
 have persisted for years, and ultimately destroyed the life of the indi- 
 vidual, and yet during the whole course of the disease albumin never 
 made its appearance in the urine. 
 
 After carefully considering all these circumstances, it seems but 
 just to say that too much stress has been laid upon the recognition of 
 minute traces of albumin as a diagnostic sign of an organic lesion of 
 the kidneys, or of its approach. Certainly, so small a loss cannot 
 produce any strain upon the system, for the simple reason that in the 
 most severe forms of albuminuria the actual amount of albumin rarely 
 exceeds more than three per cent per volume, if it reaches so high a 
 figure. It is well known from experiment that five per cent of serum- 
 albumin in solution will completely gelatinize the fluid upon boiling. 
 If now we compute this loss in comparison with the total volume of 
 
22 4 ALBUMIN'. 
 
 albumin in the blood, and attempt to estimate the total loss to the body 
 
 per day. it is too small a quantity to be worthy of consideration. 
 
 If the percentage of albumin in the urine is not more than 0.004 of 
 one per cent, or 0.008 of one per cent, tbe loss from tbe bulk of blood 
 is almost too small to be computed. It may yet be found a most 
 valuable aid as an indicator of a perfect digestion, or one which is in- 
 complete, as well as a guide to the prognosis and treatment in connec- 
 tion with diseases of the hepatic gland and the alimentary tract. The 
 presence of these traces will then come to hold the same relation to 
 these obscure diseases as a more easily recognized quantity bears to the 
 now well understood renal lesions. 
 
 (1) Heal. — The best method is to till a test-tube three-quarters full 
 of tbe urine to be tested. Hold it by the bottom between the 
 thumb and forefinger, and apply the flame of a spirit lamp or Bun- 
 sen's burner; heat the upper third gradually to the boiling-point. If 
 no precipitate is formed, it indicates the absence of albumin or the 
 alkalinity of the sample, as serum-albumin readily coagulates at 90° C. 
 162° F. in acid mediums. If alkaline in reaction, add a drop or two 
 of nitric acid until the solution is distinctly acid. Now, if a precipi- 
 tate is formed upon boiling, remaining unchanged by the addition of 
 a little more nitric acid, or becoming more decided, albumin is pres- 
 ent. But if it remains clear, albumin is absent. 
 
 The acid is added for two reasons: first, to dissolve the phosphates, 
 carbonates, and all substances likely to cause a precipitate resembling 
 albumin: and second, to neutralize any alkali that may be present 
 and hinder the precipitation of the albumin by boiling. 
 
 Acetic acid is sometimes used instead of nitric acid to acidulate the 
 solution. When acetic acid is used, this important fact should, be 
 remembered, in acidulating with this acid while boiling, just en- 
 ough should be added to neutralize, and no more, for, if rendered 
 decidedly acid, the albumin is held in solution and no coagulation 
 occurs. If, however, the solution is neutralized exactly by the acetic 
 acid, it is one of the most delicate tests. 
 
 • From the above reason, that acetic acid may hold the albumin in 
 solution or convert it into an acid albumin which is not coagulated 
 by heat, it has been thought best to render the sample acid by nitric 
 acid before applying heat, but the nitric acid is open to the same 
 objection. 
 
 Either of the above will detect 0.018 of one per cent, if not a much 
 smaller percentage. 
 
 One of the most accurate methods for detecting albumin is to wash 
 the interior of a test-tube with a four-per-cent solution of acetic acid, 
 
ALBUMIN. 225 
 
 then nearly fill the tube with the urine, and heat the superior third 
 to the boiling point while holding it by the inferior extremity. In 
 this way, if albumin be present, the superior layer will become cloudy 
 while the underlying layer remains clear; in this way a sharp distinc- 
 tion can be drawn, and the merest trace of albumin detected. 
 
 It occasionally happens that the natural acidity of the urine is so 
 great that the alkaline serum-albumin is converted into an acid albu- 
 min, which is not coagulated by heat. In such instances the urine 
 should be rendered decidedly alkaline by caustic soda or potassium, 
 and then neutralized or made faintly acid by the addition of a four- 
 per-cent solution of acetic acid, and boiled, when the albuminous pre- 
 cipitate will be quite positive. 
 
 (2) Acidulated Potassium Ferrocyanide. — Acidulate the urine 
 strongly with acetic acid, then add several drops of potassium ferro- 
 cyanide. If the solution contains albumin, a white, flocculent pre- 
 cipitate will be developed. It is said that if albumin be less than 
 one-half to two per cent, this test shows no reaction (Thomas). On 
 the other hand, in Dalton's "Physiology," he says: "This is one of 
 the most delicate tests for the presence of albumin." Here certainly 
 are two contradictory' statements. If the former be true, it is abso- 
 lutely worthless in urinary analysis, for only in exceptional cases does 
 the urine reach one and a half per cent. 
 
 (3) Acetic Acid and Sodium Sulphate. — Acidulate the urine strongly 
 with acetic acid; add one drachm of the strongly acid urine to one 
 drachm of a strong solution of sodium sulphate and boil. If any 
 form of albumin is present, a permanent precipitate will be the result. 
 This test is very exact, and does not produce any decomposition of 
 other bodies which may be present, and hence the filtrate may be 
 further analyzed. 
 
 The three following are considered very delicate tests for traces of 
 albumin in solution: 
 
 (4) Caustic Potash and Copper Test. — Pour one or two drachms 
 of the urine into a test-tube, add a drop or two of a five-per-cent solu- 
 tion of cupric sulphate, and add some liquor potassas; an excess of the* 
 potash does not interfere with the reaction. A precipitate may fall, 
 but it will be dissolved on shaking the tube, and the liquid will 
 assume a violet color. Boil the solution; no precipitate falls, but the 
 violet color will become deeper. 
 
 (5) Xanthoptrotein Reaction. — Add to the sample of urine some 
 concentrated nitric acid, and boil. Let the liquid cool, and then add 
 some ammonia. If the solution contains albumin, an orange color 
 will be produced. 
 
 15 
 
226 ALBUMIN. 
 
 (G) Milfoil's Reaction. — Add to one drachm of urine (3.887 c.c.)ten 
 minims of Millon's reagent, and heat. If the sample contains albu- 
 min in considerable quantities, a white precipitate will fall which will 
 
 become red when heated. If only a trace of albumin be present, no 
 precipitate is formed, but the fluid becomes red. The red color is 
 produced at ordinary temperatures, but it is increased by heat. 
 
 Milfoil's Reagent is prepared by adding one drachm (3.887 
 grams) by weight of nitric acid (specific gravity 1.042) to one 
 drachm (3.887 grams) by weight of pure mercury. Dissolve the 
 mercury in the nitric acid at first without, and afterwards with gentle 
 warmth. Add to this solution twice its volume of distilled water; 
 let it stand for some hours, and decant the supernatant fluid from the 
 crystals that have formed at the bottom. Keep in a glass-stoppered 
 bottle. 
 
 <7) Heller's or the Nitric Acid Test.— Vouv one drachm (3.887 c.c.) 
 or a smaller quantity of nitric acid into a test-tube, then hold it 
 obliquely and drop the urine in from the bottle, or by the aid of a 
 medicine dropper or pipette, until an equal volume has been added 
 without agitation. The urine, being of less density, will naturally 
 float upon the top of the acid. At the line of junction of the two 
 liquids, all urinary samples will gi\e a brownish-color line which will 
 vary in intensity with the condition and amount of coloring matter 
 and nrea present. 
 
 This peculiar ring of color has been considered to be the result of 
 the action of the acid on the coloring matters of the urine. Others 
 hold that it is in some way influenced by the formation of the nitrate 
 of urea, or it may be due to this formation of urea with the property 
 under these circumstances of taking up the coloring matter, as is the 
 ■case with uric acid in urine. 
 
 The only objection to this last theory is that when the crystals of 
 nitrate of urea are formed in abundance at this border line, as occa- 
 sionally happens, they can be easily taken up by a pipette, mounted 
 upon a slide, and examined under the microscope. They are then 
 iouud to be devoid of all color, and are nothing but pure white crys- 
 tals. After they have all been removed by the pipette, or allowed to 
 fall to the bottom of the tube, the color band still remains. 
 
 By others, it is held that this color band is due to the deposition of 
 acid urates, and it is also asserted that it is due to the formation of 
 hydrated uric acid. If the color band fell to the bottom with these 
 crystalline and solid substances, these theories might hold; but this 
 change appears to be the result of the action of the nitric acid upon 
 the coloring matter. 
 
ALBUMIN. 
 
 227 
 
 When the color line is not very marked and no cloud forms, and 
 albumin is present, a decided, delicate, and perfectly vrhite band is 
 formed on the surface of the acid between the two solutions. If the 
 urine is high colored and loaded with urates, a trace of albumin may 
 be obscured by them, or it may lead to the belief that the whole band 
 is albumin, and that it may be indicative of large quantities. This diffi- 
 culty may be, in a measure, obviated by gently heating the solution, 
 when the urates will disappear and the white film of albumin become 
 somewhat more distinct. 
 
 Heller has advised the use of a somewhat larger dish, with slanting 
 edges, instead of the test-tube. The urine flowing out upon a larger 
 surface gives a more marked reaction. 
 
 Hoffman and Ultzmann have advised boiling the urine with an 
 equal bulk of officinal liquor potassa, and filtering. If still not quite 
 clear, add a few drops of the "magnesian fluid" (the magnesian fluid 
 is made by dissolving magnesium sulphate and pure ammonium chlo- 
 ride, each one part, in eight parts of distilled water and adding one part 
 of liquor ammonise), warm again, and filter. This test will detect very 
 ■small quantities of albumin. 
 
 (8) To get rid of the two troublesome bands, Dr. A. W. Abbott, of 
 Minneapolis, recommends the following plan: Pour a few drops of 
 urine gently down the inside of a glass vessel containing acidulated 
 water at the boiling point. If albumin be present, a more or less 
 delicate film will form just at the dividing line between the fluid tested 
 and the clear water. This test is said to detect one-twentieth of one 
 per cent. 
 
 (9) The following test has been found to work very well, and to 
 obviate most of the difficulties experienced with Heller's method ex- 
 cept as modified by Hoffman and Ultzmann: 
 
 Pour one drachm (3.887 cc.) of chemically pure nitric acid into a 
 clean test-tube, then carefully add one-half drachm (1.942 cc.) of dis- 
 tilled water. Both solutions will remain perfectly clear and separate 
 if carefully added, but a distinct line of separation between the two 
 will be easily appreciated on account of the difference in density be- 
 tween the two solutions. Next draw up a little of the urine to be 
 examined in a pipette and allow it to flow down the test-tube, which 
 is to be held erect and not inclined. The suspected solution passes 
 quickly through the water, which acts as a filter, and strikes against 
 the acid suddenly, when a pure white film or layer of coagulated 
 albumin will shoot across the surface of the acid to the opposite side. 
 The thickness of the precipitate will depend upon the amount of 
 albumin present. On account of the perfect transparency of the acid 
 
228 ALBUMIN. 
 
 and water, if the tube is held against a dark background, the faintest 
 film can be detected separating the two fluids. 
 
 If the urine be high-colored or loaded with urates, it should be 
 diluted until almost colorless. In this way the deep color line and the 
 cloud produced by the urates, when acted upon by the acid, that so 
 often obscures the albumin in Heller's test, is almost completely over- 
 come, and the albuminous precipitate remains sharply outlined. 
 
 This method is much more delicate than Heller's. Its exact deli- 
 cacy has not been determined. After Heller's and the heat and acid 
 tests fail to show evidence of albumin, the sample can be diluted 
 many times more, and a sharp reaction will follow its application. 
 
 This method is very simple, and if carefully followed is free from 
 error. The reason for the precipitate being so positive is the clear- 
 ness of the two solutions and the precipitation of all the forms of 
 albumin. 
 
 (10) Roberts' Acid Brine Test. — The principle of this test is the 
 same as when the acetic acid and sodium sulphate are used, a different 
 acid and salt being amployed. 
 
 A standard test solution is made by adding one ounce (31.103 c.c.) 
 of dilute hydrochloric acid (IT. S. P.) to fifteen ounces (460.552 c.c.) 
 of a saturated solution of sodium chloride. 
 
 This test is used in the same way as Heller's nitric acid. One 
 drachm (3.877 c.c.) of the brine is poured into a clean test-tube, and 
 the urine allowed to run slowly down the tube so as to prevent undue 
 agitation of the two fluids and an intermingling. If albumin be pres- 
 ent in the sample, a white film or layer of coagulated albumin will be 
 found, varying in thickness with the amount present in the sample. 
 
 The advantages ascribed to this test are: (a) As a rule no color line 
 is formed, and if any, it is slight; (b) that it can be carried with less 
 danger than nitric acid; (c) it does not stain the fingers; (d) it does 
 not precipitate the urates; (e) it consolidates all forms of albumin, 
 and the sugar test applied after its use is not interfered with. 
 
 On the other side, it can be said that it is no more delicate than 
 the heat and less so than the nitric acid tests. 
 
 (11) Picric Acid Test. — When this acid is added to normal urine, 
 the only change produced is a slight yellow tinge due to the color of 
 the acid, but no precipitate occurs, and the solution remains perfectly 
 transparent. A saturated aqueous or alcoholic solution may be used 
 as a standard test; the former is the one commonly recommended. It 
 may be employed as follows. Pour one drachm (3.877 c.c.) of the 
 standard solution into a test-tube, then add the urine in the same 
 
ALBUMIN. 229 
 
 manner employed in Heller's acid test; a precipitate will form be- 
 tween the two fluids if albumin be present. 
 
 As the picric acid has a lower specific gravity than most samples of 
 urine, it is better to pour the urine into the test-tube first, and then 
 add the acid. The same result, however, is obtained in either case. 
 
 If the urine is alkaline, the sample must first be strongly acidulated 
 with acetic acid. In fact, a little acid had better be added in all cases. 
 If the urine is turbid, it should be boiled with one-fourth its volume 
 of liquor potassae, and then strongly acidulated and tested as before. 
 
 This test gives the same kind of a precipitate with the salts of pot- 
 ash as with albumin. It also precipitates all forms of albumin as well 
 as serum-albumin. The application of heat will cause a disappearance 
 of the precipitate with some of the albumins and the potassium salts. 
 
 Taken as a whole, there is some uncertainty in relation to the id- 
 liability of this test. 
 
 (12) Tanret's or the Potassio-mercuric Iodide Test. — The test solu- 
 tion is made as follows: 
 
 Iodide of Potassium, . 49.68 grains 3.219 grams. 
 
 Bichloride of Mercury, 20.83 grains 1.349 grams. 
 
 Distilled water, a sufficient quantity to make 3.21 ounces 
 <99,843 o.c). 
 
 It is employed as follows: 
 
 (a) Boil the urine to be tested with liquor potassae, and filter. 
 
 (b) Acidulate the filtrate with citric or acetic acid; the former is 
 most strongly recommended. 
 
 (c) Add a few drops of this standard solution to the acidulated 
 urine. If only a trace of albumin be present, a slight turbidity is all 
 that can be detected. When the quantity of albumin is large, a de- 
 cided cloud results. If it is abundant, a very decided precipitate will 
 be produced. The cloud resembles that which occurs when the phos- 
 phates are thrown down by heat. If employed in the same manner 
 as the nitric acid test, the two solutions will be separated by a bluish 
 disk of albumin, varying in thickness according to the quantity con- 
 tained in the sample. 
 
 When only a small quantity is suspected, pour one drachm (3.877 
 c.c.) of the test solution into a test-tube, and add the urine drop by 
 drop until an equal volume has been added. A color disk will form 
 "between the two solutions that will be either bluish-white, bluish- 
 yellow, or bluish, depending upon the amount of albumin present. 
 This test, like most of the preceding, precipitates the peptones, 
 he alkaloids, the urates when abundant, and forms a cloud when 
 
230 ALBUMIN. 
 
 mucus is present. All, however, disappear when heat is applied. 
 This test requires time and some little skill in order to obviate all 
 the possible sources of error, consequently it cannot be considered as 
 practical for general use as the heat and nitric acid tests. 
 
 (13) Olivers or the Sodium Tungstate Test. — This substance, like 
 most of the other tests, is used after the manner of Heller's. 
 
 The standard test solution is made as follows: Prepare a saturated 
 solution of sodium tungstate, one part in tour of water, add a satu- 
 rated solution of citric acid, ten parts to six of water. Add together 
 equal quantities of the two, and it is ready for using. The urine or 
 the test solution may be poured into the test-tube first, followed by 
 the one remaining. It is a very sensitive test, and said to be free 
 from all objections. Further trial, however, may prove that it pre- 
 cipitates other substances, the same as the foregoing. 
 
 (14) Pavey's Test Pellets. — This test consists in using little pellets 
 instead of solutions. They are more easily carried. They are com- 
 posed of sodic ferrocyanide, and are acidulated with citric acid. One 
 of them is crushed and placed in the bottom of a test-tube, and a 
 little urine added, or the urine can be first poured into the test-tube, 
 and the powdered pellet dropped into the suspected solution. This 
 test will produce the precipitation of albumin without the applica- 
 tion of heat. 
 
 Oleo-resins act in the same manner. 
 
 (15) TeH Papers. — These have been recommended by Dr. Oliver, 
 of Harrowgate, on account of the ease of transportation and their 
 certainty of action. They are prepared as follows: Chemically inert 
 filter paper is soaked, either in double iodide of mercury, sodium 
 tungstate, or ferrocyanide of potassium, allowed to dry and then it is 
 cut into slips of suitable size. Papers charged with citric acid are 
 prepared in a similar manner. 
 
 If the urine be turbid, it should be boiled with liquor potassae and 
 filtered; if clear, this need not be done. In either case the acid papers 
 are added until a decided acid reaction is obtained. 
 
 Having accomplished this, one of the first-named test-papers is 
 held in the urine. If only a trace of albumin be present a cloud will 
 form around the test-paper, but if more abundant, a decided cloud 
 will be formed, and the coagulated albumin will fall gradually to 
 the bottom of the tube. 
 
 These papers are said to be very delicate, and to give evidence of 
 albumin when heat and nitric acid fail. 
 
 It appears as if bedside testing of urine has been very much overesti- 
 
ALUUMIN. 231 
 
 mated. For a complete chemical and microscopic analysis is abso- 
 lutely necessary, if anything like accuracy in diagnosis is essential. 
 
 (16) Carbolic Acid Test. — This acid has been recommended to be 
 used in the same manner as Heller's nitric acid test. But the sources 
 of error are numerous, which renders it impracticable. 
 
 The exact nicety of a number of these tests have been given by Dr. 
 G-. B. Fowler, of this cit} r , as follows: 
 
 Heat and acidulation, . . . .018 of one per cent. 
 Acidulated brine, . . . .018 
 
 Picric acid, 008 
 
 Nitric acid, .... .008 
 
 Potassium ferrocyanide and acetic acid, .008 " 
 Potassio-mercuric iodide, . . .004 " 
 
 In all cases the test-tube and its contents should be viewed by re- 
 flected light against a black background as suggested by Dr. John P. 
 Munn, of this city. 
 
 Instead of using an ordinary \ test-tube, take a conical test-glass 1 . 
 and fill it two-thirds full of the test solution to be used. Then 
 add the urine very carefully to the test solution in the glass, so that 
 it may flow out upon this broad surface and not mingle with it. In 
 this way a large precipitation is likely to be the result, and its pres- 
 ence is more easily detected. 
 
 The tests which experience has proved to be the most satisfactory 
 are the heat with acidulation by acetic or nitric acid, the nitric 
 acid alone, with an equal volume of water as recommended in the 
 text, the xanthoprotein reaction, and the acid brine test. 
 
 The acid brine and nitric acid tests are both very ready methods 
 for estimating the amount in a volumetric way. If, for instance, the 
 albuminous precipitate occupies one-half of the fluid above the acid 
 or the brine, it maybe said to indicate fifty per cent; if only one- 
 fourth, twenty-five per cent. As a comparative test from day to day, 
 this is quite a practical method, but in reference to the actual per- 
 centage of albumin contained in a given specimen, it is, like all the 
 other tests recommended, absolutely inaccurate. 
 
 The only method by which anything like accuracy can be obtained 
 in estimating the quantity is by the gravimetric method. This con- 
 sists in the precipitation of the albumin upon a weighed filter, and then 
 deducting the increase in the weight of the filter from the total weight of 
 the urine from which the albumin was precipitated. The only source of 
 error in this method that cannot easily be avoided is the precipitation 
 of a small amount of coloring-matter and the earthy phosphates along- 
 
232 ALBUMIN. 
 
 with the albumin. As most of the coloring matter and phosphates 
 are removed by thoroughly washing while on the filter, this error is 
 not sufficiently great to be considered. The method is of no practi- 
 cal value to the general practitioner from the fact that it requires a 
 large amount of delicate apparatus, and also takes considerable time 
 and skill to arrive at an accurate result. 
 
 There are a huge number of methods offered by different writers, 
 all of which appear to be too complicated and uncertain to be absolutely 
 practical. They will be named and the references given only. By 
 circunipolarization; the method of Bodeker; Vogel's optical method, 
 Lang, Ilaebler, and Bornhardt Menu's method, method of P. Liborius, 
 L. Girgensohn's method, W. Roberts' dilution method. 
 
 As the actual quantity lost is so small, the knowledge of the loss 
 being y,,^,-,, or T -J- - more or less, is of no practical value in relation to 
 the symptoms, prognosis, or treatment. The volumetric analysis in 
 the test-tube from day to day is certainly a very sure index of the 
 rise and fall in the quantity of albumin and gives all the information 
 required. 
 
 Clinical significance. — The first thing to decide is whether the 
 albuminuria is of the adventitious or intrinsic variety. This can be 
 accomplished by exclusion. If the albumin persists without any 
 further evidence of structural change in the kidneys it is reasonable 
 to suppose that it is of the adventitious form. The absence of serum- 
 albumin and the detection -of the peptones or some of the derived 
 albumins in abundance would confirm the diagnosis. 
 
 If, on the other hand, the serum-albumin predominates, with casts 
 and other evidences of a structural lesion of the kidneys, the albumin- 
 uria is of the intrinsic variety. 
 
 Prognosis. — This of necessity depends upon the kind of albuminuria. 
 In the adventitious, if its cause can be removed, the prognosis is good, 
 otherwise it may terminate in the intrinsic variety. 
 
 In inherent albuminuria, the prognosis also depends largely upon 
 the cause. In connection with the fevers, acute and chronic metallic 
 poisoning, and the acute renal lesions, recovery is possible and not in- 
 frequent, but in connection with chronic venous obstruction or in a 
 well-established renal lesion the prognosis is always bad. 
 
 Treatment. — This is exclusively confined to the removal of the 
 causes. In the adventitious variety, if due to the abstinence from 
 sodium chloride, it should be added to the diet; if due to imbibing too 
 much egg-albumen, the quantity taken should be diminished; if to a 
 faulty intestinal or hepatic digestion, this should be overcome. 
 
ALBUMIN. 233 
 
 The treatment of the intrinsic variety has boon covered in treating 
 -of the various renal lesions in which it occurs. 
 
 The adventitious variety will often disappear under the influence of 
 the bile pill and the nerve tonic composed, of nux vomica and damnum, 
 see pages 26 and. 89. The diet should always be of the albuminous 
 type and limited to those substances most easily and completely di- 
 gested and assimilated. 
 
CHAPTER IV. 
 GLUCOSE OR GRAPE SUGAR. TESTS FOR GLUCOSE. 
 
 Sugar. — Glucose is found iu the urine in the condition known as 
 glycosuria or diabetis mellitus. It also occurs as the result of poison- 
 ing by urari. carbonic oxide, with a sufficient dose of morphia 
 and amyl nitrite. It has also been met with in -disturbances of the 
 medulla or base of the brain, occasionally in health and sometimes 
 after surgical operations. A trace of glucose is said to be normally 
 present both in the blood and urine, but siuce the observations of 
 Prof. Satterthwaite, who found that both uric acid and kreatin caused 
 the same reaction with the glucose tests as sugar, it is quite possible 
 that this may not be true. 
 
 A large number of tests hare been suggested from time to time. 
 
 They are, first, Moore's or Heller's. — To one drachm (3.887 c.c.) of 
 urine add an equal quantity of caustic soda or potassa, and boil. If 
 glucose be present, the mixture will at first turn to a light jellow, then 
 to an amber color, and lastly to a dark orange-brown color. 
 PI This, however, is an uncertain test, as many other organic com- 
 pounds frequently found in the urine cause the same discoloration 
 under similar circumstances. 
 
 Second, Trommer's. — Take one drachm (3.877 c.c.) of urine and add 
 12 minims of a 12$ solution of cupric sulphate ( 3 i. to § i. 3.877 to 
 31.103 c.c.) so that a very slight green color is perceptible, then add 
 to the solution one and one-half drachms (5.831 c. c. ) of liquor potassae. 
 The previously formed precipitate of the hydrated copper oxide will 
 now be dissolved and the fluid will assume a rich blue tint. Now 
 gradually heat: before precipitation occurs, the fluid becomes opaque 
 and presents a yellowish-red color, but after boiling for a feAV seconds 
 an abundant precipitate of cuprous oxide is deposited ; if sugar be 
 present, the precipitate is of a brick-red color. 
 
 The same reaction will take place without the application of heat 
 and is then called Cappezzuole's test. In this way the reaction does not 
 occur for half an hour or more. 
 
 If Trommer's test is employed in the way above described, it will be 
 
GLUCOSE OR GRAPE SUGAR. 235 
 
 found one of the most accurate, if not the most certain method for 
 detecting the presence of the glucose. It has been stated that this 
 would not reveal the presence of sugar in albuminous solutions, but 
 
 this has been found to be erroneous. 
 
 The following experiments performed by Prof. Satterthwaite, and 
 which, never having been published, are, by his permission, given 
 in detail, are interesting in showing the accuracy of this test, pro- 
 vided the above stipulated quantities be used as recommended by 
 him. 
 
 Experiment 1. — With reference to copper test for sugar in albumi- 
 nous solution. Took a 5$ serum-albumin solution to start with. 20 
 Tit (1.295 c.c.) of this 5$ solution were poured into a test-tube, and 
 2 TTL (0.129 c.c.) of a glucose solution added, then 4 minims (0.291 
 c.c.) of a 12$ sulphate of copper solution ( 3 i. to § i.) and 30 minims 
 (1.943 c.c.) of liquor potassae added and boiled. At first the reaction 
 was doubtful, the fluid turning greenish, then yellow by direct light, 
 but at the end of five minutes the reaction was good. 
 
 With such a large percentage of albumin, the fluid is apt to gela- 
 tinize and become practically solid upon boiling. 
 
 Experiment 2. — This was the same as Exp. 1, except that a 2^$ solu- 
 tion of albumin was used instead of the 5$. The reaction in this 
 case was immediately sharp and satisfactory. 
 
 Experiment 3. — Trommer's test was applied to a simple aqueous 
 solution, which contained only one grain of glucose to the ounce. ^To 
 20 minims (1.295 c.c.) of the dilute solution 4 minims (0.291 c.c.) of 
 a 12$ copper solution, and 30 minims (1.943 c.c.) of liquor potassaa 
 were added and boiled, and it gave a clear brick-red color with 
 a slight deposit. 
 
 Experiment 4. — Took 20 minims (1.295 c.c.) of a saturated solution 
 of uric acid, 4 minims (0.259 c.c.) 12$ of the copper solution, and 
 30 minims of liquor potassae. The brick-red copper deposit was thrown 
 down after boiling the solution for ten minutes. 
 
 Experiment 5. — Took 20 minims (1.295 c.c.) saturated solution of 
 kreatin, 4 minims (0.295 c.c.) of the 12$ copper solution, and 30 
 minims (1.913 c.c.) of liquor potassas. The deposit of reduced cop- 
 per was not thrown down until the solution had been boiled for seven 
 minutes, and then it was reddish-green. 
 
 Experiment 6. — Took 20 minims (1.295 c.c.) of a saturated solution 
 of tannic acid, 4 minims of the 12$ copper solution, and 30 
 minims (1.943 c.c.) of liquor potassas. A reddish deposit was thrown 
 down, the color being a sealing-wax red. 
 
 Experiment 7. — To a 5$ solution of serum-albumin one grain (0.064 
 
236 GLUCOSE OR GRAPE SUGAR. 
 
 c.c.) of glucose to the ounce (31.103 c.c.) was added. Took 20 
 minims t 1.295 c.c.) of this saccharated and highly albuminous fluid, 
 and added 4 minims (0.295 c.c.) of the 12^' solution of copper, 
 and 30 minims (1.943 c.c.) of liquor potass», and boiled. The char- 
 acteristic color reaction of Trommer's test occurred, but no precipitate 
 fell. 
 
 Experiment 8.— Took 20 minims (1.295 c.c.) of the same saccha- 
 rated albuminous fluid and applied Fehling's test. Reaction ob- 
 tained, but less perfectly than by the use of Trommer's. 
 
 Experiment 9. — Took 20 minims (1.295 c.c.) of a saturated solution 
 of hippuric acid, 4 minims (0.259 c.c.) of the 12$ copper solution, 
 and 30 minims (1.943 c.c.) of liquor potassaj. No reduction of 
 copper was produced. 
 
 Dr. Samuel Lloyd has noticed, 1 iu a series of examinations of dia- 
 betic urine by Trommer's test, that when no precipitate had occurred 
 during the boiling, a flocculent white deposit took place during the 
 cooling if the specimen contained little sugar, but an excess of the 
 urates and phosphates. This led him to make a number of experi- 
 ments to determine the accuracy of the test. Specimens containing 
 urates, phosphates, and sugar only were each submitted to the test 
 according to the usual method, a small quantity of the urine being 
 poured into a test-tube, and then a drop or tw r o of the sulphate of 
 copper solution and excess of the soda or potash solution. The result 
 was the same with the specimens containing the phosphates and the 
 urates, but with the sugar solution the characteristic color was ob- 
 served. Solutions were then prepared which contained large quanti- 
 ties of the other two iugredients, but very little sugar, and it was then 
 found that the color imparted to the supernatant fluid by this one 
 substance was sufficient to serve to color the entire precipitate, and 
 thus lead to the erroneous conclusion that the whole heavy deposit 
 was suboxide of copper, due to the presence of sugar, and that the 
 patient must necessarily be w r ell advanced in the disease. He had 
 finally concluded that, if this test was used, the phosphates should 
 first be precipitated by heat, and the urates neutralized by adding the 
 soda before the copper. 
 
 From this it would appear that if Trommer's test is used in the above 
 proportions, it still holds the first place for detecting sugar in the 
 urine. The difficulty heretofore experienced with it appears to have 
 come from no definite quantities having been laid down as the stand- 
 ard to work with. 
 
 1 New York Medical Journal, March 14th, 1885, p. 313. 
 
GLUCOSE OK GRAPE SUGAK. 231 
 
 The other substances which occur in the urine and are capable of 
 reducing the copper require several minutes' boiling to effect this re- 
 duction, but with glucose it is almost instantaneous, and in this w;iy 
 it can be distinguished. 
 
 Third, Fehling's Test. — This has heretofore been said to be a more 
 delicate copper test than that of Trommer. A number of formulae 
 and modifications have been advanced. First: 
 
 Pure crystallized sulphate of copper, . 500 grains. 
 
 Neutral tartrate of potassium, . . 2,000 " 
 A solution of caustic soda of a specific 
 
 gravity 1.12, 8,750 " 
 
 The neutral tartrate of potassium, dissolved in a little water, is first 
 mixed with a solution of caustic soda. Then the sulphate of copper 
 dissolved in about 4-J fluid ounces of water, is gradually added to the 
 alkaline liquor, which assumes a deep blue color. The whole is 
 diluted with water to the volume of 31f fluid ounces. About \ of a 
 fluidrachm of Fehling's liquor is exactly decolorized by .077 of a 
 grain of glucose. One drop of Fehling's solution will detect about 
 yoVy-g- of a grain of glucose dissolved in about \ ounce of water. 
 
 Second. It is made as follows: 
 
 Take Pure crystallized sulphate of copper, . 40 grams. 
 
 Neutral potassium tartrate, . . 160 " 
 A solution of sodium hydrate, specific 
 
 gravity 1.12, 650 " 
 
 The further preparation is the same as the above, only using 160 
 cubic centimetres in place of 4^ ounces of water, and diluting to 
 1154.4 cubic centimetres instead of 31f ounces. One cubic centi- 
 metre of this solution is exactly decolorized by ¥ i_ of a gram of glucose. 
 
 Third. Pavey's solution is made as follows: 
 
 Cupric sulphate, 320 grains. 
 
 Neutral potassic tartrate, . . . 640 <e 
 
 Caustic potash, ..... 1,280 " 
 
 Distilled water, . . -. \ -. 20 fl. oz. 
 
 The solution is made in the same manner as Fehling's, and 100 
 minims correspond to -§- grain of grape sugar, the formula for grape 
 sugar being here taken C 6 H 14 7 , while by Fehling it is taken C 6 H ]2 6 .. 
 
238 GLUCOSE OB GRAPE SUGAB. 
 
 Fourth. A modification and method described by Prof. Austin 
 Flint. Jr.. is as follows: 
 
 "Make a solution in the proportion of 370 graius of neutral tar- 
 trate of potash to a fluidounce of distilled water, and keep for use. 
 
 " Make a solution in the proportion of 95 grains of sulphate of 
 copper to a fluidounce of distilled water, and keep for use. 
 
 •• Make a solution of caustic soda in distilled water, of a specific 
 gravity of 1.12 or 164 Baume, and keep for use. 
 
 "Take half a flui drachm of the solution of copper, add half a 
 drachm of the solution of tartrate of potash, add of the solution of 
 caustic soda sufficient to make three fluidrachms. Boil the test 
 liquid, and when it is hot, add the urine drop by drop. If sugar be 
 present, the addition of a few drops of urine will produce suddenly an 
 opaque yellowish-red precipitate. If a volume of urine be added, 
 drop by drop, equal to the volume of the test, and the mixture be 
 brought to the boiling point and then allowed to cool without any 
 precipitate, it is absolutely certain that there is no sugar." 
 
 Fifth. — A former student and clinical assistant, Dr. John E. 
 Bailey, still further modified Fehling's and Prof. Flint's methods. 
 His also is composed of the three solutions, but instead of taking equal 
 quantities of the copper and neutral tartrate solution and double the 
 quantity of the third or soda solution, an equal quantity of each is 
 taken, which is more easily remembered. The solutions are desig- 
 nated 1, 2, and 3 in the order in which they are to be added, and are 
 made as follows: 
 
 Solution I. 
 
 Cupric sulphate, . 47.43 grains, 3.073 grams. 
 
 Distilled water, . . 1 fluidounce, 31.103 c.c. 
 
 Solution II. 
 
 Neutral tartrate of soda, 236.88 grains, 15.349 grams. 
 Distilled water, . 1 fluidounce, 31.103 c.c. 
 
 Solution III. 
 
 Caustic soda, . . 80.65 grains, 5. 22G grams. 
 Distilled water, . . . 1 fluidounce, 31.103 c.c. 
 
 All three solutions should be carefully filtered. It is very essential 
 in all cases to get a pure neutral tartrate salt, otherwise the test may 
 fail. In using this test, equal quantities of the three solutions are 
 
GLUCOSE OR GKAPE 8CTG-AE. 239 
 
 turned into a test-tube in their numerical order; by 80 doing no tem- 
 porary precipitation occurs. The union of these three solutions 
 develops a rich blue color. The further application of the test is the 
 same as recommended for Prof. Flint's. 
 
 The use of the neutral tartrate of soda is preferred to the potash salt, 
 experience having taught that it is less likely to fail in albuminous 
 solutions. One hundred (100) minims of this solution are exactly de- 
 colorized by one-half a grain of glucose in an aqueous solution, glucose 
 being taken at C H ]2 O . 
 
 This solution has been in use in the laboratory of the New York 
 Post-Graduate Medical School and Hospital for a number of years, 
 and it has never been known to fail. 
 
 The advantages claimed for Drs. Flint's and Bailey's methods are 
 that the three are kept in separate vials and do not decompose with 
 age, which is often the case with Fehling's. Consequently they are 
 always ready for use, and as diabetic cases are not of every-day occur- 
 rence, Fehling's solution is frequently found decomposed when it is 
 most needed. 
 
 Sixth. Dr. E. R. Squibb, of Brooklyn, has still further modified the 
 test by having only two solutions. Any two of the solutions together 
 will, after a time, decompose and render the test uncertain. The only 
 advantage claimed for Squibb's method is two bottles instead of three. 
 
 The three-bottle method is preferred. 
 
 Seventh. Dr. H. G. Piffard's Cupro-Potassic Paste: 
 
 Take of: Sulphate of copper (chemically pure), . . 1 part. 
 
 Crystalized tartrate of sodium or potassium (C.P.), 5 parts. 
 Sodic hydrate (chemically pure), . . 2 " 
 
 Mix thoroughly in a mortar. 
 
 The result will be a pasty mass, which can be transferred to a wide- 
 mouthed bottle and kept till wanted. To use it, take of the mass a 
 piece about the size of a small pea, put it in a test-tube and add about 
 two fluidrachms (7.775 c.c.) of water; boil until the mass is dissolved, 
 and the solution has a uniform, pale, and rather dirty-blue color; 
 then add two or three drops of the suspected urine, and boil again for 
 a moment. If sugar be present, the usual reaction will be manifest. 
 
 Eighth. Boettger's bismuth test consists in the action of sugar as a 
 reducing agent on bismuth. 
 
 First method. — 1. Solution of crystallized carbonate of soda; 
 strength, one part to three of distilled water. 
 
 2. Ordinary subnitrate of bismuth. Pour one drachm (3.887 c.c.) 
 of the suspected urine into a test-tube, then one drachm (3.887 c.c.) 
 
840 GLUCOSE OR GRAPE SUGAR. 
 
 of the carbonate of soda solution, and add from one to five grains of 
 bismuth. Boil the mixture, and if sugar be present, the solution will 
 first become gray and then black from the deposit of metallic bis- 
 muth. 
 
 Second method. — Pour into a test-tube one drachm (3.S87 c.c.) of 
 urine and one drachm (3.887 c.c.) of liquor potasses or soda, then add 
 from one to five grains of ordinary subnitrate of bismuth, shake and 
 boil for two minutes; first the play of colors, as in Moore's test, will 
 be observed, then a gray, and finally a black precipitate of metallic 
 bismuth will be developed. 
 
 Third method or Lowe's test. — It is almost identical with the pre- 
 ceding, the only difference being the addition of a little glycerin and 
 the use of soda instead of potash. The result is the same. 
 
 All these tests are open to objections, the bismuth being reduced in 
 like manner by sulphur, albumin, or any substance containing sulphur. 
 As albumin and sugar are frequently associated in the same sample, 
 it is only confirmatory in connection with other tests. 
 
 Silver, chromium, uranium, and tin are in a similar manner reduced 
 by the presence of sugar. 
 
 Ninth. Maumene's tin test. — To apply this test, pieces of merino or 
 any other woollen fabric are soaked in a solution of bichloride of tin, 
 and carefully dried. On wetting a piece of this cloth in the suspected 
 sample of urine, and then holding it over a spirit lamp or before the 
 fire until it becomes hot, a deep brown or black spot will appear if 
 sugar be p resent. 
 
 Tenth. Briicke's modification of the bismuth test.— Professor Briicke 
 recommends that urine containing any sulphur compound be faintly 
 acidulated with hydrochloric acid and then heated with Frohn's re- 
 agent. The reagent is made as follows: Take 23.94 grains (1.5 
 grams) of basic nitrate of bismuth, and heat to the boiling point 
 with 308.64: minims (20 grams) of water; then add 107 grains (7 
 grams) of potassium iodide, and 20 minims of lrvdrochloric acid. This 
 reagent is orange-red in color. 
 
 This solution completely removes the sulphur, but does not affect 
 the glucose. It is then filtered and the filtrate boiled for five minutes 
 with an excess of a concentrated solution of caustic potash; if a gray 
 or black color, or a blackish precipitate, is formed, the presence of 
 sugar is proved beyond a doubt. 
 
 The test, although quite accurate, is by far too complicated for a 
 ready and practical every-day test. It may occasionally be found of 
 service as confirmation proof in doubtful cases. 
 
 Eleventh. Mulder's Test. — Heat to boiling the suspected urine, which 
 
GLUCOSE OK GRAPE , 8UGAB. 241 
 
 should be colorless, or nearly so, with a solution of indigo-carmine 
 
 which has previously been rendered alkaline by sodium carbonate, and 
 a change of color is the result. It at first is blue, then green, then 
 purple, and if a large quantity of sugar be present, red, and finally 
 yellow. If this solution, while hot, is shaken so as to allow an admix- 
 ture with the oxygen of the air, the play of colors will be reversed and 
 returns to blue; but after standing, the yellow color reappears. 
 When the amount of sugar is very small, the indigo-carmine becomes 
 pale-blue only. 
 
 This test is said to detect very minute quantities of glucose. 
 
 Twelfth. Fermentation test consists in the splitting up of glucose 
 into carbon dioxide (C0 2 ) and alcohol (C 2 H O). It can be applied by 
 placing some of the suspected urine in a receptacle with a little brew- 
 er's yeast. This can be easily applied by taking two bottles, the first 
 of which shall contain the suspected fluid, together with a little brew- 
 er's yeast, and closed by a perforated cork conveying a bent glass-tube 
 which is longest in the arm not inserted into the cork. The second 
 bottle should contain lime-water and the long or external arm of the 
 glass-tube should be placed so that its mouth is immersed under the 
 fluid in bottle No. 2. Carbon dioxide (CO,) will, after a time, be 
 generated and driven off through the tube, and if allowed to discharge 
 into a solution of lime-water a white precipitate of the carbonate of 
 lime will be thrown down. This will establish the presence of sugar 
 beyond doubt, but this is not a very ready and practical test, as it 
 takes about twelve hours for fermentation to be accomplished. 
 
 Thirteenth. Polarization. — This test consists in the fact that glu- 
 cose rotates the plane of the polariscope to the right, 56. + or 57.6. 
 
 Fourteenth. Caustic Potash in Alcohol. — By adding caustic potash 
 in alcohol to a saturated solution, a precipitate of white flakes will be 
 thrown down. 
 
 Fifteenth. Quicklime Test. — An excess of quicklime added to 
 saccharated urine will cause a precipitate which, when treated with 
 alcohol, forms a white mass. 
 
 Sixteenth. Silver Test. — Add a weak solution of ammoniated 
 nitrate of silver to the urine, and boil for a time; if sugar be present, 
 metallic silver will be deposited, forming a mirror. 
 
 Seventeenth. Heinzinga Test. — Add to urine hydrate of potassium, 
 and then a few drops of molybdate or tungstate of ammonium, heat 
 to boiling, then acidulate carefully with hydrochloric acid, there will 
 result, if sugar be present, a blue color. 
 
 Among the older methods may be mentioned: 
 
 Eighteenth. The first method or that of Dr. Cruikshanks. It 
 16 
 
242 GLUCOSE OK GRAPE SUGAR. 
 
 consisted in the addition of nitric acid to urine, which converted the 
 sugar into oxalic acid, throwing it down in crystals. Next came: 
 
 Nineteenth. minefield's Test. — This test depended upon the re- 
 ducing power of glucose upon chromium; a strong solution of chromic 
 acid being taken as the standard. 
 
 Twentieth. Range's Test. — A small quantity of urine is evaporated 
 upon a white surface, and while warm a few drops of dilute sulphuric 
 acid arc dropped upon the residue. Normal urine will give a pale- 
 orange color; but if sugar be present, a deep brown and ultimately 
 black, owing to the decomposition of the sugar and a deposition of 
 carbon. This test is capable of detecting one part in one thousand. 
 
 By almost any of the above enumerated tests, the examiner with a 
 moderate amount of skill can detect the presence of glucose in the 
 urine whenever it exists in sufficient quantity to be of any practical 
 importance. But the tests which are the most practical and freest 
 from error in the hands of all are the modification of Fehling's as 
 arranged by Dr. Bailey, and Trommer's, both of which are strongly 
 recommended as standard test solutions for detecting glucose in urine, 
 as they have all the advantages and none of the disadvantages of the 
 other methods. 
 
 The Trommer's to be used in the proportions already given, and 
 not in the indefinite way in which it is often recommended. 
 
 Quantitive Analysis of Urine for Glucose. — It has generally been 
 spoken of, as absolutely necessary to determine positively the change 
 in quantity of the amount of sugar excreted daily by a diabetic patient. 
 Much has been written in regard to determining the amount of sugar 
 excreted, but as yet no practical necessity has been demonstrated for 
 such precision. 
 
 An exact determination of the daily quantity of urine voided and 
 the relative change and comparison of the specific gravity will yield a 
 very good result in reference to the change in the amount of glucose 
 excreted from day to day. Although from a chemical point of view 
 it has been spoken of as the older and crude method; clinically and 
 practically, if the quantity and specific gravity be correctly taken, it 
 yields about as reliable information as any of the methods yet intro- 
 duced. This method has been the most popular with the general 
 practitioner; for up to the present time no more ready, easily manip- 
 ulated, and practical method has been discovered. 
 
 Numerous methods have been advanced, but all, with the exception 
 of Roberts' fermentation test, have been too complicated to be practical, 
 or have depended upon a decolorization of solutions or variations in 
 shades of colors, and estimates based upon these changes. The fallacy 
 
GLUCOSE OE GRAPE SUGAR. 243 
 
 of any qualitative test based upon change or changesin color is 
 apparent, for the reason that few are endowed with the special faculty 
 of accurately distinguishing shades in color, and especially, rapid and 
 delicate transitions in these colors. Again, as these tests are applied 
 to a few minims only of the suspected sample, a wrong judgment in 
 reference to the color must lead to a great error when the computation 
 is made and applied to the large quantity of urine voided daily. In 
 a few minims the fractional error would be small perhaps in the hands 
 of an expert, but in relation to a large quantity the result must be far 
 from accurate. In fact, no two persons are apt to agree in reference 
 to delicate shades or, to say the least, there is often a difference of 
 opinion. In one instance, when several physicians were trying Feh- 
 ling's decolorization test, they could not agree, some claiming complete 
 decolorization, others the reverse. After allowing the test to stand 
 for a few minutes, however, the blue color became apparent to all, 
 which clearly showed an error in judgment on the part of one of the 
 parties. 
 
 A variation of from five to six hundred grains (32.399 to 38.879 
 grams) per day by different examiners, all estimating the quantity 
 from the same sample by Fehling's method, has frequently been ob- 
 served. 
 
 With still more delicate shades of color as evidence of different per- 
 centages, the chance for error must necessarily be very great. 
 
 In quantitative analysis in chemistry, unless it is absolutely accurate, 
 it is considered valueless. The same ought to hold true in practical 
 medicine. 
 
 It is undoubtedly quite possible for an expert with all the labora- 
 tory conveniences and repeated practice to obtain very close results 
 with any one of the methods advocated, but it cannot be expected 
 from the general examiner, and the sooner this view is adopted the 
 better. 
 
 Eoberts' fermentation test is based upon the fact that diabetic urine 
 loses density by fermentation. 
 
 The test is employed as follows: Take four ounces (124.413 c.c.) of 
 the urine to be examined, and pour it into a twelve-ounce bottle and 
 add a lump of German yeast as large as a walnut. A little more or 
 less does not appear to materially alter the result. The bottle is then 
 corked with a perforated stopper to permit of the free escape of the 
 carbon dioxide (COJ, and set aside in a moderately warm and uniform 
 temperature. An equal quantity of the sample is kept in a tightly- 
 corked bottle for a comparison of specific gravity. At the end of 
 twenty-four hours, or forty-eight at the outside, fermentation will be 
 
'24:4 GLUCOSE OE GRAPE SUGAR. 
 
 completed, and the density found to have fallen. Every degree of 
 loss is said to be equal to one grain of sugar to the ounce. By multi- 
 plying the number of degrees lost, or the number of grains per ounce, 
 by the factor .0.23, the percentage is calculated. 
 
 Provided this test was absolutely accurate, it would be a very good 
 one, and the only objection then that could be raised against it would 
 be the time needful to obtain the result. 
 
 In experimenting with this test in solutions of known strength, the 
 discrepancy has often been very great; in one instance as large an 
 error as seventeen per cent was the result, and an accurate analysis 
 was never secured. 
 
 Since experimenting with the test, it has been found that an accu- 
 rate result may be obtained provided the quantity of yeast used is 
 rightly judged, and the fermentation ke}3t at an even temperature, 
 and the urinometers used are very accurate, but experience has led 
 to the belief that it is not certain and accurate under ordinary cir- 
 cumstances. 
 
 With this, as in all quantitative tests, applied to the urine, a posi- 
 tive knowledge is required not only of the changes in the urine, but 
 of the quantity of sugar-producing elements ingested daily. 
 
 The old method, therefore, of measuring the quantity passed daily 
 and observing the changes in specific gravity yields about the same 
 results, and certainly is far more practical. 
 
 The quantitative and qualitative test for glucose as given by Max 
 Enhorn J is as follows. His article is quoted in full. 
 
 "Now, inasmuch as fermentation is not only the most exact, but 
 also the only test for sugar in the urine, the desire of bringing it more 
 into practical use seems to be justifiable. The object of this paper 
 will be to simplify, as much as possible, the method of making the 
 test, and to increase the value of it by enabling us to ascertain at the 
 same time the approximate quantity of sugar. 
 
 "Before proceeding with the proposed theme, I will give a literal 
 translation of the method of carrying out the fermentation test, as it 
 appeared in my original article: 2 
 
 "The test apparatus for this purpose is a fermentation-tube, and 
 the most convenient form is that which is described by Salkowski and 
 Leube. 3 It is made of glass, and consists essentially of four parts: (a) 
 a spherical reservoir, open at both emls; (b) a cylindrical tube, closed 
 at its upper end; (c) a somewhat narrower tube, bent so as to connect 
 
 t 
 
 1 New York Medical Record, January 22d, 1887, p. 91. 
 
 J Virch. Arch., Bd. 102, p. 268-270. 
 
 3 Salkowski and Leube: " Die Lehre vom Harn," p. 223. 
 
(JLIHJOSK OK GKRAPE SUGAR. 245 
 
 (a) and (b); (d) astand to support the other parts. A small piece (one 
 gram) of fresh commercial compressed yeast is thoroughly shaken in 
 a test-tube with about ten cubic centimetres of the fluid to be exam- 
 ined, and the spherical reservoir is filled with the resulting mixture. 
 By inclining the apparatus, the mixture easily finds its way through 
 the connecting-tube into the cylinder, completely driving out and re- 
 placing the contained air. Owing to the atmospheric pressure exerted 
 on the reservoir end of the connecting-tube, the fluid does not flow 
 back, but remains in the cylinder and tube. A little mercury is now 
 poured into the reservoir; it sinks into the connecting-tube, forcing 
 the fluid which was in the latter back into the reservoir. The cylin- 
 der is now filled with the fluid to be tested, and is shut off from the 
 air by means of the mercury, it is evident that if alcohol fermenta- 
 tion sets in, carbonic acid gas will be evolved, and, displacing the 
 fluid in the upper part of the cylinder, will force it back into the 
 reservoir. The apparatus is left undisturbed at a temperature of about 
 30 to 33° 0. (86 to 92° P.) for twenty to twenty-four hours. The 
 changed level of the fluid in the cylinder shows that the reaction has 
 taken place. The upper part of the cylinder is filled with carbonic 
 acid gas. To carry out the test as suggested by Salkowski-Leube, 
 three of these fermentation-tubes are necessary. Of these, A l is filled 
 with the mixture of yeast and normal urine, free from sugar; B with 
 the mixture of yeast and the suspected fluid, and C with a mixture of 
 yeast and a urine to which sugar has been added artificially. (C is 
 used simply to test the efficacy of the yeast.) Now, should the fluid 
 have been forced out of the upper part of the cylindrical tube B, and 
 its place taken by gas, while in A there is only a small bubble at the 
 summit of the tube, then B contains sugar. If this is not the case, 
 i. e., if B contains merely a gas bubble similar to the one in A, while 
 C, on the other hand, is partly filled with gas, then, obviously, B 
 contains no sugar. 
 
 "Being familiar with this method of carrying out the fermentation 
 test, let us examine the first point of our theme, which has for its 
 object the simplification of the method. In the above description it 
 was said that, after having filled the fermentation-tube with urine and 
 yeast, mercury must be added — in this way the cylindrical part of the 
 tube is separated from the reservoir and the air. Moreover, the test 
 is made at a temperature of 30 to 33° C, because this degree of heat 
 affords the best conditions for fermentation. The necessity of a 
 defined temperature and the addition of mercury are two conditions 
 
 1 The letters A, B, C, etc., signify the fermentation-tubes filled with the 
 different fluids to be examined. 
 
246 (il.Kc-i: OK (JKAl'K SUGAR. 
 
 which, though they may he easily carried out in a labarotory, cause, 
 
 nevertheless, some difficulties to a practical physician. Accordingly 
 I considered the following two questions: 1. Js the defined tempera- 
 ture (30 to 33° C). which is the most applicable for the fermentation 
 process, absolutely necessary., i. e., would not the ordinary tempera- 
 ture of the room give us a result sufficiently accurate? 2. Is a separa- 
 tion of the urine from the air absolutely necessary, and if so, can we 
 not separate them by something more convenient than mercury? 
 
 "In order to ascertain whether the ordinary temperature of the 
 room would be suitable for the test, I made the following two experi- 
 ments: 
 
 " Fermentation test at the ordinary temperature of the room. — 1. 
 April 23d, 1886: A, urine, acid, 1.034, sugar; B, urine, acid, 1.(20, 
 sugar; 0, urine, acid, 1.022, no sugar. After two hours: A, the 
 cylindrical part of the tube empty; B, nine-tenths of the cylinder 
 empty; C, a very small bubble at the summit of the tube. April 
 24th, 188G: A, no fluid in the cylinder; B, fluid to the depth of about 
 two lines in the cylinder; C, three small bubbles on the top of the 
 tube. 
 
 "2, May 8th, 1886: A, urine, acid, 1.022, sugar: B, urine, acid, 
 1.024, sugar: C, urine, acid, 1.034, sugar; D, urine, acid, 1.010, no 
 sugar; E, urine, acid. 1.020, no sugar; F, urine, acid, 1.024, no sugar. 
 After one hour the sugar reaction in A, B, and (' is very apparent. 
 May 9th, 1886: A, seven-eighths of the cylinder empty; B, three- 
 eighths of the cylinder empty; C, eight-ninths of the cylinder empty; 
 D, E, and P, a small bubble on the top of the cylinder. 
 
 " Both experiments clearly show that the alcoholic fermentation 
 takes place even at the ordinary temperature of the room, and thus 
 demonstrates, by the large amount of gas, the sugar reaction. Fur- 
 ther, Ave see here also in the urines not containing sugar a small 
 bubble at the summit of the tube, but this bubble is smaller than that 
 produced at 92° F. 
 
 "In a word, the fermentation test can be used in the ordinary tem- 
 perature of the room. 1 
 
 "To determine the second question, whether a separation of the 
 test-fluid by mercury or another substance (as oil) is absolutely neces- 
 sary or not, the following experiment was made: 
 
 "May 9th, 1886. — A, diabetic urine, acid, 1.034, plus mercury; B, 
 diabetic urine, acid, 1.034. plus oil; C, diabetic urine, acid, 1.034, 
 without mercury and without oil; D, normal urine, acid, 1.018, plus 
 
 1 I have made Hip fermentation test during summer and winter in my room; 
 the temperature varied from 6o to 85° F. 
 
GKLT/COSK OE GHBA.PE 8UGAE. 247 
 
 mercury; E, normal urine, acid, 1.018, plus oil; F, normal urine, acid, 
 1.018, without mercury and without oil. After one hour: A, B, and 
 C, plain sugar reaction. May 10th, 1880.— A, B, and C, the whole 
 cylinder empty; D, E, and F, a bubble on the top of the cylinder. 
 
 "Thus it clearly appears that the addition of mercury or oil has no 
 influence on the reaction. 
 
 " The above-mentioned experiments showed that the ferme7itation 
 test could be used at the ordinary temperature of the room and with- 
 out any addition of mercury or oil, but still it was a question whether 
 the minuteness of the reaction had not been lessened in a high degree 
 by this simplification. 
 
 "Starting from this point of view, I took specimens of the urine of 
 twelve healthy people, and made with them all the fermentation test; 
 to one of these specimens I added a little of a grape-sugar solution, so 
 that the urine contained one-tenth per cent of sugar; then this urine 
 was also examined by the fermentation test: 
 
 "June 4th, 1886. — A, urine, acid, 1.020, no sugar; B, urine, acid, 
 1.016, no sugar; C, urine, acid, 1.024, no sugar; D, urine, acid, 1.022, 
 no sugar; E, urine, acid, 1.020, no sugar; F, urine, acid, 1.024, no 
 sugar; G, urine, acid, 1.022, no sugar; H, urine, acid, 1.026, no 
 sugar; I, urine, acid, 1.026, no sugar; K, urine, acid, 1.026, no sugar; 
 L, urine, acid, 1.025, no sugar; M, urine, acid, 1.018, no sugar; N= 
 urine I, 10 c.c. mingled with 0.2 c.c. of a five-per-cent grape-sugar 
 solution, therefore the urine N had one-tenth per cent of sugar (here 
 the sugar could not be detected by Fehling's test). June oth, 1886. — 
 A, B, C, D, E, H, I, L, and M, a small bubble (0 0); F, = 0; G and 
 K=0; 1ST, = one-tenth c.c, empty. 
 
 "Thus we see by this experiment that the amount of gas at N (i. e., 
 in urine containing one-tenth per cent of sugar) was much larger than 
 in the other twelve normal specimens, and that it was in this way 
 possible to recognize with accuracy the presence of sugar. 
 
 " I intentionally took this large number of specimens of normal 
 urine, because the size of the gas-bubble in normal urine varies in a 
 certain degree, 1 and. I thus learned that the quantity of gas produced 
 in the cylinder by urine containing one-tenth per cent of sugar is 
 much larger than the largest gas-bubble in urine not containing sugar. 
 Therefore it is evident that the delicacy of the fermentation test is not 
 much lessened by the simplification; for even in a temperature of 92° 
 F., and with mercury, we are able to discover the presence of only 
 one-tenth per cent of sugar in a urine that has not been boiled. 
 
 1 These variations usually depend upon the degree of concentration of the 
 urine by salts, as the bubble becomes larger in more concentrated urine. 
 
248 GLUCOSE OB GRAPE SUGAR. 
 
 •• As to the time elapsing before the beginning of the fermentation, 
 I could recognize the arising of the first gas-bubbles after fifteen t<> 
 twenty-live minutes. Thus urine containing not too small an amount 
 of sugar will show the reaction even at that early time. 
 
 "As regards the number of the fermentation-tubes necessary for a 
 test, it is sufficient to take two (instead of the three above mentioned): 
 one (A) with normal urine, the other (B) with the suspected urine. 
 Whether the yeast is good or not we can see by the developed bubble 
 in A; for if the yeast be bad, no bubble will be in A: and should the 
 yeast contain sugar, then we should see in A a large displacement by 
 gas. 
 
 "All experiments I shall quote hereafter have been made in the 
 ordinary temperature of the room and without the addition of mer- 
 cury. I mention here this fact in order to avoid repetitions. 
 
 "I shall now take up the second part of my theme, namely, how 
 to ascertain the quantity of sugar by my fermentation test. 
 
 "Two methods of ascertainiug the quantity of sugar by fermenta- 
 tion have been used. One, called ' chemical/ consists in weighing a 
 definite quantity of urine before and after fermentation; the differ- 
 ence of weight caused by the escaped carbonic acid gas gives the 
 quantity of the changed sugar. The other, called 'clinical/ sug- 
 gested by Roberts, consists in the difference of the specific gravity of 
 the urine before and after the fermentation process. 
 
 ■• In the following I shall try to make use of the carbonic acid gas 
 space developed in the cylinder of the fermentation-tube to ascertain 
 the proximate quantity of sugar in the urine, a method which has 
 hitherto been used to detect merely the presence of sugar. Supposing 
 I succeed in this point, then the fermentation test, as I make it. 
 would gain much in value; for it would not only show the presence or 
 absence of sugar in the urine, but it would also give an idea of the 
 quantity of sugar present. 
 
 "If the fermentation-tube were constructed in such a way that the 
 whole quantity of carbonic acid gas, developed by the alcoholic 
 fermentation of the urine containing sugar, would gather in the 
 cylinder, then it would be easy to conclude from the development of 
 the gas volume at a given temperature and degree of barometric pr( .-- 
 sure the exact quantity of sugar. But this is not the case, for as soon 
 as some carbonic acid begins to gather on the top of the cylinder, a 
 corresponding quantity of fluid is pressed from the cylinder into the 
 reservoir. The carbonic acid developed in the reservoir escapes from 
 the surface of the fluid into the air. Thus the gas volume of the 
 cylinder does not represent the whole quantity of gas generated, for 
 
GLUCOSE OK GKRAPE sir; A li. 249 
 
 it lacks the carbonic acid which is developed in the fluid driven into 
 the reservoir. Although the gas volume of the fermentation-tube 
 does not correspond to the whole quantity of evolved carbonic acid, it 
 is nevertheless always larger or smaller, according to the greater or 
 smaller quantity of sugar in the fluid. 
 
 "It is probable that a fluid containing a certain quantity of sugar 
 would evolve in the fermentation-tubes — as they are all of the same 
 size — equal volumes of carbonic acid gas. If this be the case, then 
 we could determine by experiment the gas volumes of fluids contain- 
 ing certain percentages of sugar, and from this would be able to 
 conclude, from a certain developed gas volume in the cylinder, the 
 quantity of sugar. 
 
 "In order to be able to state easily the quantity of the gas volume 
 in the tubes, I graduated the cylindrical part (containing six cubic 
 centimetres) in cubic centimetres and fifths of a cubic centimetre. In 
 this way the quantity of the gas volume can be read from the cylinder. 
 The idea that one and the same sugar solution must reproduce in the 
 tubes equal gas volumes has been verified by experiments. I found 
 only small variations of two-fifths to three-fifths of a cubic centimetre, 
 and they depend probably upon the differences in temperature and 
 barometric pressure. In order to make the test not too complicated, 
 I intentionally did not take the temperature nor the barometric pres- 
 sure into consideration. 
 
 " The following tables show the quantity of developed gas volumes 
 in specimens of urine containing definite percentages of sugar. To 
 determine these quantities, several samples of normal urine were 
 mixed with grape-sugar solutions, and the following experiments were 
 then made: 
 
 " 1. May 29th, 1886: A, normal urine, acid, 1.021; B, normal 
 urine, acid, plus one- half per cent of sugar; 0. normal urine, acid, 
 plus one-fourth per cent of sugar; D, normal urine, acid, pins one- 
 fourth per cent of sugar. May 30th, 1886: A, a small bubble on the 
 top of the cylinder; B, = 2J- c.c. gas; 0, = -| c.c. gas; D, = f c.c. 
 gas. 
 
 "2. May 31st, 1886: A, normal urine, acid, 1.020; B, normal 
 urine, acid, plus one per cent of sugar; C, normal urine, acid, plus 
 one-half per cent of sugar; D, normal urine, acid, plus one-half per 
 cent of sugar; E, normal urine, acid, plus one-fourth per cent of 
 sugar. June 1st, 1886: A, a small bubble on the top of the cylinder; 
 B, = 5f c.c. gas; C,=2f c.c. gas; D, = 2 c.c. gas; E,=f c.c. gas; F, 
 = i c.c. gas. 
 
 "3. June 1st, 1886: A, normal urine, acid, 1.022; B, normal urine. 
 
250 GLU0O8E ()K GRAPE SUGAR. 
 
 arid, plue one per cent of sugar; C, normal urine, acid, plus three- 
 fourths per cent of sugar; D, normal urine, acid, plus one-half per 
 cent of sugar, dune 2d, 1880: A, a small bubble on the top of the 
 cylinder; B. = ">§ cc. gas; C,=3f c.c. gas; D,=2| c.c. gas. 
 
 "4. June "id. 188G: A, normal urine, acid, 1.00G; B, normal urine, 
 arid, plus one per cent of sugar; C, normal urine, acid, plus one-half 
 per cent of sugar; D, normal urine, acid, plus one-fourth per cent of 
 sugar, dune 3d, 1880: A, a small bubble on the top of the cylinder; 
 B, = 5f c.c. gas; 0,=2| c.c. gas; D,=| c.c. gas. 
 
 "5. June 24th, 1880: A, normal urine, acid, 1.024; B, normal urine. 
 acid, plus one per cent of sugar; C, normal urine, acid, plus three- 
 fourths per cent of sugar; D, normal urine, acid, plus one-half per cent 
 of sugar; E, normal urine, acid, plus one-fourth per cent of sugar; F, 
 normal urine, acid, plus one-eighth per cent of sugar. June 25th, 
 1880: A, a small bubble=0; B,=5 c.c. gas; C,=4 c.c. gas; D,=21 
 c.c. gas; E, = f c.c. gas; F,= T \, c.c. gas. 
 
 "6. October 21st, 1880: A, normal urine, acid, 1.018; B, normal 
 urine, acid, plus one-half per cent of sugar; C, normal urine, acid, 
 plus three- fourths per cent of sugar. October 22d, 1880: A, a small 
 bubble on the top; B,=2± c.c. gas; C,=3f c.c. gas. 
 
 "7. October 23d, 1880: A, normal urine, acid, 1.020; B, normal 
 urine, acid, plus one-half per cent of sugar; C, normal urine, acid, 
 plus three-fourths per cent of sugar; D, normal urine, acid, plus one 
 per cent of sugar. October 24th, 1880: A, a small bubble on the top 
 of the cylinder; B, = 2| c.c. gas; C, =3f c.c. gas; D,=4f c.c. gas. 
 
 "8. October 20th, 1880: A, normal urine, acid, 1.020; B. normal 
 urine, acid, plus one-fourth per cent of sugar; C, normal urine, acid. 
 plus one-half per cent of sugar; D, normal urine, acid, phis three- 
 fourths per cent of sugar. October 27th, 1880: A, a small bubble on 
 the top; B,= -fa c.c. gas; C,=l T 9 o c.c. gas; D, — 3f c.c. gas. 
 
 "0. November 1st, 1880: A, normal urine, acid, 1.022; B. normal 
 urine, acid, plus one-fourth per cent of sugar; C, normal urine, acid, 
 plus one-half per cent of sugar; D, normal urine, acid, plus three- 
 fourths per cent of sugar; E, normal urine, acid, plus three-fourths 
 per cent of sugar; F, normal urine, acid, plus one per cent of sugar. 
 November 2d, 1880: A, a bubble on the top = 0; B,= I c.c. gas; C,= 
 If c.c. gas; D, = 3| c.c. gas; E,=3f c.c. gas; F, — 5 c.c. gas. 
 
 "10. November 2d, 1880: A, normal urine, acid, 1.018; B, nor- 
 mal urine, acid, plus one-fourth per cent of sugar; C, normal urine, 
 acid, plus one-half per cent of sugar; D, normal urine, acid, plus one- 
 half per cent of sugar; E, normal urine, acid, plus three-fourths per 
 cent of sugar; F, normal urine, acid, plus one per cent of sugar. 
 
GLUCOSE OK (JRAI'K SUGAR. 251 
 
 November 3d, 1886: A, a small bubble on the top; ]'>,= [ c.c. gas; 
 C,=2£ c.c. gas; D,=2 c.c. gas; E, = 3£ c.c. gas; F,=4$ c.c. gas. 
 
 "If we take the numbers found in every experiment, then we have; 
 
 "For one per cent of sugar the gas volume equals 5§, 5§, of, 5, 4|, 
 5, 4f c.c. 
 
 "For three-fourths per cent of sugar the gas volume equals 3§, 4, 
 
 Q3 Q2 Q2 Q3 93 pn 
 
 "For one-half per cent of sugar the gas volume equals 2|, 2f, 2, 
 2f, 2|, 2|, V s , 1 T V l|,2i, 2 c.c. 
 
 "For one-fourth per cent of sugar the gas volume equals §, |, f, £, 
 
 2 2 3 1 1 p n 
 
 "For one-eighth per cent of sugar the gas volume equals ^ c.c. 
 
 " By this table it becomes evident that the numbers for the quan- 
 tity of the gas volume in different samples of urine containing the 
 same percentages of sugar are always approximately equal, and differ 
 at the most by three-fifths cubic centimetres. 
 
 "The average numbers quoted in the table are: One per cent of 
 sugar equals 5 c.c. gas; three-fourths per cent of sugar equals 3-f c.c. 
 gas; one-half per cent of sugar equals 2 c.c. gas; one-fourth per cent 
 of sugar equals -f c.c. gas; one-eighth per cent of sugar equals y 1 ^- c.c. 
 gas. 
 
 " I intentionally avoided ascertaining the quantity of the gas vol- 
 umes in smaller proportions than in quarters (one, three-fourths, one- 
 half, one-fourth), in order that the differences of the gas volumes 
 might be as great as possible, and that they could be easily distin- 
 guished from each other. 
 
 "With one per cent of sugar the gas volume is 5 c.c; thus the gas 
 fills nearly the whole cylindrical part of the fermentation-tube. If 
 the urine contain a little more than one per cent of sugar, then the 
 whole cylinder will be occupied by gas; the urine, pressed into the 
 cylinder, will deliver all its carbonic acid into the air, and will give 
 us in this way no means of ascertaining how much more than one per 
 cent of sugar it has contained. Therefore, if a sample of urine is 
 given to us for examination, and we make the fermentation test in the 
 graduated fermentation-tube, we shall be able to say on the following 
 day, i. <?., after the fermentation has taken place, whether the urine 
 contains sugar or not, and if sugar, then how much of it, whether 
 one eighth, one fourth, one-half, three-fourths, one per cent, or more 
 than one per cent; but we shall not be able to say by the first test 
 alone how much more than one per cent of sugar the urine may con- 
 tain. 
 
 " In older to ascertain by this fermentation test approximately the 
 
252 t.l.l I 08E OB «.U Al'K SUGAR. 
 
 quantity of sugar in urine containing more than one per cent of 
 sugar, it is necessary to dilute it with water. 
 
 "Diabetic urine of a straw color, and with a specific gravity of 
 1.018 to 1.02'.\ wa> usually diluted by me two times; of 1.022 to 
 l.o28, fire times: 1.028 to 1.038, ten times. The test is to be made 
 with the diluted urine. After the reaction has been completed, the 
 gas volume of fche fermentation-tube is read, and thus the quantity of 
 sugar ascertained: in this way the original (not diluted) urine will 
 contain, in proportion to the amount of dilution, two, five, or ten 
 times more sugar than the diluted one. 
 
 " As an example for the quantitative fermentation test, the follow- 
 ing experiment may be mentioned: 
 
 "June 28th, 1886: A, diabetic urine, 1.040, diluted ten times; B, 
 diabetic urine, 1.038, diluted ten times; C, diabetic urine, 1.020, 
 diluted two times: D, normal urine, 1.010. June 29th, 1886: A,= 
 3\ c.c. : B.=2t c.c. ; C, = 5 c.c. gas: D, a small bubble on the top of 
 the cylinder. Thus A has 3V c.c. gas = £ per cent of sugar, the urine 
 has been diluted ten times, therefore the original urine contains 74 
 per cent of sugar; B, = 2£ c.c.= 4 per cent X 10=5 per cent of sugar; 
 C,=5 c.c. =1 per cent x2=2 per cent of sugar; D, no sugar. 
 
 "This method of ascertaining the quantity of sugar by fermenta- 
 tion I applied during several months in the examination of the urine 
 of the diabetic patients of the German Hospital, and I was fully satis- 
 fied with the result. I also compared several times the results found 
 by fermentation with the numbers given by the quantitative Fehling's 
 solution test. As bearing on this point, the following two experi- 
 ments may be mentioned: 
 
 "1. Fermentation test. — June 10th, 188G: A, diabetic urine, 1.040, 
 diluted ten times; B, diabetic urine, 1:026, diluted five times; C, 
 diabetic urine, 1.020, diluted five times; D, normal urine. June 
 11th, 188G: A. = 41 c.c. gas=over £ per cent x 10 = more than 74_ per 
 cent of sugar; B,= 2 c.c. gas = 4 per cent x 5 = 24 per cent of sugar; 
 
 C, = l c.c. gas = over \ per cent x 5 = more than 14, per cent of sugar; 
 
 D, no sugar. 
 
 "Fehling's test. — A. = 7i per cent; B, = 2 per cent; C, = 2 per 
 cent of sugar; D, no sugar. 
 
 "2. Fermentation test. — June 14th, 1886: A, diabetic urine, 1.032, 
 diluted ten times: B, diabetic urine. 1.03 s , diluted ten times; C, 
 diabetic urine, 1.024, diluted five times; D, normal urine. June 
 15th, 188G: A. =2f c.c. gas=4 per cent x 10=5 per cent of sugar; B,= 
 3? c.c. gas=£ per cent x 10=74 per cent of sugar; C, = f c.c. gas=£ 
 per cent x 5 = 14, per cent of sugar; D, no sugar. 
 
GLUCOSE OK GRAPE SUOAK. 
 
 25: 
 
 " FehUng's Test.—A, = o per cent; B, = 6| per cent; C,=lfper 
 cent of sugar; D, no sugar. 
 
 " If we now compare the results of the quantitative test by Fai- 
 ling's solution with the results found by the fermentation test, we find 
 that they are not always absolutely equal, although the difference is 
 but slight. In this way it appears that the method of ascertaining 
 the quantity of sugar by the gas volume in the fermentation tube 
 gives true and approximately correct results. 
 
 " The advantages of this mode of 
 ascertaining the quantity of sugar con- 
 sist in its being neither troublesome 
 nor complicated, and it can also be 
 employed by every physician. Urine 
 containing albumin can be directly 
 examined for sugar by the fermenta- 
 tion test; 'it is not necessary to sepa- 
 rate the albumin before applying the 
 test, as in other methods/ That is an- 
 other point in favor of the fermenta- 
 tion test. 
 
 " In order to make the quantitative 
 determination of sugar yet easier, we 
 have written on the cylinder figures 
 showing the percentages of sugar. A 
 fermentation-tube bearing this scale 
 shows directly, by the level of the 
 urine, the per cent of sugar, and can 
 be therefore called ' Fermentation Sac- 
 charometer.' 
 
 "From a study of the experiments detailed in this article we may 
 formulate the following conclusions: 
 
 "First.— The fermentation test can be made in the ordinary tem- 
 perature of the room. 
 
 "Second. — The addition of mercury is not necessary. 
 
 " Third.— -The volume of developed gas in the cylinder gives us an 
 idea of the approximate quantity of the sugar present in the urine." 
 
 Fig. 53.— Fermentation Saccharo- 
 meter. 
 
CHAPTER Y. 
 NITROGENOUS EXCRETORY SUBSTANCES. 
 
 There are a number of groups of nitrogenous substances which 
 represent the physiological metamorphotic transformations of the 
 body, some of which appear normally in the urine, and are the com- 
 plete products of tissue waste. But the larger number are found in 
 the blood or the various organs and fluids which constitute the animal 
 organism. Some of them appear constantly in the urine, but in such 
 small quantities that they are not easily recognized, and consequently 
 afford no practical information; others appear as abnormal constitu- 
 ents, and for the same reasons are equally unimportant. Still the 
 time may not be far distant when each of these complex substances 
 may be more easily recognized and, when occurring in the urine, they 
 will be found to be indicators of diseased conditions; their presence 
 or absence enabling the physician to attain greater skill in diagnosis. 
 
 They are given in tabular form to show their great variety, 
 and as indicative of the manifold number of products which may be 
 formed when their normal development is interrupted. It also sug- 
 gests a variety of these incomplete products as the cause of the great 
 diversity of symptoms classed under the general term uraemia or 
 ursemic poisoning. 
 
 1. Urea, CH 4 N 2 0, or (NH,) a CO 15. Cystin, C 3 H,NS0 2 
 
 2. Uric Acid, C;H 4 N 4 3 16. Benzoic Acid, HC,H 6 O a 
 
 3. Kreatin, CiHoN.Oj 17. Tyrosin, C 9 H n N0 3 
 
 4. Kreatinin, C 4 H 7 Nr 3 18. Hippuric Acid, C 9 H 9 N0 3 
 
 5. Allantoin, C 4 H 8 N 4 3 19. Phenylic Acid, CHoO 
 
 6. Sarkosin, C 3 H,N0 2 20. Glycocholic Acid, C 20 H 43 NO» 
 
 7. Hypoxanthin, CoH.N.O 21. Taurocholic Acid, C 20 H 4: ,NSO, 
 
 8. Xanthin, C 6 H 4 N 4 2 22. Indican, KC 8 H NSO 4 
 
 9. Carnin, C 7 H 6 N 4 3 23. Indigo, C B H 6 N 9 
 
 10. Guanin, CsHoNsO 24. Indol, C 8 H 7 N 
 
 11. Kynurenic Acid, C 20 H 14 N 2 Og + 25. Skatol, C U H N 
 
 + 2H 2 = C 2 „H 18 N 2 4 26. Inosite, C H 12 O 
 
 12. Glycin, C 2 H 2 (NH 2 )0(OH)C 2 H 5 - 27. Cerebrine, Ci,H 33 N0 3 
 
 N 3 2 28. Lecithine, C 42 H 84 NPO 
 
 13. Taurin, C 2 H,N0 3 S 29. Neurine, C 6 H 13 N 
 
 14. Leucin, C H 13 NO 2 
 
NITROGENOUS EXCRETORY SUBSTANCES. 255 
 
 UREA (CILN./J). 
 
 Next to water, urea is the most abundant and important normal 
 ingredient found in urine. It constitutes nearly one-half of the 
 solid constituents. The average amount of urea excreted daily is 
 estimated by physiologists at about 550 grains (35.637 grams). Ad- 
 mitting the daily average of urine voided to be 50 ounces (1555.170 
 c.c), and the above figure the quantity of urea excreted, the per- 
 centage of urea eliminated will be 2.2 per cent per diem. All these 
 figures are liable to very wide variations from day to day, and from 
 hour to hour, in a state of perfect health and, of course, to a still 
 greater extent in disease. 
 
 The kind and quality of food, the quantity of fluid taken, the 
 amount of exercise, and the hour of the voiding of the urine, all have 
 their influence in determining the quantity of urea to be formed and 
 excreted. The activity of the integumental and alimentary excretion 
 also must not be overlooked. 
 
 Eemembering all these facts, and especially those relating to diet 
 and exercise, the absolute daily quantity of urine excreted must be 
 ascertained, and the test made from the mixed sample to obtain any- 
 thing like trustworthy information. The examination of the urine 
 for one day will be of no service, but it must be repeated for several 
 days in succession, and these results must be added together and 
 divided by the number of examinations and days to yield anything 
 like approximate accuracy. 
 
 With all this, the quantitative test must be accurate and the calcula- 
 tions carefully computed, otherwise the greatest error will be the 
 result. 
 
 Unless every article of diet was carefully analyzed, in conjunction 
 with the greatest possible accuracy in quantitative analysis of urine, 
 no positive information could be obtained, and even then a highly 
 nitrogenous meal might slip through the alimentary tract undigested 
 and unabsorbed. 
 
 When all these possible chances for error are considered in ascer- 
 taining the precise quantity of urea eliminated and its relation to the 
 amount of urea-forming elements imbibed, and the variously inter- 
 rupted metabolic transformations, the practical importance of esti- 
 mating the precise quantity of urea eliminated is reduced to the 
 minimum, if not absolutely lost, in reference to any information re- 
 garding diseased processes. 
 
 The exact amount of urea excreted may be determined, but it fur- 
 nishes no information as to the source and cause of the non-elimina- 
 
256 NITROGENOUS EXCRETORY SUBSTANCES. 
 
 tion. It simply assures the examiner that the diminution in specific 
 gravity Lb due to a deficient elimination of urea, and as this is about 
 the only cause for a diminished density, we can in all cases assume 
 it to be due to this. The knowledge that the loss of urea is three- 
 tenths or five-tenths of one per cent is of no practical value. It 
 neither aids in diagnosis, prognosis, nor treatment. 
 
 There are a number of methods for the quantitative analysis of 
 urea. Most of them, however, have certain objections and uncertain- 
 '.its. which, -with the above reasons, renders them very troublesome 
 and almost useless. A few of them, however, will be given. Among 
 these may be mentioned the methods of Russell and West, Liebig, 
 Davy, Fowler, Squibb, and Doremus. 
 
 The test of Russell and West is one of the most accurate in use. 
 There are, however, some serious objections to it. The outfit is 
 somewhat expensive and easily broken. It is difficult to manipulate 
 unless the examiner is accustomed to such work. There is also 
 danger from inhaling the fumes of the bromine, and. the laboratory, 
 office, or house may become filled with its pungent odor. 
 
 The apparatus which has been in use at the laboratory of the New 
 York Post-Graduate Medical School and Hospital consists of gradu- 
 ated pipettes, and a registered collecting and a generating bulb tube, 
 the one to hold the solutions and the other to collect the gas set free; 
 a pneumatic trough on long legs, with a perforated stopper, arranged 
 to receive the generating tube below and the collecting tube above. 
 
 The directions for using are: Fill the small pipette up to the neck 
 with the sample to be tested; this will measure exactly five cubic cen- 
 timetres (77.161 minims); let it flow down the bulb, then pour in 
 water until it rises to the top of the constriction. The amount of 
 Avater to be added to reach this point is fifteen cubic centimetres 
 (231.485 minims). 
 
 Put in the long stopper, and see that no air is below it. 
 
 Fill the measuring tube, and invert it in the trough, which has 
 previously been filled with water, and drop it into the socket to steady 
 it until the generating tube has been attached. Fill up the bulb 
 tube witli the hypobromate solution. The amount required for the 
 test is 28 cubic centimetres. This, however, does not always fill the 
 tube, and water has to be added to displace all the air. 
 
 Pull the long stopper over the perforated cork, insert the bulb 
 tube from below, and slip the measuring tube into the socket over 
 the perforated cork and bulb tube as quickly as possible to prevent 
 the loss of any of the gas. 
 
NITROGENOUS EXCRETORY SUBSTANCES. 257 
 
 Warm the bulb until it feels quite hot, or keep it in a sufficiently 
 warm place. 
 
 If the five cubic centimetres of urine give off more nitrogen gas 
 than the measuring tube will hold, dilute the urine with an equal 
 volume of water, and take five cubic centimetres of the dilution, read 
 off the result on the measuring tube, and multiply by two. It is al- 
 ways best to dilute the urine. 
 
 If the urine contains albumin, heat to boiling with two or three 
 minims of acetic acid, filter, and take five cubic centimetres of the 
 filtrate. 
 
 The figures 1, 2, and 3 marked on the measuring tube are to be 
 read 1, 2, or 3 grams of urea for each 100 cubic centimetres. 
 
 The hypobromite solution is prepared by first making a caustic 
 soda solution, and then adding the bromine. 
 
 To make the soda solutions, 100 grams of pure caustic soda are dis- 
 solved in 250 cubic centimetres of distilled water and filtered. When 
 cold, the addition of 25 cubic centimetres of bromine completes the 
 hypobromite solution. As this keeps badly, it is better to make the 
 soda solution, which keeps well in large quantities, and only add the 
 bromine at the time of using. 
 
 To make just the required 28 cubic centimetres, take 22.4 cubic 
 centimetres of the caustic soda solution, and add 5.6 cubic centimetres 
 of bromine. But owing to the danger in measuring the bromine, it 
 is much better to take the whole bottle which holds 10 cubic centi- 
 metres, and add 40 cubic centimetres of the soda solution. From 
 this mixture the required 28 cubic centimetres can easily be mea- 
 sured and transferred to the bulb tube with safety to the manipu- 
 lator. 
 
 The bromine should be opened and added to the soda solution in 
 the open air, with the back to the wind. 
 
 It takes an ordinary one-ounce vial of bromine, price 35 cents, to 
 make 10 cubic centimetres. 
 
 The conversion of the metric system is made by considering one 
 gram or cubic centimetre equal to 15.43234874, and allowing 480 grains 
 or minims to the ounce. 
 
 1. gram, . . = 15.4323 + 
 
 minims. 
 
 2. " = 30.8646 + 
 
 it 
 
 3. " = 46.2970 + 
 
 14 
 
 5. cubic centimetres = 77.1617 -f- 
 
 li 
 
 5.6 " " = 86.4211 + 
 
 (< 
 
 10. " " = 154.3234 + 
 
 << 
 
 15. " " = 231.4852 + 
 
 " 
 
 17 
 
•_'"> s NITROGENOUS KX< 1:1 i< >i: Y SUBSTANCES. 
 
 22.4 cubic centimetres = 345.6846 -f- minims. 
 
 25. " « = 385.8087 + 
 
 28. •' " = 432.1057 + 
 
 40. •' " = 1.2860 + ounces. 
 
 100. grams, . . = 3.2850 + 
 250. cubic centimetres = 8.0376 -}- " 
 
 The above-described apparatus is the one which has been used for 
 several years past, both in experiments and for testing urine. It lias 
 been greatly modified and made quite simple by Opjohn. 
 
 Davy's, like the Russel and West method, is based upon the split- 
 ting up of the urea into nitrogen, carbon dioxide (C0 2 ), and water. In 
 the Russel and West test, the carbon dioxide (CO.,) is absorbed by the 
 caustic alkali or hypobromite solution; in Davey's, by the hypo- 
 chlorate solution. 
 
 Liebig's is still more complicated, but by it [or that of Davy in the 
 hands of an expert chemist, very accurate results can be obtained. 
 But in both there are so many chances for error and so many cor- 
 rections to be made, that, practically speaking, for every-day office 
 work they are not to be recommended. 
 
 The test introduced by Dr. G. B. Fowler, of New York City, is 
 easily manipulated and is quite practical. All the appliances needed 
 are a long glass cylinder capable of holding 10 or 12 ounces (311.034 
 c.c. or 373.242 c.c), and graduated in ounces and fractions; two 
 large and accurate urinometers, one registering densities from 1.000 
 to 1.030, and the other from 1.030 to 1.060. The whole cost being 
 about five dollars. 
 
 The principle of the test consists in the liberation of the nitrogen 
 gas and the carbon dioxide (C0 2 ), by the action of the liquor soda? 
 chloriuatis or Labarraque's solution. 
 
 The test is used as follows: Take seven ounces (217.314 c.c.) of the 
 chlorinated soda solution of a known density of 1.045, and multiply it 
 by seven, add one ounce (31.103 c.c.) of urine having a specific 
 gravity, say of 1.010. As the evolution is so sudden, the specific 
 gravity of the combined fluids has to be accounted for before unit- 
 ing. Take 7 ounces of the soda solution at 1.045x7 = 7.315, add to 
 this the one ounce (31.103 c.c.) of urine with a density of 1.010 and 
 divide by eight, and it will give 1.040f as the specific gravity of the 
 combined fluids, viz., 1.045x7 = 7.315 + 1.010 = 8.325-^8 = 1.040&. 
 At the end of an hour or more, the density will have fallen; if to 
 1.039, it indicates a loss of If degrees in density. By multiplying 
 this loss by the factor 7.791, it will indicate the number of milligrams 
 of urea lost in every 100 cubic centimetres of urine,'or, if we multiply 
 
NITROGENOUS EXCRETORY SUBSTANCES. 
 
 259 
 
 the loss by the factor .77, it will give the amount lost in percentage; 
 in this example it would indicate a loss of 14.65 milligrams in every 
 cubic centimetre, or 1.46 per cent. 
 
 Fig. 54. 
 
 Glass Cylinder Graduated in Ounces or 
 
 Cubic Centimetres. 
 
 Fig. 55. 
 Urometer of Doremus, Keduced about 
 One-third. 
 
 The following method, as given by Dr. Charles A. Doremus/ of this 
 City, is the most practical of all. 
 
 1 New York Medical Record, March 14th, 1885, p. 302. 
 
260 OTTROGENOITS EXCRETORY SUBSTANCES. 
 
 " The form of apparatus shown in the figure has been found to 
 yield results so closely in accord with theory that its employment for 
 rapid clinical examination of the urine may lead to a more frequent 
 analysis for urea on the part of the physician and be the means of 
 securing data concerning the elimination of so important an excre- 
 mentitious substance which will be beneficial. 
 
 "The manipulation of the urometer is simple in the extreme. By 
 inclining it, the long arm may be filled with the hypobromite to the 
 bend at the bulb. By means of the nipple pipette, a measured vol- 
 ume of the urine (1 c.c.) is injected slowly up the long arm by com- 
 pressing the nipple. A rapid decomposition of the urea takes place, 
 the bubbles of nitrogen rising in the long arm, while the dis- 
 placed liquid flows into the bulb, which serves as a reservoir. With 
 a little care the urine may be delivered at a rate that permits the de- 
 composition to take place without loss of gas. The graduation on 
 the glass indicates the weight of urea in the urine used. 
 • " Two forms of apparatus are made, one graduated to read fractions 
 of a gram (0.00 to 0.03 per 1 c.c. of urine), the other to show grains 
 of urea in the fluidounce of urine. When the volume passed in 
 twenty-four hours is known, the calculation of the analysis is very 
 easy. Total quantity of urine voided, 1.600 c.c; urea in 1 c.c. of 
 urine (result of analysis) 0.024 grams; urea in 1.600 c.c = 0.024X 
 1.600 c.c. = 38.4 grams. When the centesimal graduation is used, 
 the weight of urea in 100 volumes of urine is ascertained by multi- 
 plying the result of the test by 100. This gives what is commonly 
 termed the percentage of urea. This is not strictly correct, but the 
 true percentage can be calculated when the specific gravity of the 
 urine is taken thus: specific gravity of urine, 1.020; urea in 1 c.c. of 
 urine, 0.02 grams; 100 c.c. of urine would weigh 102 grams if the 
 specific gravity was 1.020, therefore, 
 
 102 : 100 : : 2 : x = 196, the true percentage. 
 
 " When the tube graduated in grains is used, the calculation of 
 the percentage is a more complicated arithmetical problem. The 
 ounce contains 455.7 grains. From this, the specific gravity, and the 
 result of the analysis the computation can be made. 
 
 "The hypobromite solution is prepared according to the formula 
 of Knop, by dissolving 100 grams of sodium hydrate in a 250 c.c. of 
 water. This solution may be kept in a bottle with a paraffined stopper. 
 Bromine is mixed with this in the proportion of one volume to ten; 
 2 c.c. of bromine with 20 of the sodium hydrate will suffice for two 
 tests. After the bromine has united with the alkali, the liquor is 
 diluted with its own volume of water. 
 
NITROGENOUS EXCRETORY SUBSTANCES. 26! 
 
 " When using English weights, six ounces of sodium hydrate are 
 dissolved in a pint of water to make the alkali. The bromine should 
 be added to this in the proportion of one to ten, and the liquid diluted 
 with its own volume of water. A fresh, good, hypochlorite will serve 
 for the hypobromite when the latter cannot be obtained. 
 
 "The normal quantity of urea voided is two per cent or .02 grams 
 per c.c. or 10 grains per ounce. The elimination of a diminished or 
 increased quantity of urea is speedily determined by the use of the 
 apparatus. 
 
 " Messrs. Eimer & Amend supply either form at a very moderate 
 price." 1 
 
 As already explained, there is no very practical information to be 
 obtained from such analyses, on account of the numerous sources of 
 error and the many daily variations independent of disease. 
 
 Further than this, the non-elimination of urea does not indicate its 
 accumulation in the blood, and even if it did, it proves nothing, for 
 experimentally it has been proven that hypodermic injections of urea 
 produce none of the effects commonly witnessed in so-called uraemic 
 attacks, but large doses are more likely to produce the opposite or a 
 soothing influence upon the nervous system. 
 
 There is not the slightest doubt that incomplete physiological 
 metamorphosis is the cause of the so-called uraemic manifestations. 
 But just what the irritating and poisonous substance is has not as 
 yet been clearly elucidated. 
 
 Taking all these things into consideration, it appears that very lit- 
 tle, if any, additional information is obtained by knowing the precise 
 number of grains or the percentage of urea lost. The loss of density 
 in connection with the quantity, as indicated by the urinometer 
 affords equally as much information. 
 
 Clinical Significance of Urea. — Urea naturally is more abundant 
 in the urine of children than in that of adults, which is explained by 
 the greater amount of muscular activity and the growth and develop- 
 ment requiring more nitrogenous food. 
 
 Urea is also increased during the period of rest following muscular 
 activity in the adult. 
 
 Urea is increased in quantity during the early activity of all acute 
 and febrile diseases. The only recorded exception to this is Frerichs' 
 case of acute atrophy of the liver, in which he found the urine 
 deprived of urea. In other cases, he found it increased. 
 
 As these acute diseases advance and the renal cells undergo pro- 
 gressive metamorphotic changes and lose their eliminating power, 
 the quantity of itrea is diminished. This non-formation and elim- 
 
■Ji'rJ NITUor.KXOrs I XOUKTOKY Sl/HSTANCKs. 
 
 ination of urea with the retention of incomplete products in the 
 circulating blood appears to he the great cause for the increased 
 bodily .temperature, and is the principal factor in exciting and main- 
 taining the cerebral manifestations. If, for any reason, the incom- 
 plete products accumulate very rapidly, they almost completely over- 
 throw the nervous centres, and a fall in or a low bodily temperature 
 is the result. It is a firm conviction based upon an extended necropsy 
 study that in all the acute diseases the height of the attack and the 
 prognosis rests almost exclusively upon the minute changes in the 
 hepatic and renal epithelial cells. "When this fact is more generally 
 accepted and acted upon, the mortality in connection with all acute 
 and severe diseases and after severe surgical operations will be 
 diminished, other things being equal. The greatest antipyretic will 
 be that drug or that plan of treatment which will prevent the retro- 
 grade metamorphosis of the hepatic and renal epithelial cells and sus- 
 taiu their nutrition and elimi native activity. 
 
 During the defervescence of these diseases, there is a state of phy- 
 siological inactivity and the urine contains but very little urea. From 
 this time on, however, the urea in the urine will steadily increase in 
 quantity, in direct proportion to the return of the functional activity 
 of the epithelial corpuscles of the kidneys, until the normal standard 
 has again been attained. 
 
 If there has been a permanent impairment, it is apt to remain below 
 normal. 
 
 It is a well-known clinical fact that in all forms of renal lesions 
 there is a diminution in the quantity of urea excreted, but this is not 
 the case in connection with the chronic diseases implicating the other 
 visceral organs. Peculiar nervous manifestations are the rule with 
 the renal lesions and the exception with the other chronic diseases. 
 
 With glycosuria the urea is increased in the urine up to the time 
 that the renal cells fail, and then a decrease in the quantity of urea 
 eliminated is noticed, followed by marked nervous symptoms, uraemia, 
 and death. 
 
 From these clinical and pathological observations, this assumption 
 is justified, that the function of the renal epithelial cells is to pick up 
 from the blood the urea-forming elements, convert them into com- 
 pletely formed urea, and discharge them into the lumen of the urinif- 
 erous tubules. 
 
 If the urea accumulated in the blood was in direct proportion to its 
 disappearance in the urine, this theory would not be sustained, but 
 since this is not the case, it would appear to more fully substantiate 
 the idea here advanced. The elimination of large quantities of water, 
 
NITROGENOUS EXCRETORY SUBSTANCES. 208 
 
 which is principally discharged through the Malpighian tufts, and but 
 slightly, if at all, through the epithelial cells, increases the quantity 
 of urea excreted, and consequently its action in regard to this agent 
 must be purely mechanical. Passing over the excretory cells in large 
 quantities, it keeps the free surface clean and possibly by a suction 
 force helps to draw the solid particles from the protoplasm or through 
 the rods of Heidenhain. Therefore, the quantity of urea eliminated 
 is one of the great indicators by which we are enabled to judge of 
 the extent and degree of retrograde metamorphosis going on in the 
 renal epithelial corpuscles. But a careful microscopic study of the 
 epithelium of the casts will give more accurate information in regard 
 to the condition of the kidneys. 
 
 uric acid (C B H 4 N 4 0,). 
 
 It is well known that uric acid is one of the products resulting from 
 proteid metabolism, but as to the exact point of its formation, there 
 is considerable doubt. It is a normal ingredient of the urine and is 
 apparently a less complete product of tissue waste than urea. By 
 some it is thought to be antecedent to the formation of urea. It has 
 been found in the blood, liver, and spleen, and it has been 
 claimed that it was more abundant in the spleen than at any other 
 portion of the body. But about an equal quantity is found in the 
 portal and hepatic blood. From this abundance in the spleen an 
 abnormal quantity in the urine has been attributed to a faulty action 
 on the part of that organ, but its presence in the urine after the 
 removal of the spleen upsets this argument. 
 
 The views already advanced in relation to the acidity of the urine 
 and the formation of urea and our clinical data point towards a 
 similar method of formation for uric acid and traces its origin to the 
 liver. 
 
 The chemico-physiological action of the liver is to develop the uric- 
 acid-forming elements which are taken up from the blood, and are 
 finally discharged into the uriniferous tubules as completely formed 
 uric acid. This is borne out by our clinical data, for in all cases in 
 which uric acid is abundant, the functions of the liver appear to be 
 incompletely performed and there is also a hypertrophic condition of 
 the renal cells. A typical pathological example of this is to be found 
 in diabetes, in which }3rimary changes in the liver are followed by an 
 hypertrophic swelling of the epithelial cells, and finally their total 
 destruction. Here an abundance of uric acid in the urine is not 
 infrequent. The lack of an abundance of this acid in primary lesions 
 
264 MTKoi.EN.US KXORETOKY S1BSTANCES. 
 
 of the kidneys also points towards the renal cells as the final seat of 
 production. 
 
 The finding of the small crystals of uric acid in the renal epithelial 
 cells, when sections are made from these organs, is also proof of their 
 formation at this point. 
 
 Uric acid requires from ten to fifteen thousand parts of water to 
 hold it in solution. It is also less soluhle in acid than alkaline solu- 
 tions. On account of this great insolubility, and its liability to be 
 deposited in the renal organs, and the frequency of its occurrence, it 
 becomes one of the excreta which is most likely to induce a permanent 
 renal lesion. This condition has been considered the principal ex- 
 citant of Bright 's. 
 
 Careful clinical observation demonstrates that this condition cannot 
 be directly traced to any special kind of food. It is quite as likely to 
 appear with vegetable as animal diet. That it has its origin in the 
 nitrogenous compounds is, however, quite certain. The explanation 
 of its occurrence upon a vegetable diet appears to be this. The 
 carbonaceous substances are more easily transformed than the nitro- 
 genous: over-indulgence in the former, therefore, exhausts the hepatic 
 transforming power, so that the nitrogenous elements are only in- 
 completely acted upon, the quality of bile becomes impaired, and 
 finally uric acid is found in abundance in the urine. The return to a 
 well-selected mixed diet will often obviate the difficulty; in other 
 cases, a small allowance of purely albuminous diet is followed by good 
 results, but in the larger proportion of cases the deficiency in the 
 quality of the bile must be compensated for before anything like a 
 permanent cure can be effected. 
 
 In some instances the appearance of uric acid in the urine may be 
 due to an incomplete oxidation into complete urea, but in the larger 
 number the cause - is farther back and due to the incomplete hepatic 
 metabolism. 
 
 The question of a uric acid diathesis is often raised. It would 
 appear from the above that there is no condition truly deserving of 
 the title uric or uric acid diathesis. The symptom accredited to such 
 a condition is its appearance in the urine in abundance; the cause is 
 an interruption in the physiological functions in the liver and the kid- 
 neys. It frequently occurs in families in which the methods of living 
 are such that the liver is constantly overworked and incompletely 
 supplied with oxygen. The children and grandchildren live as their 
 forefathers have done, and consequently suffer in like manner. A 
 change of habit, however, will cause a disappearance of the symptoms, 
 which argues strongly against a diathesis. 
 
NITROGENOUS EXCRETORY SUBSTANCES. 265 
 
 The crystals of uric acid may accumulate in the pelves of the 
 kidneys, forming what is commonly known as a renal calculus, their 
 discharge giving rise to severe and sometimes dangerous symptoms, 
 known as renal or nephritic colic. After their escape from the 
 ureters, they may lodge in the bladder and form the nucleus for a 
 uric acid or even a phosphatic calculus, or, in fact, any form of cystic 
 stone; or they may be discharged with the urine, causing painful 
 micturition or "scalding." 
 
 When abundant, they are plainly visible to the unaided eye. 
 
 The qualitative test for determining the presence of this acid is 
 known as the murexide reaction, and is employed as follows: 
 
 Place a small quantity of the reddish crystalline deposit or some of 
 the crystals in a watch-glass or on a glass slide; add four or five drops 
 of nitric acid, and heat very cautiously over a spirit lamp or Bunsen's 
 burner. The uric acid will dissolve, and a reddish-yellow residue 
 will be obtained. Ammonia vapor or a small drop of ammonia added 
 to the residue will produce a beautiful purplish-red color; on the 
 subsequent addition of a little solution of caustic potash, it will assume 
 a violet tint. 
 
 It has also been found that uric acid has the property of reducing 
 copper in a similar manner to sugar (Pavey and Satterthwaite). It, 
 however, requires longer boiling, and the copper test should be em- 
 ployed in the following proportions: 
 
 Take one drachm (3.887 c.c.) of the urine, add twenty (1.295 c.c.) 
 minims of a twelve-per-cent solution of sulphate of copper, then add 
 two and one-half (9.719 c.c.) of liquor potassae, and boil. At the end 
 of ten minutes' steady boiling, if uric acid be present, the reduction 
 will be effected and a reddish deposit will be produced, which, after 
 standing for a little while, is as positive as that of glucose. 
 
 The quantity can be determined in two ways; first, by precipitating 
 with hydrochloric acid and collecting the crystalline deposit upon a 
 weighed filter; and second, by the method suggested by Dr. Pavey. 
 This also consists in the reducing power of uric acid on cupric 
 sulphate. 
 
 Both methods, however, are too complicated to be of any practical 
 value to the general practitioner, and a further description of them is 
 omitted. 
 
 Diagnosis. — This is readily made when the crystals are found in 
 the urine. 
 
 Prognosis. — Depends upon the treatment and the physician's suc- 
 cess in regulating the patient's diet and habits. 
 
 Treatment. — If due to a deficient supply of oxygen, this should be 
 
266 NITROGENOUS KXCRETORY SUBSTANCES. 
 
 increased: in fact, in all these eases they should take pains to exercise 
 freely in the open air. The next step is to regulate the diet, either 
 placing them upon a limited mixed, or one which is exclusively 
 nitrogenous. . The main object is to improve the stomach and intes- 
 tinal digestion, that absorption and further assimilation can be as 
 easily effected as possible. 
 
 If there is reason to believe that the quantity and quality of bile are 
 deficient, a little may be added in the way of fel bovis inspissatum, 
 which in itself is often quite sufficient to remove the difficulty and 
 cure the disease. 
 
 All forms of tonic cholagogues will be found of service. 
 
 Tonics only do good by improving the general condition of the 
 digestive tract. If the abnormal condition is attributable to a de- 
 pression of the nervous system, the nerve tonics should be used, and 
 one of the best for its influence upon the nervous mechanism of the 
 liver is damiana and its preparations, either alone or in combination. 
 The dilute nitro-hydrochloric acid in ten-minim doses often proves 
 itself of service as a tonic to the hepatic function: it, however, is more 
 palliative than curative. 
 
 kreatix (C 4 H 9 N 3 OJ. 
 
 This is one of the products of muscular metamorphosis, and 
 probably never occurs in the urine under its own form. By losing 
 one element of water, it is converted into kreatinin, which is one of 
 the normal constituents of the urine. The finding of kreatin in a 
 sample is generally believed to be due to the process of obstruction 
 which causes an element of water to be joined to kreatinin. 
 
 kreatinin (C 4 H.N 3 0) 
 
 is one of the complete products of tissue metamorphosis, and is 
 always present in urine. The quantity eliminated daily is quite 
 small, 15.432 grains (1 gram). It is one of the most powerful or- 
 ganic alkalies found in connection with the animal economy. There- 
 fore, it is reasonable to suppose that the relative proportion existing 
 between the formation and elimination of uric acid and kreatinin 
 must largely govern the reaction of the urine. But on account of the 
 small quantity and the difficulty of recognizing the presence of the 
 latter, the examination for kreatinin in the urine has not yet been 
 made practical. 
 
NITROGENOUS EXCRETORY SUBSTANCES. 2^)7 
 
 ALANTOIN (C„H 8 N 4 : ,) 
 
 is found in the alantoic fluid of the foetus and in the urine of animals 
 for a few days after birth, and may he found in the excreta in minute 
 quantities later in life. 
 
 It is one of the products resulting from oxidization of uric acid, 
 and ordinarily is further transformed and eliminated as urea. 
 
 It has been found in the human urine after taking tannic acid. 
 
 SAKKOSIN (CJ-I.N'OJ 
 
 appears to be derived from kreatin, and only appears in the urine 
 when large quantities have been ingested. Its presence prevents the 
 precipitation of the urea by mercury, and consequently interferes, 
 when present, with the quantitive estimation by this method. 
 
 HYPOXANTHIN (C 5 H 4 N 4 0) ' 
 
 or sarkine is a normal constituent of muscles, and has been found in 
 the spleen and medulla of the bones. It has been found in the blood 
 and urine in connection with leucocythsemia. Bence-Jones also 
 found it in the urine of a boy nine years old, as a crystalline deposit. 
 Hypoxanthin crystals were found by Lebon in a vesical calculus. 
 
 XANTHIN (C 5 H 4 N 4 2 ). 
 
 Xanthin appears to be a higher oxide of the former. It was first 
 discovered in a urinary calculus, but has since been recognized as 
 a urinary crystalline deposit. It is very insoluble in water, requiring 
 1,500 times its bulk at 100° C. (180° F.). 
 
 The clinical sig7iificance of hypoxanthin and xanthin is chiefly in 
 their insolubility, especially in the case of the latter, and consequently 
 their tendency to form calculi. 
 
 CARNIN (C 7 H 8 N" 4 0..) AND GUANIN (C.H.N.O).'^ 
 
 These two substances, up to the present time, have only been found 
 in extracts from the tissues of the body, and have not been traced into 
 the urine in their own form. __ " 
 
 KYNURENIC ACID (C 20 H 14 lSr.,O 6 . +2H 2 0). 
 
 Kynurenic acid has, so far, only been found in the urine of dogs. 
 
L'''' v MTHot.K.Nols EXGRBTOBY SUBSTANCES. 
 
 glycin (C,H,(NH,)0(OH) C a H 6 N 9 O a ). 
 
 Glycin luis not been traced into the urine as a distinct element, 
 but is one of the nitrogenous products which may be obtained by the 
 decomposition of hippuric acid or bile acids. 
 
 taurin (C a H 7 NO,S). 
 
 This is a constituent normal to the hepatic secretion, but occasion- 
 ally passes out of the body in the urine. It is not easy to detect its 
 presence, and is therefore of no practical value. 
 
 LEUCIN (C 6 H, 3 N0 3 ). 
 
 This substance is occasionally found in the urine in an incomplete 
 crystalline form, in connection with tyrosin. It has been found in 
 connection with acute yellow atrophy of the liver, acute phosphorus 
 poisoning, leucocythaemia, typhoid fever, small-pox, etc. Its clini- 
 cal significance is the same as tyrosin. 
 
 Scherer's Test for Leucin. — If pure leucin is evaporated with 
 nitric acid, a colorless, almost imperceptible residue remains. Add 
 hydrate of soda, the leucin dissolves, and according to its purity 
 forms a colorless, or more or less colored fluid. If it be collected upon 
 a piece of platinum foil, it forms an oil-drop, which does not wet the 
 platinum, but rolls about without adhering to it. This is also quite 
 characteristic of very impure leucin. 
 
 cystin (C s H 7 NSO„). 
 
 This crystalline substance has been found in connection with urinary 
 calculi, and also as a urinary sediment. But at present our knowl- 
 edge of it is very meagre and its clinical significance very uncertain. 
 
 BENZOIC ACID (HC 7 H 5 2 ) 
 
 is one of the non-nitrogenous compounds resulting from a splitting up 
 of hippuric acid, and is only found in the urine in connection with a 
 decomposition of this acid, and after eating freely of asparagus. 
 
 TYROSIN" (C H n NO.,) 
 
 has been found in the urinary sediment as fine needle-like crystals 
 collected into feathery masses. In alkaline solutions they often form 
 rosettes, composed of the fine needles arranged radially. On boiling 
 with Millon's reagent (see page 226), the fluid will become red. 
 
NITROGENOUS EXCRETORY SUBSTANCES. 269 
 
 Piria's Test for Tyrosin. — Gently warm with strong sulphuric 
 acid, add chloride of iron, a violet color will he produced if the crys- 
 tals are tyrosin. 
 
 It has, like leucin, hcen found in connection with acute yellow 
 atrophy of the liver, acute poisoning by phosphorus, leucocythsemia, 
 typhoid fever, small-pox, etc. 
 
 Clinical significance. — The appearance of leucin and tyrosin in 
 the urine is unquestionably indicative of a very marked interruption 
 in the metabolic processes of the body, and especially of the liver, and 
 is evidence of the great severity of the primary disease. 
 
 hippuric acid (C 9 H NO 3 ). 
 
 This substance is found in abundance in the urine of herbivora, but 
 in the human subject only 4.409 grains (0.35 grams) are excreted 
 daily. It crystallizes in the shape of fine needles or four-sided prisms. 
 It is soluble in 600 parts of cold water. Its quantity in the urine is 
 increased by eating plums, red whortleberries, bellberries, mulberries, 
 asparagus, and by taking benzoic acid, oil of bitter almonds, toluol, 
 cinnamonic acid, kinnic acid, etc. 
 
 It has also been found in abundance in the acute fevers, diabetes, 
 cholera, etc. 
 
 Clinical importance. — A vegetable diet appears to increase the for- 
 mation of this acid. From this and the fact that benzoic acid or the 
 benzoates have a tendency to increase this acid in the urine, it was at 
 one time much lauded as a specific for the uric acid diathesis. It 
 was, however, found of no special benefit, and if the reasons already 
 advanced be true in relation to the formation of urea and uric acid, 
 there is no physiological grounds for assuming that an increased for- 
 mation of hippuric acid is going to produce a change m the metabolic 
 action of the hepatic and renal cells in relation to the oxidation and 
 formation of the uric acid. 
 
 The use of benzoic acid and its compounds may be of service in con- 
 nection with alkaline urine, and has often been found a great aid in 
 cystic inflammations. 
 
 PHENOLIC ACID (C 6 H 6 0). 
 
 This acid only occurs in the urine. At one time it was regarded as 
 a normal constituent, but it is believed to be, more accurately speak- 
 ing, a product of decomposition. After carbolic acid poisoning it 
 has been found by several observers, while others have failed to detect 
 its presence. 
 
270 XITKot; K.Nols |\t liKTHHV Sl'BSTAN< is. 
 
 TAUKOCIIOLIC AND GLYCOCnOLIC ACIDS (C a(J IT 46 NSO,) 
 
 and (C f .H 4 ,N0.).1 
 
 These two are known by the common name of the biliary acids. 
 They are proteid compounds which have their origin in the liver, and 
 normally are poured into the alimentary tract with the bile. Here 
 they aid in digestion, and are again reabsorbed and reconverted either 
 by the hepatic cells or while in the blood. They may be found in 
 connection with icterus or an over-production of bile, with all acute 
 febrile diseases in which there is a marked blood poison, with acute 
 poisoning by antimony, copper, phosphorus, *and arsenic, and in acute 
 yellow atrophy of the liver. 
 
 Their principal clinical significance is that they can be found in the 
 urine a day or two in advance of the biliary pigments. They may 
 even be found when no pigment escapes. 
 
 The test for the bile acids or salts is Pettenkofer's, which is em- 
 ployed as follows: 
 
 Prepare a standard solution of cane sugar of the strength of one 
 part to four of distilled water. Add one minim (0.0G4 c.c.) of the 
 saccharated solution for every ounce (31.103 c.c.) of the suspected 
 sample, then a few minims of sulphuric acid; this will decompose the 
 bile acids, and be followed by the formation of cholic acid. If the 
 solution contain less than one five-hundredth of one per cent, no 
 further change will occur; if, on the other hand, there is more than 
 one five-hundredth of one per cent, the addition of a little more sul- 
 phuric acid will be followed, first by a cherry-red color, which soon 
 changes to a deep violet. 
 
 The bile acids have to be first precipitated and isolated before this 
 test can be applied, and for this reason it is not of practical value in 
 connection with urinary analysis. 
 
 Strassburgh's modification is applied to the urine as follows: Dip 
 a piece of filter paper into the fluid, and let it dry completely; put one 
 drop (0.064 c.c.) of sulphuric acid on the dried filter paper, and let 
 it run off; after a few seconds a deep violet color is developed, best 
 seen by transmitted light. 
 
 This, unfortunately, like Pettenkofer's and all its modifications, is 
 inaccurate and uncertain in urinary samples, and consequently devoid 
 of practical value. 
 
 Both tests also give nearly the same reaction with solutions contain- 
 ing albuminates, amyl alcohol, ethereal oils, olein, oleic acid, and the 
 salts of morphine and codeia. The only method of differentiation is 
 a spectroscopic examination. 
 
NITROGENOUS EXCRETORY SUBSTANCES. 271 
 
 INDOL (C 8 H 7 N), INDICAN (KC B H„NSOJ, AND INDIGO (C e E , N.,0 ). 
 
 These three substances are closely allied to each other. They are 
 supposed to originate as indol, which is developed by the liver, al- 
 though pancreatic fermentation has also been considered as the place 
 and means of its formation, while experimental investigation has 
 led to the belief that it only develops in the latter organ when bac- 
 teria are present, and that its development is due to their action. 
 
 There is no doubt but that indol is present in the alimentary canal, 
 and that some of it passes out with the fasces, and gives rise, in part at 
 least, to their peculiar odor. The remaining portion is absorbed with 
 the chyme, and appears in the urine as indican. Here it is estimated 
 by its conversion into indigo blue. 
 
 Among the coloring matters a similar substance was observed by 
 Heller, and named uroxanthine, but it has since been found to be 
 identical with indican. 
 
 Its presence can be detected by the method of Jaffe modified by 
 Senator. 
 
 Pour two drachms (7.775 c.c.) of urine into a test-tube, and add an 
 equal quantity of fuming hydrochloric acid, and then a concentrated 
 solution of chloride of lime, drop by drop, until a blue color is fully 
 developed. Shake the mixture with two drachms (7.775 c.c.) of 
 chloroform, which will sink to the bottom and be more or less deeply 
 tinged with indigo if indican be present. 
 
 The quantitative test of Jaffe is too complicated to be of any prac- 
 tical value. 
 
 Indican is said to be always present in normal urine, but in very 
 small quantities. By different observers it has been found to be in- 
 creased by a meat diet, carcinoma of the liver, cholera, cholera 
 morbus, diarrhoea originating in the small intestines, markedly in ob- 
 struction to the small, and slightly with obstruction to the large in- 
 testine, in Addison's disease, with nervous exhaustion, especially 
 affecting the spinal cord, in urina spastica, frequent coitus, onanism, 
 etc., and with every irritation to the urinary tract, nephritis, Bright's, 
 uraemia, typhoid and intermittent fever, etc. 
 
 Clinical significance. — From this large list of different conditions, 
 to which many others in all probability could be added, it is almost 
 impossible to draw any practical deduction, except that it indicates an 
 increased and possibly incomplete proteid metabolism. 
 
 It has been suggested as a means of diagnosticating lesions of the 
 small intestine or occlusion of its lumen; but since so many other con- 
 ditions produce a like result, much of its value is lost. If its quantity 
 
272 NITROGENOUS EXCRKTORY SUBSTANCES. 
 
 could be easily calculated, it might be an element in differentiation 
 between a lesion involving the large and small intestine; but, owing 
 to the time required and the uncertainty of the result, it can hardly 
 be considered as affording reliable proof in so acute a condition as ob- 
 struction to the lumen of the small intestine. Theoretically, it is a 
 very nice point of differential diagnosis, but, practically, the patient 
 might easily die before a positive result could be obtained. 
 
CHAPTER VI. 
 
 URATES, PHOSPHATES, AND CHLORIDES. 
 URATES. 
 
 The uric acid may be combined with soda, ammonia, potash, lime, 
 or magnesia, forming a urate. The urates of ammonia and soda are 
 the most common and may be either neutral or acid in reaction. 
 
 These salts occur in high-colored urine when the quantity is dimin- 
 ished and its density increased. 
 
 Such urine when first voided is clear, but on cooling becomes 
 cloudy or a decided deposit is developed. The sediment may be only 
 a faint cloud, or it may be nearly white, a deep pink, or a decided 
 reddish deposit. The latter, when abundant, is known as the brick- 
 dust deposit. 
 
 They are usually only deposited in acid urine, but may at times be 
 found in faintly alkaline samples. 
 
 The urates have to be distinguished from the phosphates and 
 albumin. 
 
 They are distinguished from the former by heat, which precipitates 
 the phosphates and dissolves the urates ; alkalies and the carbonates 
 also dissolve them, the reverse being true of the phosphates. 
 
 From albumin they are differentiated by heat and nitric acid, which 
 causes the urates to disappear and the albumin to be precipitated. 
 
 The white urates of children might be mistaken for the phosphates,, 
 but the above tests will at once decide the question. 
 
 Occasionally, when the urine is very concentrated and the urates 
 unusually abundant, they may be deposited almost as soon as they are 
 expelled; but, as a rule, the sample must cool before they make their 
 appearance. Normal urine at a very low temperature will generally- 
 deposit the urates. 
 
 There is no evidence that certain kinds of food increase their for- 
 mation, but incomplete digestion, absorption, and assimilation from 
 any cause which interferes with the perfect nitrogenous transformation 
 promotes their development to an unusual degree. 
 18 
 
274 PHOSPHATES. 
 
 They appear to be increased, no! bo much by a Large production of 
 uric acid, as by its incomplete formation. 
 
 In all forms of acute diseases, Buch as pneumonia, typhoid Eev< r, 
 and all conditions accompanied by increased bodily temperature, the 
 urates an' abundant. As the disease improves and the physiological 
 processes become more completely performed, they gradually decrease 
 in quantity. 
 
 The same is true in gout: during the attack they are abundant, as 
 the patient recovers they disappear. In gout, it matters little what 
 kind of diet is allowed, provided it is cut down to the limit of perfect 
 transformation and assimilation by the diseased system. This is the 
 explanation for the ready recovery of a gouty patient upon a purely 
 nitrogenous diet. In most cases, the rightly adjusted mixed diet will 
 afford the most satisfactory results. In other cases, the very j>resence 
 of the starches and sugars are the causes which prevent the perfect 
 proteid metabolism and retard recovery. In such a case, a purely 
 nitrogenous diet will produce a cure where the most judiciously selected 
 mixed or an exclusive non-nitrogenous diet would continually make the 
 disease worse. Consequently each case must be separately analyzed 
 and treated accordingly. 
 
 In the urine of children when teething, an abundant, white deposit 
 of the urate of ammonia is not of infrequent occurrence, and has often 
 been mistaken for a phosphatic deposit. 
 
 The urates are occasional^ found in excess after any severe mental 
 exertion, physical exercise, or profuse perspiration, and indicate only 
 a physiological change. 
 
 With organic disease of the viscera and especially the liver, or with 
 an incompletely performed gastric, intestinal, and hepatic digestion, 
 the urates appear in the urine in abundance. 
 
 Clinical signified nee. — From the above-enumerated causes and con- 
 ditions, only one conclusion can'.be deduced; which is, that the urates 
 •are only of importance when they are continuous, and in all cases 
 indicate an incomplete metabolic transformation of the proteids 
 which has chiefly to do with a faulty action on the part of the liver. 
 
 Treatment. — The most speedy and certain relief will follow a well- 
 regulated diet, plenty of out-door exercise and possibly the addition 
 of some of the numerous cholagogue tonics. 
 
 PHOSPHATES. 
 
 These salts occur in pale urine of alkaline reaction and diminished 
 density. The phosphoric acid is combined with soda, lime, or mag- 
 
PHOSPHATES. 275 
 
 nesia, forming a phosphate. The two former may be combined in 
 such a way as to form an acid or alkaline salt. 
 
 Heat,. when applied to faintly acid urine, will drive off tin; carbon 
 dioxide (C0 2 ), and if the phosphates are present in abundance the fluid 
 will become turbid. Such samples may be mistaken for those con- 
 taining albumin, but one drop of nitric acid will dissolve the salts and 
 cause an albuminous precipitate to become more apparent. In this 
 way the two can at once be distinguished from each other. 
 
 Heat precipitates the phosphates, but causes the deposit of urates 
 to disappear. The phosphates occur after alkaline fermentation has 
 been developed. The urine may be cloudy, when first voided, from 
 the presence of the phosphates. 
 
 Clinical importance. — The phosphate of soda and potassa are always 
 in solution, but the phosphate of lime may form an amorphous or 
 crystalline deposit. The phosphate of magnesia may also form a 
 crystalline deposit. 
 
 The phosphates are derived both fronTythe food and the metamor- 
 photic changes going on in the body. During the early stage of all 
 inflammatory conditions while the exudation is being poured out, they 
 are decreased in the urine, but after this stage they progressively 
 increase, and with the subsidence of the process they decrease to the 
 normal standard. The same phenomenon is noticeable in connection 
 with all acute febrile conditions. In meningitis, the same disappear- 
 ance, rise, and fall has been observed. A similar change has been sup- 
 posed to occur in connection with excessive mental strains and in 
 certain forms of indigestion. But as yet no very definite clinical data 
 are to be derived from the study of these ingredients. In relation to 
 the above-named inflammatory conditions and acute diseases, the 
 chlorides bear about the same relation, and being more easily esti- 
 mated yield all the practical information required. 
 
 With a highly vegetable diet, with injuries to the spine, in mania 
 and with many nervous disorders, as well as in elderly people, the 
 hepatic functions will be incompletely performed. With such con- 
 ditions there is apt to be an incomplete formation of uric acid and 
 consequently a fall in the acidity and apparent increase of the phos- 
 phates in the urine. In fact, the urine may become continuously 
 alkaline, the deposition of the phosphates persistent, and a formation 
 of a phosphatic calculus almost certain. It is of importance to recog- 
 nize this condition, as the treatment depends wholly upon the property 
 of forming uric acid, and every measure should be instituted that will 
 increase the total quantity of this acid formed. 
 
 An opposite condition or over-acidity may give rise to alkaline urine 
 
276 0HLOBIDE8. 
 
 and a deposition of the phosphates. This is brought about by the 
 over-prodnction of uric acid which irritates the genito-urinary tract, 
 excites a decomposition of the urine, alkaline fermentation, and the 
 precipitation, of the phosphates. With this variety the urine will pre- 
 viously have been highly acid. 
 
 The treatment for this is directly opposite to that for the previous 
 condition. The production of the uric acid must be decreased. 
 
 The urinary symptoms being nearly the same, a close study of the 
 clinical symptoms and the digestive processes in general are absolutely 
 essential for a differential diagnosis between the two. 
 
 With obstructive lesions to the urinary tract, with partial retention 
 and alkaline fermentation, the same alkaline urine with a phosphatic 
 deposit will be observed. Here the condition is, more strictly speak- 
 ing, a local one, and has to be treated as such, and when treated in con- 
 nection with a regulated diet the difficulty is soon relieved. 
 
 CHLORIDES. 
 
 Chlorine is found in the urine combined with potassium, ammonium, 
 and sodium. The last, however, is the salt of special interest. 
 
 A nitrate of silver solution is the most practical for both quantita- 
 tive and qualitative analysis. 
 
 Liebig's volumetric process with a solution of nitrate of mercury, 
 or Mohr's with nitrate of silver, are undoubtedly the most accurate 
 tests, but too complicated to become generally useful. 
 
 For a complete description of those tests the reader is referred to 
 more extended works. 
 
 For practical work, a standard nitrate of silver solution is made 
 by adding one part of nitrate of silver to eight parts of distilled 
 water. 
 
 Before testing for the chlorides, the urine should be acidulated with 
 a few drops of nitric acid to prevent the precipitation of the phosphates 
 which otherwise would occur. 
 
 Add one minim of the silver solution to the sample of urine to be 
 tested. If the suspected solution still remains clear and transparent, 
 it indicates the total absence of the chlorides. 
 
 If the solution becomes generally, but only slightly turbid, it indi- 
 cates the presence of one-tenth of one per cent of the chlorides. 
 
 If cheesy lumps are deposited and the supernatant fluid and pre- 
 cipitate remain unchanged, the chlorides are present in quantities 
 ranging from one-half to one per cent. 
 
 The normal amount of chloride of sodium discharged in the urine, 
 
CHLORIDES. 277 
 
 admitting that 200 grains (12.959 gram) are eliminated daily in 50 
 ounces (1555.174 c.c.), would be a fraction over one-tenth of one per 
 cent. Consequently the slightest increase or decrease will he readily 
 appreciated by the above solution. If we allow a smaller quantity than 
 normal, there is apt to be a precipitate, for then the quantity remain- 
 ing is sufficient to cause a cloud. 
 
 The chlorides, like all other normal ingredients of the urine, are 
 subject to wide variations dependent upon the quantity taken into the 
 system daily and the amount of water eliminated. 
 
 In health, the taking of an excess of the chloride of sodium is not 
 indicated by its increase in the urine for several days, and after its use 
 is discontinued it takes several days for it to disappear, hence an accu- 
 mulative action is observed. This, however, does not appear to be the 
 case in disease. 
 
 Fortunately for this test, the urine is usually decreased in quantity 
 which readily renders the increase in the chlorides very apparent. 
 
 If fifty ounces (1555.174 c.c.) be taken as the standard daily secre- 
 tion of urine, it will be easy to compute the comparative quantity of 
 solids present, by evaporating down the whole amount if it exceeds 
 that number, or by diluting it with distilled water if it has a less 
 volume. 
 
 Clinical significance. — In all acute inflammatory processes where 
 there is a marked fibro-plastic or serous exudation, the inflammatory 
 deposit is usually found to contain an abundance of the chlorides, 
 phosphates, and carbonates, and at the same time they are deficient 
 or absent in the urine. 
 
 The diseases in which they are especially important are pneumonia, 
 typhoid fever, pleurisy with effusion, cholera, and in fact in all acute 
 febrile conditions, especially if there is much exudation. Their reap- 
 pearance in the urine is always indicative of improvement or of the 
 reabsorption of the inflammatory exudation, other things being equal, 
 and often tells of approaching recovery when all the clinical symp- 
 toms remain apparently unchanged. 
 
 If, on the other hand, after returning in the urine they should sud- 
 denly disappear or become greatly diminished in quantity, while the 
 clinical symptoms apparently remain about the same, it is always a 
 bad omen and indicates an exacerbation, due to an extension or the 
 development of a new inflammation, and renders the prognosis un- 
 favorable. 
 
 Consequently, by a daily examination for the chlorides in severe 
 cases of pneumonia, where the patient is too feeble for a satisfactory 
 physical examination, valuable information may be obtained, and it 
 
278 CHLORIDES. 
 
 will enable the attendant to prognosticate and treat the ease more in- 
 telligently. 
 
 One very import ant fact to be remembered is, that the physician often 
 is not called to see the case until the height of the inflammatory pro- 
 cess has been reached, and therefore there will be no time when the 
 chloride of sodium is absent from the urine, for it has already begun 
 to be reabsorbed and eliminated. 
 
 The most important clinical fact is, as to whether it continues until 
 the marked rational symptoms indicative of recovery have been 
 developed. By observing these conditions, the physician can always 
 he in advance of the ordinary symptoms with his treatment. 
 
 The examination for the chlorides is most important in pneumonia, 
 on account of the extensive exudation, but should not be neglected in 
 any severe or acute inflammatory disease. 
 
 A peculiar cloudiness spontaneously forming in the urine, in cases 
 of severe fevers, has by some observers been found to indicate an almost 
 certain restoration to perfect recovery. Although unexplained by 
 them, it is probably due to the abundant reappearance of the urates, 
 phosphates, and chlorides. 
 
CHAPTER VIL 
 
 ADVENTITIOUS COLORING-MATTERS; BILE PIGMENT; FAT; 
 MUCUS; BLOOD OR HEMOGLOBIN. 
 
 ADVENTITIOUS COLORING-MATTERS. 
 
 Under this beading, a large number of substances will be mentioned, 
 most of which have been considered at some time as the true coloring- 
 matter of the urine, while a few have been classed as derived pigments. 
 Their large number and diverse nature will at once show the un- 
 certainty existing in the minds of the chemists as to the true coloring- 
 principle of urine. 
 
 They are: 1st, the urochrome (Thudichum); 2d, indigo, of which 
 there are three varieties described: the white, red, and blue. The 
 white form is also called, 3d, indican (Shunk) or, 4th, uroxanthiri 
 (Heller); it is capable of being converted into red indigo or, 6th, 
 urrhodin (Heller), or into blue indigo; 7th, indigotin or, 8th, uro- 
 glancin (Heller); 9th, urohematin (Harley and Scherer); 10th, uro- 
 bilin (JafE); 11th, hydrobilirubin (Maly); 12th, purpurin (Bird and 
 Prout); 13th, uroerythin (Heller, Bird, and Prout); 14th, urophoepne 
 (Heller and Ziegler); 15th, urian (Shunk); 16th, urianin (Shunk); 
 17th, uromatin (Harley); 18th, cyanourin (Braconnot); 19th, urrho- 
 dinogen (Thudichum); 20th, uromelanin (Thudichum); 21st, uropit- 
 tin (Thudichum); 23d, chromogen (Thudichum); 23d, urosin; 24th, 
 urosacin; 25th, hemophin; 26th, melanogen. 
 
 Many of these are synonyms, the same or an almost identical sub- 
 stance having been discovered at about the same time and inde- 
 pendently named by each discoverer. Many others are derivatives 
 from some more fixed pigment. 
 
 The three of importance are uroliEematin, urochrome, and the 
 indigo forms. The former is unquestionably the primary source of 
 a large number of this list, which under different analyses have 
 yielded a slight difference in the atomic formulas. TTrohamiatin or 
 urochrome — the latter name being preferable — is, in all probability, 
 
280 ADVENTITIOUS COLORING-MATTERS. 
 
 derived directly from the coloring-mutter of the blood, and is the sub- 
 stance which gives its peculiar yellow color to the normal urine. 
 
 The tests for these substances are based upon colors or shades of 
 color, or on extended chemical analysis, both being impracticable in 
 general medicine. 
 
 Indican as a coloring-matter has been found to be increased in the 
 urine in such a wide range of diseased conditions, and its detection 
 and quantitative analysis are so uncertain, as to render its presence 
 or absence of little practical importance (see page 271). 
 
 CI i>iival significance. — The dark, reddish-yellow color of the urine 
 with all forms of fevers is ascribed by Heller to uroerythin and an in- 
 crease in the normal coloring-matter, but there is some doubt about 
 uroerythin being a special coloring-substance developed as the result of 
 disease; it appears more likely to be a derivative of urohaematin, and 
 the color of the urine and its variation in disease is better explained 
 under the haematoglobinuria theory, which may cause a number of 
 slightly different pigments to be discharged, as a result of the rapid 
 destruction of the haemoglobin. 
 
 BILE PIGMENTS IN URINE. 
 
 The biliary coloring matters are the only other pigments of real im- 
 portance. They give to the urine varying shades of color from brown- 
 to green. 
 
 The test for them is G-melin's bile, or the nitro-nitrosic acid test. 
 It is employed as follows: place some of the suspected urine on a clean 
 white porcelain dish, then add a few drops of nitric acid containing 
 a good proportion of nitrous acid until the two run together. Kadi- 
 ating from the point of contact, there will be observed the following 
 play of colors, green, blue, violet, red, and last a dirty yellow. 
 
 If biliverdin only be present, the green is absent, and the play of 
 colors will then be blue, violet, red, and dingy yellow. 
 
 Briick's test is as follows: Pour the suspected urine on a white por- 
 celain plate, add a few drops of dilute nitric acid, and then some 
 strong sulphuric acid instead of the nitrous acid. The same play of 
 colors will be the result. A test-tube can be used instead of the plate 
 if found more convenient. The contrast of colors, however, will not 
 be so striking as is the case with a white background. 
 
 The fluid should be absolutely free from alcohol, as this will cause an 
 abundant formation of nitrous acid, and the same color rings, even in 
 the absence of bile pigment. 
 
 Indican in the urine may lead to an error, but by making sure that 
 the green, blue, violet, and red are all present in regular order, no 
 
ADVENTITIOUS COLOKING-MATTER8. 281 
 
 mistake will be made, for the indican only produces green and yellow 
 zones under the same circumstances. 
 
 In cases of long-continued high temperature, bile pigments may be 
 present in the urine, and yet not respond to the tests; the reason for 
 this has not been explained. 
 
 In such instances, if it is necessary to determine the presence of 
 bile, Huppert's method may be used; this is as follows: Precipitate 
 the urine with milk of lime, and filter. Take a piece of the precipi- 
 tate, of the size of a hazel-nut, and place it in a test-tube, and fill the 
 tube half full of alcohol, add sulphuric acid until it retains an acid 
 reaction after shaking. Warm this fluid, and the color will be ex- 
 tracted from the precipitate; filter and boil the filtrate. If bilirubin 
 is present in the urine, it will combine with lime and be precipitated; 
 the acid will set it free, and it will be dissolved by the alcohol, form- 
 ing a yellowish-green solution. The more acid the quicker the re- 
 isponse. Long boiling may produce a blue color. 
 
 Why this reaction is not due to the alcohol as in the other case is 
 not explained, and possibly this may be the source of the reaction and 
 not the biliary pigments. 
 
 Many oxidizing agents will produce various shades of green when 
 applied to urine containing bile pigment. Iodine and atmospheric 
 air produce a grass-green. A pure caustic potash solution, strength 
 one part to three of water added to urine, with an excess of hydro- 
 chloric acid, will produce an emerald green color if bile pigment be 
 present. (Ultzman's test.) 
 
 Clinical significance. — Bile pigment may be found in the urine in 
 a very large number of diseases, viz., obstruction to the ductus com- 
 munis choledochus or its hepatic tributaries from any cause, and in 
 cases without obstruction, such as poisoning by the various severe 
 fevers in which jaundice is a common symptom. It is also observed 
 in yellow, malarial, and relapsing fevers; and with typhus, some cases 
 of typhoid, scarlatina, small-pox, acute yellow atrophy of the liver, 
 epidemic jaundice, and pneumonia; also with animal poisons, such as 
 pyasmia, septicaemia, puerperal fever, rabies, snake bites, etc.; and 
 again in connection with poisoning by the minerals, phosphorus, mer- 
 cury, copper, antimony, and with chloroform and ether, and after 
 severe mental emotions, fright, anxiety; concussion of the brain, 
 asphyxia, excessive production of bile, congestion of the liver, etc. 
 
 Grm elm's test is unquestionably the most practical, but from the 
 large range of conditions giving rise to the appearance of bile pig- 
 ments in the urine, little practical importance can be attached to it. 
 
 The presence of bile pigment in the urine, however, may be said 
 
282 
 
 MUCUS. 
 
 to be indicative of one of three things: an occlusion of the bile ducts r 
 an over-production, or an inability on bhe part of the system to com- 
 pletely reconvert tin- constantly reabsorbed pigment. 
 
 In functional derangements of the liver, it is quite important to 
 know whether there is a deficient or an over-production of bile, and 
 the presence or absence of these pigments may be turned to accoun 
 in helping to decide the question. 
 
 AVhen there is a deficient production both in quantity and quality, 
 bile pigment will not be apt to appear in the urine, but with over- 
 production it is quite likely to be found. 
 
 FATTY MATTERS. 
 
 Fat is rarely seen in the urine except in cases of chyluria. Acci- 
 dental cases, however, are excepted, for it is not uncommon that the 
 specimen brought to the examiner is in a dirty bottle, which has 
 contained some oily matter. 
 
 Test for fat. — Agitate fresh urine with an equal volume of sulphuric 
 ether in a narrow cylinder, and let the mixture stand for twelve or 
 twenty-four hours. It will separate into three parts, a superior of 
 ether, and an inferior of urine, while between the two there will be a 
 thin yellow oil} T layer. The sample, which previously was milky, will 
 become perfectly clear. This oily layer may be siphoned or decanted 
 off. 
 
 Evaporate the ether from the fluid removed, and the result will be 
 little yellow globules looking like butter, and often having a rancid 
 odor. This fatty material, on the application of a gentle heat, will 
 melt into a yellow oil which slowly solidifies on cooling. 
 
 Fat occurs in the urine as the result of epithelial disintegration 
 in some forms of chronic renal disease, but even then it only occurs 
 in microscopic quantities. 
 
 MUCUS. 
 
 This substance usually occurs in the normal state as a faint and in- 
 distinct cloud after the urine has stood a few hours. It is most 
 abundant near the bottom of the fluid and especially in the urine of 
 the female. 
 
 The chemical test for mucus is to add acetic acid drop by drop un- 
 til fine fibrillated bands of mucus, which are often tortuous in out- 
 line, begin to fall. 
 
 By adding a little iodine or iodide of potash with the acetic acid, 
 
BLOOD HAEMOGLOBIN. 283 
 
 these delicate bands of mucus which are thrown down are rendered 
 more visible. 
 
 Tartaric acid and very weak solutions of the mineral acids wiil give 
 the same reaction. The precipitate in all cases is dissolved by an 
 excess. 
 
 These tests are rather uncertain. The cloud which is seen to form 
 in the fluid is quite as certain evidence of the presence of mucus. 
 
 Clinical significance. — Continued irritation of the urinary tract 
 without inflammation and the formation of pus will often increase the 
 mucus to an easily perceptible amount. Usually, however, the in- 
 creased quantity is associated with an inflammatory condition and the 
 more or less abundant formation of pus. 
 
 "With such conditions as a urethritis, catarrh of the bladder, cystitis, 
 ureteritis or pyelitis, the mucus is often very abundant, forming large 
 and tenacious ropy strings in the urine. It is also present in large 
 quantities in cases of metritis and vaginitis. 
 
 BLOOD HAEMOGLOBIN. 
 
 It sometimes happens that after a hemorrhage from the urinary 
 tract the corpuscles are dissolved and cannot be found by microscopic 
 examination. In hemoglobinuria, few if any corpuscles are found. 
 In such cases it may be necessary to employ a chemical test for the 
 detection of the presence of blood. The guaiac or Heller's test may be 
 used. 
 
 The guaiac test is employed as follows: Add a few drops of the 
 tincture of guaiacum to a small quantity of urine in a test tube; then 
 add about as much ozonized ether (a solution of peroxide of hydrogen 
 in ether) as there is urine. If blood-coloring matter be present, a sap- 
 phire blue color will be produced. 
 
 Another method is to add equal parts of tincture of guaiacum and 
 oil of turpentine in a test-tube to an equal volume of urine; if blood 
 be present a deep blue color is produced. 
 
 Heller's test. — The urine is rendered alkaline with liquor potassa or 
 soda, heated to the boiling point, and set aside. The precipitated 
 phosphates are of a greenish or reddish color if the blood-coloring mat- 
 ter, haemoglobin, be present. 
 
 Spectroscopic examination, however, is the only certain method by 
 which the presence of the blood-coloring matter can be detected, but 
 this is not convenient for ordinary use. 
 
 Clinical significance. — The appearance of dissolved blood-corpuscles 
 or soluble haemoglobin in the blood is found chiefly in hemoglobinuria 
 
L K4 BLOOD HAEMOGLOBIN. 
 
 and is only of importance in such cases. If its presence could be 
 easily ascertained, and if present in minute quantities, it might be of 
 ureat service in all cases of high-colored urine in showing whether 
 the color represented blood destruction or was due to some other 
 cause. 
 
OHAPTEK VIII. 
 
 HOW TO USE THE MICROSCOPE; RED BLOOD-CORPUSCLES; 
 LEUCOCYTES; MUCUS. 
 
 How to use the microscope and mount samples. — The instrument 
 should have a solid base, and be placed upon a firm, but rather low 
 table. The direct rays of the sun should not be used for illumination. 
 A north light is generally considered the best. If good daylight is not 
 to be obtained, a small kerosene hand lamp will answer sufficiently 
 well. A student's lamp will give a very perfect light. 
 
 It is always best to look through the instrument with both eyes 
 open; at first this will be impossible, but a little practice will soon 
 overcome the difficulty. 
 
 Of the two reflecting mirrors, the concave is the one most used in 
 urinary examinations. 
 
 The best combination for urinary work is a good f inch objective 
 which will magnify the object from 60 to 100 times; and a good ^ or £ 
 objective which will magnify the object from 250 to 400 times. With 
 these lenses a medium eye-piece should be used. 
 
 Every instrument should be furnished with a ' ' nose-piece," a brass 
 attachment which is screwed into the end of the barrel and carries two 
 or more lenses on a revolving arm. By it the lenses can be shifted 
 almost instantaneously, and in this way much time is saved. A gen- 
 eral survey should be made with the low power and then the special 
 object resolved with the high power. 
 
 The first thing to be acquired in using the microscope is to learn 
 how to arrange the mirror so as to get the direct reflection of the 
 light through the lens, tube, and eye-piece. This is accomplished by 
 shifting the mirror until the right angle is obtained. 
 
 The next step is to learn how to focus the instrument upon the ob- 
 ject to be examined. As the working distance between the face of 
 the lens and the cover glass is only a small fraction of an inch, consid- 
 erable difficulty is often experienced by the beginner. 
 
 The object having been mounted and placed on the stage, the barrel 
 is caused to descend until the objective is brought nearly down to the 
 
286 BOW TO D8E THE MICROSCOPE. 
 
 cover. The examiner now looks through bhe eye-piece and gradually 
 Lowers the barrel, at the same time following it down with his eye un- 
 til blurred objects commence to appear in the sample. TheD by 
 changing from the coarse to the fine adjustment a few turns of the 
 latter one way or the other, as may be required, will bring the object 
 distinctly into focus; at the same time the slide is held or moved at 
 will witli the opposite hand until every object has been completely 
 studied. This rule should invariably be adopted: with one hand 
 keep the fine adjustment screw in motion so that every part may be 
 accurately focussed; at the same time keep moving the slide until every 
 part under the cover glass has been brought into the field of vision. 
 In this way a thorough analysis of the sample is made. 
 
 Urinary sediments are usually most abundant near the margin of 
 the cover-glass. If there is danger of missing the objects sought after, 
 a strip of tissue or filter paper may be laid at the edge of the cover on 
 one side, which will cause a current and float the solid particles over 
 to that edge of the cover, when they can easily be found. 
 
 The next step is to mount the object. The necessary implements 
 are slides, cover glasses or circles, pipettes, and a pair of small 
 forceps. 
 
 The cover glasses should be thin and scrupulously clean. A 4$ 
 solution of acetic acid will be found the best liquid to remove all 
 grease and by rubbing with a silk handkerchief, old linen, or tissue 
 paper, they can be rendered very free from dirt. After cleansing, 
 they should be handled with the forceps, or by their edge only if the 
 lingers are to be used. Finger marks on the surface arc seen as 
 foreign objects. 
 
 The best pipettes are made from quarter-inch glass tubing, which 
 should be cut at right angles at both ends and never pointed. A 
 square end pipette is much better than a tapering extremity, for the 
 reason that there is a much larger space to draw the sediment through. 
 The length of the tubes may vary from six to ten inches (15 to 25 cen- 
 timetres;. For crystals and heavy deposits, one finger is placed over 
 one end of the pipette, while the free extremity is passed to the bottom 
 of the vessel containing the sediment, and then the finger closing the 
 opposite end is quickly removed. The finger is then replaced and the 
 pipette and its contents quickly withdrawn from the fluid. By this 
 method the solids are caused to run rapidly up into the lumen of the 
 tube in considerable quantities. One or two drops should be allowed 
 to escape and then one should be secured on a perfectly clean slide. 
 The main object is to gauge the drop so that it will be just covered by 
 the circle used and none allowed to flow outside. If there is too much, 
 
BL00D-00EPU8CLES. 287 
 
 the cover glass may float and be kept in constant motion, or all the 
 sediment washed out. Too small a drop is preferable to an unduly 
 large one. 
 
 The circle should now be placed over the sample. This is best 
 accomplished by seizing one edge with the forceps; thou place the 
 under side of the opposite edge first on the slide near the drop, then 
 bring it in contact with the urine, followed by a sliding motion so 
 that the under surface of the cover may be moistened. Then 
 gradually let down the side held by the forceps. By following this 
 rule, the formation of air-bubbles under the circle is prevented. The 
 specimen is now ready for examination. 
 
 If casts are to be looked for, the pipette is used in the same manner 
 as before, with this exception, viz., instead of going deep into the 
 deposit, the introduced end should be stopped just at the superior 
 border or a little above the sediment, and, instead of letting the fluid 
 rush in rapidly, the finger should be removed cautiously so that the 
 sample will run in gradually. By moving the tube around, the ex- 
 aminer can often skim off the top of the solid portion. It should be 
 mounted as before. The reason for this method is that casts, being 
 lighter than the other solid ingredients, collect on the top of the ap- 
 parent sediment, where they are most abundant and consequently 
 they are more likely to be secured at this point. 
 
 A failure to observe this important rule in many samples contain- 
 ing large numbers of casts results in their being overlooked and 
 reported by the examiner as absent. Eepeated trials should be made 
 before saying that casts are or are not present. 
 
 Never return the contents of the pipette to the sample under exam- 
 ination, as it will stir up the sediment and prevent any further satis- 
 factory search until several hours have elapsed. 
 
 BLOOD-COEPUSCLES. 
 
 The red blood-disks only will be dealt with at this time. Under 
 the microscope the normal corpuscle will be found to be perfectly 
 round, and very faintly tinged with yellow by their contained hae- 
 moglobin. If only one disk be present in the field, it is at first hard 
 to recognize or to distinguish any color, but concentration and com- 
 parison with other objects will usually enable the examiner to appre- 
 ciate its presence. If a number are collected together, the color is 
 quite apparent, and if abundant, a distinctly reddish tint is plainly 
 seen. Their average diameter is ¥ ^Vo °^ an incn > 6.9 mmm. The 
 red disk is biconcave and consequently is thicker toward the periphery 
 than at the centre or free margin. The result is that it has two focal 
 
288 
 
 HOW TO USB THE MK'KOSCOPE. 
 
 centres. When the rim is in exact focus, the centre appears as a dark 
 spot surrounded by a light zone which in turn is encircled by a dark 
 ring representing the thin margin. When the centre is in exact focus, 
 
 Fig. 56.— Blood-Corpuscles as seen with the Square Ocular Micrometer (Keyes). 
 
 it will be light and transparent, surrounded by a single broad and 
 dark band of considerable width. This peculiar optical property has 
 led occasional observers to believe that the red corpuscles contained a 
 
 Fig. 57.— Human Blood-Corpuscles. 
 
 a, Globules showing double contour; 6, globules turned on edge; c, the same in rouleaux, like 
 coin. Highly magnified tRollett). 
 
 nucleus, which, however, is not true, but is a microscopic delusion. 
 By exciting a current in the fluid while looking at them, they will be 
 seen to turn on their edges, when their biconcavity becomes more 
 
BLOOD. 
 
 289 
 
 easily apjireciated. Wlien very abundant, they sometimes adhere 
 together by their flat surfaces like rolls of coins and are known as rou- 
 leaux. 
 
 In urine, they are likely to undergo destructive changes and become 
 altered in character. It" the watery element of. the urine is abundant, 
 the haemoglobin will absorb it and cause the corpuscles to swell, 
 become spherical, lose their color, and finally disappear altogether. 
 Just before dissolution they often appear like rings or shells (Fig. 58, 
 b). Strong alkalinity of the urine produces alike result. If deprived 
 of their water, they become shrivelled and shrink, forming irregular 
 star-shaped or crenated disks. After having undergone this transfor- 
 mation, they are hard to recognize by those not familiar with this 
 change. The red corpuscles sometimes undergo slight amoeboid 
 movements. 
 
 Fig. 58. — Human Red Blood-Globules. 
 
 a, With haemoglobin; b, without haemoglobin. 
 
 Highly magnified (Rollett). 
 
 . 59.— Human Blood-Corpuscles 
 
 Crenated. 
 Highly magnified (Rollett). 
 
 Clinical significance. — Blood-corpuscles may be found in the urine 
 after any operations on and in the immediate vicinity of the genito- 
 urinary tract. They may occur with urethral stricture or stone, cal- 
 culi in the bladder, ureters, or pelves of the kidneys. Also with in- 
 flammation of the urethra, bladder, ureters, or renal pelves and 
 kidneys; and with villous, sarcomatous, or carcinomatous tumors of 
 the bladder. 
 
 Blood in the urine is also found in cancer, sarcoma, and tubercle of 
 the kidneys, suppurative nephritis, irritation by crystals in the kidneys, 
 acute diffuse nephritis, and in some of the other forms of nephritis; in. 
 purpura hemorrhagica, scorbutus, scurvy, pernicious anaemia, leuco- 
 cythaemia, eruptive fevers, yellow fever, continued and malarial 
 fevers, acute and chronic congestion, injury with or without rupture 
 of the renal tissue or urinary tract, emboli, thrombosis, and infarc- 
 19 
 
L".Mi LEUCOCYTES. 
 
 tion of the renal vessels, phthisis, wasting diseases, and parasites of 
 the kidneys. 
 
 In females, it is found during menstruation, pregnancy, and in con- 
 nection with uterine diseases. 
 
 Certain irritative medicines, viz., turpentine, cantharides, squills, 
 and all irritating diuretics will cause it. 
 
 Some consider blood in the urine quite diagnostic of certain forms 
 of chronic kidney lesions; but experience has shown it to be present 
 occasionally in all forms. 
 
 From this very long list of causes for blood in the urine, there are 
 few, if any, cases in which its origin can be positively stated. 
 
 If blood casts are found in the sample, it is positive evidence that 
 some of the blood came from the kidneys. "With severe injuries and 
 symptoms of injury to the kidneys, the presence of blood in the urine 
 would strengthen the diagnosis of rupture of the organ. But hemor- 
 rhage may occur after injury and no laceration be found at the ne- 
 cropsy. 
 
 Clots of blood indicate external hemorrhage or blood from the ure- 
 thra or bladder. 
 
 LEUCOCYTES. 
 
 This term, for convenience and the inability to differentiate be- 
 tween the white blood- cell, a mucus, and a pus 
 <$£=* m corpuscle, is applied to all. 
 
 /s^\ When they are examined m an indifferent fluid, 
 
 | the following appearances will be observed: 
 
 €1 (^ The white blood-corpuscle is a round granular 
 
 Fig. 60. - Ordinary body from ^ttW to -^Vo of an inch (10 to 8 mmm.) 
 
 Appearance of Pus. •' d u « u . a u u \ ^ / 
 
 in diameter, m which the nucleus is faintly visible. 
 
 The mucus-corpuscle is about the same size, and has a granular 
 appearance and a little more distinct nucleus. 
 
 The pus-corpuscle also has about the same size and appearance; if 
 any difference exists, it is a little more granular. 
 
 The differences, if any, may be stated as follows: 
 
 1. White Mood-corpuscles, nucleus least distinct. 
 
 2. Mucus-corpuscles, nucleus most distinct. 
 
 3. Pus-corpuscles, granular appearance most distinct. 
 
 These variations are more theoretical than real. Even under the 
 most favorable circumstances it requires a skilled observer to appreci- 
 ate these fine points of distinction. "Withdraw the favorable condi- 
 tions, and replace them by the opposite and also degenerative changes 
 
LEUCOCYTES. 
 
 291 
 
 to which they are constantly subject, and it becomes absolutely 
 impossible to tell one from the other. 
 
 Some observers go so far as to say that there are marked differ- 
 ences in the same kind by which varying grades of constitutions can 
 be detected, and an accurate diagnosis and prognosis established. 
 This, however, seems impossible from the great difficulty to isolate 
 such cells normally, and the many retrograde changes they are likely 
 to undergo from the time of development to the time of examination. 
 
 All that can be said with any degree of certainty when they are 
 found in the urine is that there is a catarrhal or inflammatory condi- 
 
 Fig. 61.— Pus in Various Stages of Development. 
 
 tion of the genito-urinary tract, or that the contents of a pus basin 
 have found their way into the sample of urine under examination. 
 
 When any of these corpuscles are in aqueous solutions, they tend to 
 imbibe the water, swell up, and become less granular, or even trans- 
 parent. In too concentrated solutions, they give up their water and 
 shrink. 
 
 In the former case, the nuclei will be a little more transparent; in 
 the latter, they are still more difficult to find. 
 
 If they are acted upon by acetic acid, the granules tend to leave the 
 body of the protoplasm and accumulate in the nucleus. This causes 
 an opacity of the nuclei and clearness of the remaining portion, so 
 that the nuclei now stand out in bold relief. The number of nuclei 
 
392 muous. 
 
 will depend upon the rapidity and incompleteness of their develop- 
 ment. If the formation has been slow and as near perfect as pos- 
 sible, not more than two nuclei will be found, but with a more rapid 
 production, three,, four, five, six, or more will make their appearance, 
 and be found in one protoplasmic mass. This reaction of pus-cells 
 with aortic acid is very marked, and confirms the diagnosis. 
 
 The many changes in the reaction of the urine are a fruitful source 
 for variation in these corpuscular elements. From hour to hour they 
 may undergo changes which will materially alter their general char- 
 acter. 
 
 Frequent expectoration into the chamber is not an uncommon 
 cause for leucocytes of the mucus variety in the urine. 
 
 These white corpuscles often exhibit marked amoeboid movements. 
 
 Leucocytes may be found in the urine in quantities varying from 
 ODe to hundreds to each slide examined. 
 
 6 
 
 Fig. 62.— Highly Magnified Leucocytes. 
 a. Putting out processes; 6, having withdrawn processes (Rollett). 
 
 Clinical significance. — Their presence indicates a gonorrhoea, gleet 
 stricture of the urethra, prostatitis, prostatic abscess, catarrh of the 
 bladder, tumors, pyelitis, pyelonephrosis, cancer and tuberculosis of 
 the kidneys, also renal calculi. 
 
 In large quantities they are indicative of a cystitis, pyelitis, or a 
 pyelonephrosis. 
 
 In the female, they may come from the vagina or uterus. 
 
 MUCUS. 
 
 This substance is very frequently seen in microscopic examinations 
 of urinary samples, and, on account of the frequency with which it is 
 confounded with casts, it is of no little importance. 
 
 It usually occurs as delicate films or streaks, which may run more 
 
mucus. 293 
 
 than across the field of vision. Their outlines are more or less irregu- 
 lar, and at places almost invisible. By following one of these bands 
 along its course, it will often be found to terminate in an irregular 
 mass of mucus. This in itself would distinguish it from a cast. In 
 other cases, its ends become more and more irregular and ragged, and 
 are ultimately lost in the fluid. Their exact point of termination is 
 often indefinitely marked. 
 
 By some writers, mucus casts or plugs are described and said to 
 come from the renal and seminal tubules and the follicles of the pros- 
 tate gland. 
 
 They are described as long mucus plugs which are often branched, 
 and when they are generated in the seminal tubes are said to have 
 associated with them spermatozoa. This peculiar formation, as ordi- 
 narily represented by Whittaker's plates, has never been observed by 
 the author. 
 
CHAPTEE IX. 
 
 URIC ACID, OXALATES, URATES, PHOSPHATES, MICROSCOPIC 
 
 PIGMENTS. 
 
 UEIC ACID. 
 
 AVhen absolutely pure, this acid is a crystalline substance without 
 color. The crystals are of many shapes and compound forms. They 
 may be rhombic, lozenge, spindle, barrel, or even dumb-bell in shape, 
 or they may form tables, prisms, and long and short rods. They may 
 also be deposited as stars, or by an aggregation of some of the simple 
 
 
 <&> 
 
 Fig. 63.— Irregular and Dumb-bell Crystal Fig. 64. — Irregular Forms of Uric Acid 
 
 op Uric Acid. Crystals. 
 
 varieties develop into stars, bundles, or even balls and spikes, or spiked 
 crystals. 
 
 Their distinguishing feature in the urine is that they are almost 
 always colored. It may be only a faint yellow tint, but the rule is a 
 decided reddish or brown shade. 
 
 The crystals may be easily recognized by the naked eye, but under 
 ordinary circumstances the color is clear and decided, making them 
 easy of recognition. There is nothing else in the urine that they caL. 
 be mistaken for. Their clinical significance has already been noted 
 (p. 264). 
 
 In rare instances they do not become colored, but retain their 
 
OXALATK OK IJMIO. 
 
 29* 
 
 normal whiteness, and are then known as the white^crystals of uric 
 acid. 
 
 Fig. 65. — Uric Acid Rosettes. 
 
 Fig. 66. — Uric Acid Rosettes and Irregu- 
 lar Forms op Crystal. 
 
 OXALATE OF LIME. 
 
 It was once believed that oxalic acid did not exist free in the human 
 system, but of late it seems to have been proven that it does, and that 
 it is eliminated from the blood in its pure form. It, however, most 
 
 a 
 
 I 
 
 *9*<f£ 
 
 Fig. 67. 
 
 Fig. 69. 
 
 Fig. 68. 
 Oxalate of Lime Crystals. 
 67, Ordinary forms; 68, typical forms, rectangular octahedra; 69, irregular and dumb-bell 
 forms. 
 
 frequently occurs in the urine in combination with calcium, forming: 
 the lime oxalate crystals. Their typical form is rectangular octa- 
 hedra, but anomalous forms are occasionally found having the form 
 of amorphous lumps, dumb-bells, or square columns with pyramidal 
 ends. 
 
296 OXALATE OF LIME. 
 
 They are insoluble in water, alcohol, ether, ammonia, alkalies, and 
 acetic acid, but are soluble in the mineral acids, and to some extent 
 in sodium phosphate and urate. 
 
 From uric. acid they arc distinguished by their insolubility in alka- 
 lies, and from the phosphates by their insolubility in acetic acid. 
 
 Under the microscope they appear as minute, little squares with 
 cross markings and of a pure white color, resembling somewhat a 
 folded square envelope. In size, they range between xcW to j^- - of 
 an inch, 4.535 mmm. to 50.679 mmm.; the latter are rarely found, 
 the small size usually predominate. The dumb-bell forms are infre- 
 quent, and range in size from y^Vu to jfo of an inch, 16.933 to 
 4.2.332 mmm. The other forms are also rare. If a side view is 
 obtained, the most common shape is the octahedron, or double pyra- 
 mid, two pyramids base to base. 
 
 They might be mistaken for some of the uric acid forms, but the 
 color will establish their character, and the size will differentiate 
 between them and the triple phosphate. 
 
 Urine containing oxalate of lime is always acid, of an amber tint, 
 and contains finely cloudy mucus. 
 
 Oxalates in the urine may be the result of certain kinds of vegetable 
 food that contain an abundance of oxalic acid, from an incomplete 
 metabolism of the waste products of the body, or from deoxidization 
 of urea and uric acjd, as in urine from acid fermentation. Some appear 
 to have proven that they come directly from pre-existing oxalic acid 
 in the blood joining with the lime, either in the blood or the proto- 
 plasm of the epithelial cells lining the uriniferous tubules, more 
 probably in the latter. 
 
 This method of formation helps to explain their presence in the 
 uriniferous tubules and in the substance of the cells. 
 
 Clin iced significance. — The presence of oxalate of lime crystals 
 in the urine does not appear to be characteristic of any particular dis- 
 ease. They are, without doubt, the result of mal-assimilation, whicli 
 can generally be traced to an incompletely performed hepatic diges- 
 tion and one in which there is an over-production of a poor quality of 
 bile. If they are deoxidized or incompletely oxidized urea or uric 
 acid as some believe, it still argues in favor of the primary difficulty 
 being located in the liver. 
 
 With nervousness, hypochondriasis, dyspepsia, and indigestion they 
 make their appearance in the urine, and also in some forms of renal 
 colic, forming a calculus by being aggregated together (mulberry 
 calculus). 
 
 The most satisfactory treatment is plenty of open-air exercise, with 
 
URATES. 
 
 297 
 
 a free administration of dilute nitro-hydrochlorie acid. But foremost 
 of all is a strict attention to the diet and digestive functions. 
 
 Great care must be exercised to guard against taking anything that 
 will not be easily and completely digested. 
 
 Some vegetable substances contain an abundance of oxalic acid or 
 the oxalates. This should be remembered, and such articles of diet 
 should be avoided. 
 
 URATES. 
 
 Of these there are several forms: the amorphous, and the urates of 
 lime, ammonia, soda, and potash. The ammonia and soda salts are 
 crystalline and can be recognized as such under the microscope. All 
 the urates are more or less colored in the urine, either brown or 
 brownish-yellow, like uric acid. 
 
 Fig. 70.— Urate op Soda, Showing Spiked or Hedge-hog Crystals. 
 
 The urate of soda is generally in the form of round balls of con- 
 siderable color, at other times they have fine, spike-like projections 
 from their surface, when they are called the hedge-hog crystal; it is 
 this form only that can be positively regarded as the urate of soda. 
 Another form is described as round balls with fine lines radiating 
 from the centre, but these crystals so closely resemble carbonate of 
 lime that it is very hard, if not impossible, to distinguish them from 
 each other. If deeply colored, they are probably urates; if white, 
 carbonate of lime. 
 
 The urate of ammonia is seen as opaque, spherical masses, some- 
 times round or incompletely dumb-bell-shaped, often lying across 
 each other at right angles, forming crosses; or aggregated together, 
 resembling rosettes. 
 
 It is difficult, if not impossible, to distinguish the urate of soda from 
 the urate of ammonia, unless the spiked balls or hedge-hog crystals 
 
298 PHOSPHATES 
 
 arc distinctly marked. By their color it is impossible to separate one 
 from the other. 
 
 The addition or the formation of a free acid decomposes them, with 
 the formation of a soluble salt and later the deposition of uric-acid 
 crystals. 
 
 The urates may be distinguished from the phosphates upon the 
 slide by holding it, until quite warm, in the flame of an alcohol lamp 
 or Bunsen's burner. If the deposit is composed of urates, it will 
 disappear; but if made up of phosphates, it will become more 
 decided. 
 
 When the urates and phosphates are both present, the heat will 
 cause a marked diminution in the amount of sediment present, but 
 not a complete disappearance. 
 
 PHOSPHATES. 
 
 There are two classes: the earthy and alkaline. The former is the 
 only group of any practical importance in microscopic urinary ana- 
 lysis. The earthy phosphates are found in alkaline urine of low 
 density as a white aud not very abundant precipitate. The urine, 
 when first voided, is sometimes cloudy from their presence, the re- 
 verse being the case when the urates are in abundance. In this way, 
 they may be differentiated at the time they are expelled. 
 
 When the urine is first voided, they are usually in the amorphous 
 state and only occur in this form with an alkaline reaction. 
 
 They are present when the food taken contains a large amount of 
 the carbonates, vegetable salts, the malic, tartaric, and citric acids; 
 continuous loss of sleep, nervous exhaustion from any cause, and ex- 
 cessive mental strains of all kinds, and in certain forms of dyspepsia, 
 which prevents the formation of sufficient acid. 
 
 This condition is often met with in connection with constant 
 brain workers, who habitually take but little exeicise. Such persons 
 regularly pass turbid urine, due to the presence of the phosphates and 
 diminished acidity. Quantitative analysis of such samples will usually 
 show a diminution rather than an increase in these salts. From 
 this it would appear that their presence is due to diminished acidity 
 and not to an increase in the quantity of the phosphates. 
 
 Their perceptible presence, therefore, does not of necessity indicate 
 a diseased condition, but rather the taking of large quantities of the 
 above mineral substances, or a diminution in the acid production. 
 An abstinence from certain forms of diet, and plenty of out-door exer- 
 cise will often prove sufficient to cause their non-appearance and con- 
 sequently effect a cure. 
 
I'JIOKI'IIATKS. 
 
 200 
 
 The only special danger from the continuance of such a condition 
 is the formation of a phosphatic calculus. 
 
 The treatment of this condition refers more to the regulation of the 
 diet and exercise than to the administration of drugs. 
 
 The taking of mineral acids does not improve the condition, except 
 in so far as it improves the general digestive and assimilative powers. 
 
 The triple phosphates, when slowly and perfectly crystallized, 
 occur as white, transparent prisms, with bevelled edges. All grades 
 of imperfect crystals are also met with. When rapidly crystallized, 
 they are deposited in a variety of stellated, feathery forms. These can 
 
 Fig. 71.— Stellar Phosphate op Lime— Crystalline Forms. 
 a, Stars; b, fans; c, bundles; d, rods; e, bottle-shaped. 
 
 easily he developed artificially by adding ammonia to urine. At one 
 time this form was supposed to be due to the phosphates uniting 
 with a very large quantity of ammonia. They occur as a white deposit 
 or as a flocculent cloud resembling mucus, or as an iridescent scum 
 on the surface of the urine; the two latter are the most frequent. 
 
 When the urine is faintly acid, boiling will cause quite a distinct 
 cloud, which disappears instantly upon adding one minim of nitric 
 acid. 
 
 The triple phosphates can occasionally be found in urine when first 
 voided. This condition indicates retention of urine from some cause, 
 
•'><>ll MICROSCOPIC PIGMENTS. 
 
 stone in the bladder, cystitis, and an alkaline decomposition before it 
 is expelled. 
 
 They arc, however, more frequently found in urine which has under- 
 gone alkaline fermentation outside the body; in fact, they are a pro- 
 duct of this change. 
 
 They are occasionally found in conjunction with uric acid, urates, 
 or oxalate of lime in the same sample and at the same time. In such 
 cases, it is quite probable that the urine has not completely lost its 
 acidity, and the previously formed acid deposits have not yet been com- 
 pletely liquefied. 
 
 As a rule, they are extra-vesical products, and therefore of no 
 great clinical importance. 
 
 The stellar 2)ho$phaic of lime is of rare occurrence and of no clini- 
 cal importance. Under the microscope it appears in colorless crystals 
 arranged in sheaves or rosettes. Its distinguishing features are its 
 whiteness and arrangement with the clubbed formation of the peri- 
 phery. 
 
 In this it differs from the rosettes of uric acid, which are pointed 
 at the periphery, and which in the urine almost always have a deep 
 yellow or brown color. 
 
 The stellar phosphate occasionally is developed just at the time the 
 urine is changing from the acid to the alkaline reaction. But most 
 frequently it seems to appear as an accidental formation in urine that 
 has stood for a time in the laboratory. 
 
 It has no clinical significance. 
 
 MICROSCOPIC PIGMENTS, 
 
 Under this heading, blood, bile, urinary, and miscellaneous pig- 
 ments will be considered. 
 
 Irregular bodies varying much in size are often found in examining 
 urine, and they have considerable color, which is either yellow, brown, 
 or red. Many of these j)articles are undoubtedly masses of desqua- 
 mated epithelial cells or disintegrated corpuscular elements in which 
 all evidence of a nucleus is absent; or they may be foreign bodies which 
 have taken up the coloring matter of the urine or been colored before 
 entering. They are, however, seldom met with, unless the urine con- 
 tains blood or bile. From this it would appear reasonable to consider 
 them as albuminous masses of varying shapes and sizes, which have 
 attracted to themselves little particles of blood pigment or some of its 
 derivatives, either melanin, urochrome of Thudichum, urobilin or pur- 
 purin of Prout, uroerythin of Heller, or indican. In other cases, 
 biliverdiu or bilirubin or some of their derivatives cause the color. 
 
MICROSCOPIC PIGMENTS. -'501 
 
 When carefully studied with a perfect and high-power Ions and a 
 strong light, they are without doubt very minute crystalline forma- 
 tions, probably derived from some of the normal or abnormal color- 
 ing matters present. 
 
 In cases of jaundice, all the desquamated epithelial cells and m;i 
 of protoplasm will be stained deep yellow. 
 
 These pigmentary bodies are of no special value, but often give 
 rise in the minds of the students to the inquiry, Where do they 
 come from and what d o they indicate ? 
 
 It has been said that they were usually abundant in renal disease, 
 and especially so in the lesions commonly included under the term 
 chronic Bright's. The reverse, however, has been more often the case. 
 
 Many of the reddish flakes and delicately tinted scales resembling 
 butterflies' wings are nothing more than little imperfections or hollows 
 on the surface of the glass slides that have retained some of the red 
 oxide of iron — used by the mechanic in polishing the glasses. They 
 are often puzzling, and have caused many a mistake or new dis- 
 covery. 
 
CHAPTER X. 
 
 EPITHELIAL CELLS ; SPERMATOZOA. 
 
 Epithelial Cells. — It is well known that there is great variety in 
 the form of the epithelial elements found in the urine, some of which 
 are] derived from the urinary tract, and others from the generative 
 organs, while a smaller number may come from the air-passages, the 
 mouth, or the skin. But, of all these, the variety known as flat or 
 
 %^h . * 
 
 $Mi )y m> 
 
 ^B 
 
 Fig. 72. — Cells found in Urine. 
 
 Each division of the scale equals 0.0033 mm., or 3.3 jx— roughly, 8« #. The large flat cells 
 average, probably, from 40 to 55 or 60 ii in their greatest diameter. Fifty cells, measured care- 
 fully by the author, averaged 49 tt in their greatest diameter, and 37 jj. in the diameter at right 
 angles with that one. 
 
 pavement epithelium, the tailed cells, and the small angular cells 
 commonly called " renal, " have given rise to the most discussion. 
 
 Naturally, epithelial cells from the urinary tract are found in either 
 sex. On the other hand, the urine of the female is almost invariably 
 said to contain a peculiar sort of large and angular cell that has been 
 
EPITHELIAL CELLS. 
 
 :;o:; 
 
 regarded as peculiar to the sex. But all varieties, sizes, and forms of 
 epithelial cells may come from the bladder, the ciliated form excepted. 
 The structure of the bladder distinctly explains this, because it is 
 divisible into three separate layers. The innermost or deepest is com- 
 posed of several rows of small cells varying in size and shape, but 
 usually cuboidal or rounded in outline. When these cells are shed 
 rapidly they increase in size and have a more globular form, espe- 
 cially in catarrhal conditions or when the membrane is inflamed in 
 any way. The intermediate plane is made up of a single or in part 
 double layer of pyriform cells. Their tail-like prolongations are 
 either single or double, but usually single, and fitted in between the 
 epithelial cells of the deeper layer. Their rounded or outermost ends 
 fit into depressions in the inferior face of the superficial cells. 
 
 Eig. 73.— Cells prom Urine Removed Through an Abdominal Opening into the Bladder. 
 
 The third or outer layer is composed of a form of flattened cells called 
 transitional. These cells are made up of large masses of protoplasm 
 which usually appears to have two or more nuclei, but often this 
 phenomenon is an optical illusion, and one at least of the apparent 
 nuclei is produced by the fossa on their lower surface where it rests 
 upon the underlying corpuscles. In cases of an ordinary catarrhal con- 
 dition or inflammation, the epithelial membrane may be cast off in 
 separate layers or with its three layers adhering together and appear- 
 ing as such under the microscope. But a careful examination of the 
 mucous membrane of the renal pelves, of the ureters, and of the vagina 
 demonstrates that in all these regions the membrane is composed of 
 three layers of cells similar to those found in the urine (Fig. 72 and 
 Fig. 73) and from the bladder, ureters, and renal pelves (Fig. 74). Kow, 
 though the variety known as vaginal epithelial cells has been said to 
 be the most common in the female, investigation shows that they are 
 
304 EPITHELIAL CELLS. 
 
 quite as likely to come from the bladder, and even form the ureters 
 or the pelves of the kidneys. There is another quite interesting 
 point of medico-legal interest in connection with these cells, some 
 alleging that they are always absent in the virgin. The author's 
 attention was especially called to this subject when making a necropsy 
 upon a female patient, aged eighteen, who had died twenty-four hours 
 after a fracture of the skull. When the kidneys were examined they 
 unexpectedly gave every macroscopic evidence of a chronic parenchy- 
 matous metamorphosis. The urine was desired for examination, to 
 see if it contained evidence of the renal lesion, which it did in every 
 particular. It was also found to contain an abundance of large flat 
 cells identical with those commonly called vaginal, and single, and 
 bifid-tailed cells also were abundant. In this case, the urine was not 
 withdrawn through the urethra, but the bladder, which happened to 
 be distended, was opened from the abdominal cavity, and its contents 
 were withdrawn through a clean syringe. Excluding the vagina, and 
 tracing the origin of these flat cells to the bladder, their frequency in 
 the female and rarity in the male can be explained as follows: From 
 the loose attachment of the bladder to the movable anterior wall of the 
 vagina there is of necessity greater mobility in the female than in the 
 male. The frequent motion and tendency to pouching of the trigonum 
 vesica?, and the more frequent over-distention in the female, naturally 
 tend to excite a mild catarrh, which damages the epithelial cells, 
 loosens their attachments, and easily accounts for their frequent and 
 abundant desquamation. On the other hand, the firm attachments 
 of the male bladder to the surrounding tissue, and its less mobility 
 and distensibility, tends to hold the epithelial cells in their proper rela- 
 tions. 
 
 Another point of considerable interest in this connection is the 
 dependence upon the tailed cells as diagnostic of pyelitis. One of 
 Professor Satterthwaite's former students, Dr. Creedon, now of Globe 
 Village, Mass., while working in the laboratory, prepared with great 
 care specimens of the epithelial cells from the different portions of the 
 urethra, bladder, ureters, pelves of the kidneys, and renal tubules. He 
 made accurate measurements and also drawings of the cells removed 
 from the various regions. The result of his research was that single 
 and bifid-tailed epithelial cells were present throughout the mucous 
 membrane of the urinary tract, from the meatus urinarius to the 
 papilla? of the kidneys. He further found that the renal epithelial 
 cells and those from the deeper layers of the urinary tract and from 
 the uriniferous tubules of the kidneys also corresponded exactly in size 
 and shape in all the specimens and in the different regions. Of course, 
 
KJ'ITHKLIAL CKLLS. 
 
 105 
 
 various sizes and shapes existed throughout. This careful observa- 
 tion was strong evidence in favor of the impossibility of locating with 
 certainty the source of any given variety of epithelial cells when found 
 in the urine. These experiments were made upon subjects in whom 
 the membrane was free from any inflammatory process at the time of 
 death. If the membrane was the seat of any inflammatory action, the 
 rapid metamorphosis, subdivision, and desquamation of the cells 
 would tend to make the similarity still greater. In the instance 
 already cited, the tailed epithelium, both single and bifid, was abun- 
 dant, but there was no evidence of pyelitis or any inflammatory condi- 
 tion of the urinary tract at the necropsy. There was, however, 
 catarrh of the bladder. To establish more certainly the close similar- 
 
 c. d. 
 
 Fig. 74. 
 a, Cells from ths vagina; b, the six cells on the left came from the trigonum vesicae, and 
 the six to the right from the fundus of the bladder; c, cells from the ureter; d, cells from the 
 renal pelvis. 
 
 ity in the shape and size of the epithelial cell in the various regions 
 and layers, further examinations of the mucous tract were made, with 
 the following result: A necropsy was made on another female, aged 
 eighteen. Specimens were carefully prepared from the pelves of the 
 kidneys, the ureters, the fundus and trigonum of the bladder, and the 
 vagina. Drawings and measurements were made of the various kinds 
 of cells from the different regions, also of the cells found in the urine 
 taken from the bladder at the first necropsy. In all the different 
 regions, and in both cases, the size and shape so closely corresponded 
 that no apparent difference could be made out, as is well illustrated 
 by the drawings. The various specimens were also measured and 
 20 
 
306 EPITHELIAL CELLS. 
 
 the figures corresponded. The only variation that conld be detected 
 in the flat cells was a Blight difference In size, those from the vagina 
 and bladder being a little larger than tbose from the other two 
 regions. The middle layer of the vagina contained cells that ap- 
 proached the spindle frm more than the poyramidal kind. 
 
 Renal epithelial cells have often been described as occurring free in 
 the urine, and as being recognizable as such under the microscope, 
 but the writer's opinion is that it is absolutely impossible to diag- 
 nosticate with certainty between renal cells and those of the deeper 
 layer of the mucous membrane of the urinary tract. Either one 
 might be mistaken for the other. Buccal epithelial cells may occa- 
 sionally find their way into the urine, as when the receptacle for the 
 urine served the purpose of a spittoon. They are, however, said to be 
 distinguished from the vaginal cells by a more regular outline and by 
 being larger. Specimens of these cells were prepared for comparison, 
 but in size and shape they presented so many points in common that 
 no marked difference could be drawn. Measurements of these cells 
 gave the same results as those taken from the urinary tract and the 
 vagina. 
 
 Ciliated epithelial cells are occasionally found in urine and may 
 come from the air-passages through the sputa, but are more likely to 
 come from the uterus or the Fallopian tubes in the female, and the 
 ejaculatory ducts, vesiculas seminales, or vas deferens in the male. 
 
 The results obtained by Dr. Creedon, and the above observations 
 furnish additional proof of the untrustworthiness of the statement of 
 Professor Ebstein in von Ziemssen's " Cyclopaedia of Medicine," vol. 
 XV., p. 574, that the occurrence of tailed epithelial cells in purulent 
 urine was the most positive indication that the patient had pyelitis. 
 
 The conclusions deduced from this study are: that flat epithelial 
 cells are found in the urine of females more frequently than in that 
 of males'; that they originate both in the vagina and in the bladder, 
 probably more frequently in the bladder and the urinary tract; that 
 they desquamate more frequently and in larger numbers from the 
 female bladder on account of its loose attachment and greater 
 mobility, and consequently are more frequent after the termination 
 of virginity; that isolated angular "renal" cells cannot be dis- 
 tinguished from those of the third layer of epithelium at any point; 
 and that no distinctive features can be ascribed to any cell or set of 
 cells, by which its place of origin can be determined. But by a 
 complete chemical and microscopic analysis, together with a complete 
 history, very accurate results can be obtained. 
 
SI'KKMATOZOA. 
 
 30V 
 
 BPEEMATOZOA. 
 
 These microscopic bodies are frequently met with both in the male 
 and female urine, but of the two, the latter is most likely to contain 
 them. 
 
 They require a high power to distinctly bring out their outlines, 
 although they can be recognized with a two-thirds objective. 
 
 Under favorable circumstances they are 
 found to be composed of a head and tail 
 united by an intermediate cylindrical body 
 or middle piece. The head consists of a 
 flattened ovoid mass, with a central depres- 
 sion on each side. They will appear broad or 
 narrow depending upon the part presenting, 
 whether the flat surface or the edge. The 
 head is -^-^ of an inch (4.233 mmm.) long, 
 and T oio¥ °f an mc -h (2-539 mmm. ) thick, and 
 is thickest at the attached end, which causes 
 the free extremity to appear pointed. The 
 tail is a tapering film projecting from the 
 central piece, having a length of -^- ¥ to ^ ¥ 
 of an inch (20 to 16 mm.). 
 
 They are sometimes with their fluid 
 medium found in large quantities and from 
 their albuminous nature will cause a cloud 
 to appear in the urine upon the application 
 of heat or the addition of nitric acid. 
 
 They are only of practical importance in suspected cases of rape,, 
 and especially if the medico-legal side is in question. 
 
 They may be found in the mucus of the vagina after coitus, and 
 have been known to retain their physiological activity for several days. 
 Under favorable circumstances they may retain their power of activity 
 for as long a period as ten or fourteen days. This probably in a 
 measure accounts for the uncertainty of the date of impregnation and 
 the exact duration of pregnancy. 
 
 They may be abstracted from soiled linen, by carefully soaking in 
 a one-per-cent solution of sodium chloride for fifteeu or twenty 
 minutes. 
 
 When found in the urine, they are generally inactive. 
 
 In one instance they were found at the necropsy in the cavity of the 
 uterus of a young woman who had committed suicide by jumping 
 from the third-story window. 
 
 Fig. 75. — Human Spermato- 
 zoa. 
 
 1, In profile, the tail not re- 
 presented: 2, viewed on the 
 flat: b, head; c, middle piece; 
 rf, tail; e, end piece of tail 
 (Quain's " Anatomy.") 
 
CHAPTER XI. 
 
 VEGETABLE ORGANISMS: FUNGI. 
 
 VEGETABLE ORGANISMS. 
 
 {a) Sphero-bacteria or micrococci are minute spherical particles of 
 protoplasm not more than s6 fl 00 of an inch (1 mmm.) in dia- 
 meter. Their protoplasm is believed to consist of an outer envelope 
 and cell contents; the cell wall closely resembling cellulose. They 
 resist the action of alkalies, acids, heat, and cold to a wonderful degree. 
 They refract light, and are decidedly colored by some reagents. 
 
 These bodies, like all bacteria and bacilli, multiply by transvere fis- 
 sion. In this way they form, chains, clumps, or large globular masses. 
 
 t % - n 
 
 * i 
 
 •<v 
 
 Fig. 76.— Sphero-Bacteria (Genus Micrococcus), x 700. 
 
 1. a. Single; b, zooglcea. 2. a, in pairs (diplococcus forms); b, in tetrads; c, in chains 
 (sometimes designated a streptococcus. (Delafield and Prudden, "IHandbook of Pathological 
 Anatomy and Histology.") 
 
 When packed together in these large masses they form what are 
 called by some zooglceas; and it is supposed that they are held together 
 by a delicate film of intercellular substance. They do not grow into 
 rods or filaments, like other forms, and according to Cohn have no 
 independent power of locomotion, thus differing from the bacteria 
 proper and the bacilli. 
 
 Under the microscope and in urine they appear as minute highly 
 refracting dots, and if suspended in the fluid show an active Brownian 
 movement. "When single and isolated it is hard to distinguish them 
 from minute fat droplets or granules of protoplasm. But they can 
 be distinguished when aggregated together by their uniform size, and 
 
VEGETABLE ORGANISMS. 309 
 
 by being disposed at equal distances from one another. Fortunately 
 they are frequently found in rows, pairs or large accumulations. 
 
 If dividing rapidly, they often appear dumb-bell like in shape, and 
 have a to-and-fro movement. When dividing more slowly, they are 
 seen forming rows or chains of four, six, or more linked together. 
 Under favorable circumstances, they frequently form the globular 
 masses united together by an intercellular substance. 
 
 Occasionally a transverse and longitudinal fission takes place at the 
 same time, and groups of four-celled " sarcinae forms" are produced. 
 
 All these different forms may be found in a single sample. 
 
 The globular masses are very common in urine, and it is sometimes 
 difficult, if not impossible, to say whether these masses are groups of 
 micrococci, degenerated epithelial corpuscles, or masses of transformed 
 protoplasm. It often requires a staining reagent and an unusually 
 high power to solve the question, but with them it is not difficult, 
 except when the cells are single. 
 
 Micrococci may be so abundant or develop so rapidly that urine 
 even at first, or a clear sample will soon be opaque, and in some cases 
 white dots as large as the head of a pin can be recognized with the 
 unaided eye. They then usually become stained by the absorption of 
 the coloring matter present in the urine. 
 
 They require for their growth a nitrogenous pabulum, oxygen,, 
 moderate temperature, moisture, and a faintly acid or alkaline- 
 medium. 
 
 (b) The sarcina is another microscopic vegetable organism of the 
 sphero-bacteria type and is one of the lowest orders of saccharomycetes,. 
 They were first described by Goodsir in 1842. 
 
 There are two principal varieties described, the sarcina ventrieulr 
 and s. urinse. Both are found in the urine. Still other varieties have 
 been mentioned. 
 
 The sarcina ventriculi is described as coming from the stomach in 
 connection with a number of diseases, and with the vomited matter 
 occasionally fall into the urine. 
 
 The sarcina urinae is probably developed outside of the sample and 
 accidentally gets into it. In either case, the sarcina appear under 
 the microscope as little collections of sphero-bacteria arranged in 
 groups of four, sixteen, sixty-four, and so forth, which have a tend- 
 ency to divide or split off from the mother mass in the same numer- 
 ical order. 
 
 They differ from similar micrococci formations in this, that the^ 
 spherules are larger, have a diameter of y-g-^o-jj of an inch (1.58? 
 mmm.), in their peculiar arrangement and division. 
 
310 VEGKTAULK OKC.AXISMS. 
 
 The only difference between the s. ventriculi and 5. urinre is a 
 Blight variation in size, the spherules of the former being a little 
 larger: the diameter of the spherules of the s. urmae coming between 
 <>f the 5. ventriculi and the micrococci proper. 
 
 The author has never found either of the above forms, and Prof. 
 Satterthwaite, who has had a very large experience in urinary 
 analysis, also informs him that he has never met with them. 
 
 (c-) Micro-bacteria or Simple Bacteria. — Under this title many 
 forms of organisms have been described, but of late the unqualified 
 term has become a distinct order by itself, so that now the term is 
 empirically limited to rod-shaped bacteria, in which the length ami 
 breadth have a certain relation to each other. A simple bacterium 
 must he just one half as broad as it is long. Their length is T -o3hnr of 
 an inch (2.53!) mmm.), and their breadth o,,, 1 ,,,,, of an inch (1.269 
 mmm.). 
 
 This variety is the one most frequently found in all samples of 
 
 /. 
 
 >;->/ 
 
 /•' / 
 
 t 2 
 
 Fig. 77.— Micro-bacteria (Genus Bacterium). 
 
 1, Bacterium termo; 2, bacterium lineola. Specimens stained with fuchsin. X 600. (Dela- 
 
 field and Prudden, " Handbook of Pathological Anatomy and Histology.") 
 
 urine. It may be well to observe here that they will vary much in 
 size, notwithstanding the above arbitrary rule. 
 
 They are often quite abundant and render the urine cloudy by 
 their presence in the same way as the micrococci. They may be 
 found immediately after drawing the urine with a catheter; this, how- 
 ever, is exceedingly rare except when the urine is alkaline before it is 
 voided or in connection with cystitis and pyelitis. 
 
 In one case in which there was no cystitis or pyelitis, and in which 
 the urine was acid, it persistently contained bacteria in abundance 
 when first voided or was withdrawn by a carbolized catheter. The 
 patient was suffering from an atrophic form of diffuse nephritis and 
 the urine was heavily loaded with albumin. 
 
 As a rule, an hour or two elapses after voiding before they make 
 their appearance. If the urine is free from epithelial cells or albu- 
 minous elements, it will often stand exposed to air for days without any 
 bacteria being found in it. The rapidity and the abundance of their 
 formation appears to be influenced by the amount of albumin pri- 
 marily in the sample. 
 
VEGETABLE ORGANISMS. 311 
 
 (d) Vibriones. — These are organisms of the micro-bacteria type, 
 and are found in the urine at any time after it has been expelled from 
 the bladder. They vary considerably both in size and shape, and are 
 found most frequently and abundantly when decomposition has be- 
 come established. 
 
 When viewed under the microscope, they are about one-three-thou- 
 sandth of an inch (8.4GG mmm.) long, and quite broad compared with 
 other forms. They are always in motion, and are propelled by a 
 spiral or twisting motion; sometimes they revolve upon their own 
 axis at a tremendous rate of speed. It is quite evident that they are 
 not dependent upon the fluid for this motion, for they move as rapidly 
 against the current as with it. This movement of the whole organ- 
 ism differs from the Brownian movement, which consists in a con- 
 stant motion of the granular particles compos- 
 ing the mass of protoplasm. 
 
 (e) Leptothrix. — This is a micro-bacterium 
 or vegetable organism that appears under the 
 microscope as a minute filamentous body hav- 
 ing considerable length and but little breadth. 
 It is usually found in scrapings from the buccal 
 
 . , , . , , , , „ . . . , Fig. 78. — Leptothrix 
 
 cavity and m the contents or carious teeth. Buccalis *-ith micro- 
 
 T , , , . i j n • coccus Colonies from 
 
 It was at one time supposed to be in some way the mouth of a healthy 
 
 . i -i-i •■ ,1 p i - p Person, Stained with 
 
 connected with, it no the cause or, certain forms gentian violet, x eoo. 
 
 <; i li i.iij_-i_i i (Delafleld and Prudden, 
 
 of aphthous sore mouth, but it has since been "Handbook of Pathoiogi- 
 
 n Tii iii-i.i.£xii i cal Anatomy and Histol- 
 
 found to be a normal habitant of the buccal cav- ogy."> 
 ity. It occasionally finds its way into the urine. 
 
 (/) Desmo-bacterium is the one exciting considerable interest in 
 reference to the causation of certain infectious and contagious diseases, 
 and requires a few words. 
 
 A typical bacillus is a rod-shaped body, the length of which is more 
 than twice the breadth. In general, its length is about one-ten- 
 thousandth of an inch (2.539 mmm.), and the breadth one-eighteen- 
 thousandth of an inch (1.411 mmm.) or less. The length and breadth 
 vary with the variety. 
 
 The two micro-organisms which are most likely to be found in 
 the urine are the bacillus tuberculosis and the gonococcus, the former 
 reaching the urine through the medium of the sputum, or incases in 
 which there is a tubercular lesion of the genito-urinary tract the lat- 
 ter would be swept in during micturition. 
 
 The different varieties of bacilli can only be distinguished by their 
 minute variations in size and shape and their behavior with certain 
 
3 1 2 
 
 VIJ.KTABLE ORGANISMS. 
 
 aniline dyes, or by cultivation. The latter, however, is wholly im- 
 practicable for general use. 
 
 It is not at all likely that their detection in the urine will ever be 
 necessary or will yield any very satisfactory results if attempted. 
 
 Bacteria in general are said to be plain, jointed, or mono-tailed, 
 depending upon the stage and rapidity with which they are dividing. 
 This, however, according to the present classification, would be more 
 applicable to vibriones, leptothrix, and bacilli, but not to the simple 
 bacterium. 
 
 At this point, it may be said that in highly putrescent fluids all 
 forms of bacteria multiply rapidly and are apt to be undersized, while 
 
 'A 
 
 f 
 
 / 
 
 y 
 
 s 
 
 p. 
 
 N 
 
 Fig. 79.— Bacillus Tuberculosis. X about 800. 
 (Delafield and Prudden. " Handbook of Pathological Anatomy and Histology.") 
 
 in less putrescent fluids they divide more slowly, are more perfectly 
 formed, and larger than the average. 
 
 The volumetric bulk, on the contrary, will be greatest in the first 
 instance, least in the latter, while the vitality will be least in the former, 
 and greater in the latter case. 
 
 Up to the present time, it is a mooted question whether bacteria 
 cause fermentation and putrefaction or are a concomitant product of 
 this change. Pasteur and believers in his germ theories are strong 
 in their belief that these micro-organisms must be introduced into the 
 substance before new micro-organisms can be developed. 
 
 The opponents of these theories believe that they are developed as 
 the result of fermentation. 
 
VEGETABLE ORGANISMS. 313 
 
 The germ theorists claim that all diseases have a separate and dis- 
 tinct bacillus or micro-organism for each given disease. In some 
 instances, this at first seems quite probable; but if we observe that, 
 as a rule, the germ, which was supposed to be essential to some 
 particular disease, is found in reality in every human individual with- 
 out producing the malady, it is not surprising that we should be 
 sceptical on the subject. In almost all the instances where the local 
 seat of the disease can be easily reached, careful research reveals in 
 healthy subjects precisely the same micro-organisms. This raises the 
 question, might not this prove true in the more deeply seated diseases, 
 provided as careful a search could be made in perfectly sound sub- 
 jects ? They may not be either the cause or the products of the 
 disease, but intermediate agents between the true cause and the effect. 
 
 These micro-organisms may yet be found to be important factors in 
 producing disease. It has been a firm conviction for a long time 
 that they bore the same relation to a disease that a hod-carrier does 
 to the erection of a wall or building. He neither produces the bricks 
 and mortar, prepares the foundation, nor lays the wall. So with the 
 bacillus. It has not been proven to produce the poison, to prepare the 
 system for its reception, nor institute the building up of the disease. 
 
 It appears, therefore, that these four conditions must be considered 
 in every abnormal process. The preparation of the system for the 
 reception of the poison, the means of transportation of the poison, 
 and the builder of the disease. Thus far, only one of the four has 
 been mastered, which is the laying of the foundation; the cause and 
 medium of transportation, and the elements which set the poison in 
 motion remain as yet absolutely an unsettled question. 
 
 The foundation of every disease is unquestionably laid by dissipa- 
 tion and everything which tends to diminish a perfect physiological 
 standard, namely, bad air, bad food, and bad hygienic surroundings, 
 as well as over-work, either physical or mental or both. 
 
 The part attributable to the micro-organisms is rather that of the hod- 
 carrier depositing the poison upon suitable ground for further growth, 
 development, and destruction. There is no doubt in reference to time 
 intervening between the introduction of the poison and the result. 
 
 It may be that the poison attaches itself to these bacilli ; and as they 
 increase in number it also becomes more virulent, until finally there 
 is enough developed to produce a given result. Or, it may be that, 
 by their rapid multiplication, with their active movements, they spread 
 out until a weak point is reached and the poison thus gains access to 
 the system. 
 
314 VEGETABLE ORGANISMS. 
 
 Accepting this view of the subject, the bacilli areas important as 
 
 the actual cause of the disease, and perhaps even more so. 
 
 Antiseptic treatment is still called for and possibly may be fonndof 
 still greater service. The efficacy of antiseptics now appears to be in 
 preventing the activity of their movements and in controlling their 
 
 growth ami development which prevents the development and spread 
 of the poison. 
 
 If these micro-organisms were the absolute cause of the disease and 
 acted as a poison, it would seem as if they ought in every instance, 
 and on every subject to "work alike, the same as acids and alkalies, 
 but the quantity introduced appears to have an inverse ratio to the 
 result attained. This is often exemplified in purely contagious dis- 
 eases, where a little poison from a very mild case will produce in the 
 second person a very intense attack and vice versa. 
 
 Again, it does not seem possible to find and appreciate enough 
 different varieties to account for all the known diseases. 
 
 Fig. 80.— Desmo-bacteria (Genus bacillus). Bacillus Anthracis, from Spleen of Mouse In- 
 oculated with the Bacillus. Specimen Stained with Methylen Blue. X 600. 
 (Delafield and Prudden, " Handbook of Pathological Anatomy and Histology.") 
 
 In the case of the modified anthrax virus it was found that pro 
 tective inoculation killed a larger percentage in protecting the re- 
 mainder than if the animals were left to the original disease, which 
 was poor encouragement for the stock raisers. This also tends to sub- 
 stantiate the fact that slow and perfect development increases the 
 destructive power. 
 
 Unless better results can be secured in the diseases affecting the 
 human race little good can be hoped for from a modified virus and 
 protective inoculation. 
 
 The differences in the reaction of the bacilli with different staining 
 methods may be explained by the variation in their age and method 
 of production. It is a well-known fact to every one familiar with his- 
 tological and pathological work, that all forms of organic protoplasm 
 stain differently at different stages of their development, and as a result 
 of the various retrograde changes which they undergo. Why is it not 
 just as reasonable to attribute the different reactions of different stain- 
 
I ■• it in r; I . 
 
 3 1 5 
 
 ing reagents to such changes as it is when they occur in the centre 
 and periphery of an epithelial carcinoma? No one seems fco have 
 thought it necessary to attribute different causes to these two points. 
 
 FUNGI. 
 
 There are two important forms found in connection witli urinary 
 analysis— the mould and the yeast or sugar fungi. 
 
 (a) The penicillium glaucum is that variety of fungus which forms 
 mildew. It occurs quite frequently in urine that is slightly acid or 
 commencing to turn alkaline. It may appear with or without the 
 presence of albumin or sugar. It is composed of three parts: the 
 mycelium which is made up of an interlacing network of sporules; 
 
 Fig. 81.— Penicillium Glaucum Showing Mycelium, Stipes, and Thalli. 
 
 the stipes or stems are surmounted by their thalli and grow upwards 
 from the mycelium, and from the branching tufts the sporules are 
 constantly being desquamated. 
 
 What is most commonly seen under the microscope is the single 
 sporule, and occasionally a thallus and still more infrequently the 
 mycelium. 
 
 The sporules are usually oval, considerably larger than a pus-corpuscle. 
 They have quite a clear cell contents with a distinct nucleus. In 
 focussing down upon them, they are found to have greater depth than 
 pus or blood-corpuscles with which they are sometimes confounded. 
 Two, three, or more are often found joined together with an occasional 
 branching thallus. By the latter they are positively distinguished 
 from pus or blood, and this also distinguishes them from yeast fungi. 
 
 {b) Torula cerevisim, or yeast fungus. "When yeast is placed in a 
 
316 FUNGI. 
 
 fermentable fluid, its cells multiply not by fusion, as in lower algae r 
 but by the budding fourth of young cells from the parietes of a pre- 
 existing spore. In the course of a short space of time, one cell will 
 have developed into three, four or five more complete cells which 
 remain in continuity until the plant stops growing, but separate and 
 return to the parent form if the fermenting process is checked or 
 arrested. If the process continues to full development, a mycelium 
 will be formed, from which stipes shoot upward and are surmounted 
 by a spherical thallus. It is the bursting of the thalli and the setting 
 free of the sporules that causes their appearance in the urine. 
 
 (c) The SaccliaromycescerevisKE, or S. urince, is almost identical, if 
 
 Fig. 82.— Representing Yeast and Sugar Fungus. Showing Mycelium, Stipes, and Thalli. 
 
 not isomeric with the former. This plant grows in the same way as the 
 torula, by a jn-ocess of budding. The cells are usually round and 
 have a thin investing membrane which incloses a finely granular sub- 
 stance, containing one or two transparent spots called vacuoles. 
 These spots are little cavities filled with a clear fluid. The cells 
 usually are single and about -^-^ of an inch (12 mm.) in diameter. 
 The majority are isolated, but occasionally two or more are joined, 
 forming moniliform chains. 
 
 It is only by finding a stem and its attached thallus that we can be- 
 positively sure that the sporules are of the yeast or sugar variety, and 
 not due to the penicillium glaucum. 
 
CHAPTER XII. 
 
 CASTS. 
 
 There are two principal types of casts: the blood and the hyaline; 
 in connection with the latter, there is a large modification as may be 
 seen by a single glance at the following table: 
 
 Small. Large. 
 
 f 1. Blood 
 
 2. Hyaline 
 
 3. Epithelial 
 
 4. Nucleated 
 
 Casts. -J 5. Finely granular. . . 
 
 I 6. Coarsely granular. 
 
 7. Fatty 
 
 I 8. Tubular 
 
 (^ 9. Cork screw 
 
 The blood cast is simple, and easily understood. It is produced 
 by an exudation of all the constituents of the blood, and a matting 
 together and entanglement of the blood-corpuscles by fibrin elements 
 in the lumen of the uriniferous tubules. They are discharged from 
 the tubes in masses, representing perfect casts of the portion of the 
 kidney from which they have escaped. They are found in the urine 
 as little plugs of blood-corpuscles with parallel sides and rounded ends. 
 This variety is only met with in acute congestion, hemorrhagic infarc- 
 tions, hematuria, acute diffuse nephritis, and acute exacerbations of 
 the chronic diffuse nephritis. The presence of blood casts in the urine 
 is the only positive evidence of hemorrhage from the kidneys. Their 
 presence alone does not indicate organic renal disease. Some call the 
 hyaline, with a number of blood-corpuscles attached to them, blood 
 casts, but this is erroneous. Blood casts are not common. 
 
 The hyaline cast is not so thoroughly understood, but it is gen- 
 erally believed that a peculiar fibrinous substance is thrown out of the 
 blood into the uriniferous tubules, and when discharged independent 
 of the epithelial cells, it is known as a hyaline cast, but with attached 
 epithelial corpuscles, in various stages of retrograde change, the various 
 forms tabulated are produced. 
 
31S 
 
 CA8T8. 
 
 A single cast of this variety may be found in urine without indi- 
 cating any renal lesion. But their continuance in any appreciable 
 number is always an indication of some retrograde change. 
 
 1, Small blood. 
 
 Fig. 83.— Casts. X 500. 
 
 2, Small hyaline. 
 
 3, Small epithelial. 
 
 - 
 4, Large blood. 
 
 7, Small nucleated. 
 
 5, Large hyaline. 
 
 1 65 
 
 Finely granular. 
 
 9, Coarsely grauular. 
 
 By an epithelial cast is meant one in which the epithelial cor- 
 puscles are attached to, or implanted, in this hyaline plug, having 
 been separated from the basement membrane, and still retaining the 
 appearance of renal epithelial cells. Casts of this kind are usually 
 found in the acute parenchymatous metamorphosis of the kidneys, 
 and in the acute diffuse nephritis, or in connection with acute exacer- 
 bations. 
 
OASTS. 
 
 319 
 
 The nucleated cast is one, in which the protoplasm of the epithe- 
 lial cells has been obliterated, and only the nuclei can be recognized 
 
 Fig." 84.— Casts. X 500. 
 
 10, Large nucleated. 
 
 41! 
 
 <*> 
 
 40 
 
 13, Small fatty. 
 
 / 
 11, Finely granular. 
 
 12, Coarsely granular. 
 
 14, Small corkscrew. 
 
 15, Small tubular. 
 
 16, Large fatty. 
 
 17, Large corkscrew. 
 
 n 
 
 18, Large tubular. 
 
 as they adhere to or are implanted in the hyaline substance. The 
 inability to recognize the protoplasm is caused by the cells becoming 
 
320 
 
 CASTS. 
 
 infiltrated with fine particles of effete material and the imbibition of 
 an albuminous fluid until everything is indistinct but the nucleus. 
 
 This form of cast is met with in the acute parenchymatous meta- 
 morphosis of tbf kidneys, in diffuse lesions, and in acute exacerbations- 
 it indicates a still greater retrograde change in the epithelial cells. 
 
 Fig. 85.- Casts x 1,200. 
 
 .■•■ i 
 
 
 1, Hyaline. 
 
 2, Epithelial. 
 
 3, Nucleated. 
 
 F 7 ' 
 
 : 
 
 4, Finely granular. 
 
 5, Coarsely granular. 
 
 0, Fatty east. 
 
 The finely granular cast is one in which the epithelial cells are 
 not only cloudy, but are also infiltrated with fine granular particles, 
 some of which are oil-globules of minute size, aud others granular 
 detritus probably from incomplete products of tissue metamorphosis 
 drawn from the blood, and in part from the further destruction of the 
 epithelial protoplasm itself. 
 
CASTS. 
 
 321 
 
 This form of cast represents a still greater destructive change, and 
 is met with in a well-established acuto lesion, or in the commence- 
 ment of a chronic lesion. 
 
 The coarsely granular cast is simply one representing a more 
 advanced degree of the former process, with more abundant and 
 larger fat droplets, and a still greater destruction of the epithelial 
 protoplasm. 
 
 This form is met with at the end of an acute lesion, but more fre- 
 quently indicates a chronic parenchymatous metamorphosis or a 
 diffuse lesion of the renal glands. 
 
 The fatty cast is one in which the metamorphotic process has 
 almost, if not completely, destroyed the protoplasm of the epithelial 
 corpuscle, which has been replaced by fat droplets of varying sizes, 
 which are easily recognizable. The cast may have a large or small 
 diameter, but the former is the more common. 
 
 This form indicates an advanced stage of the chronic parenchyma- 
 tous metamorphosis or a chronic diffuse lesion of the kidneys. 
 
 The tubular cast is a rare variety, and is formed by a plug of 
 hyaline matter in the lumen of the uriniferous tubule and a thin 
 ensheathing layer of the same material behind the epithelial cells ; 
 in this manner the corpuscular elements are detached from the base- 
 ment membrane and discharged. They appear under the microscope 
 as a perfect ring of epithelial elements. Occasionally the central 
 plug will be observed protruding from one or the other extremity. 
 
 This variety might be considered as a curiosity. 
 
 The corkscrew cast is produced by a twisting of the body of the 
 cast upon its own axis, so that it resembles the spiral of a corkscrew. 
 This opinion is based upon numerous sections of the kidneys that 
 show this peculiar arrangement in the straight tubules, some of which 
 have the casts still lodged in them. 
 
 Some believe that all forms of casts (the blood, hyaline, and tubu- 
 lar excepted) can be, and are frequently formed by the transformation, 
 desquamation, and matting together of the epithelial cells without the 
 aid or the presence of this fibrinous or hyaline material. This may 
 be the case in a few instances, but in the vast majority the hyaline 
 material forms the basis of all casts. In either case the microscopic 
 appearances are the same. 
 
 The peculiar arrangement of the tubular cast appears to denote 
 that the protoplasm is clogged by the hyaline material, which cuts 
 off the nutritive supply, prevents the free escape of the effete material, 
 and enables the substances, which should pass through, to push the 
 cells from their attachment to the underlying basement substance. 
 21 
 
31'2 CAM-. 
 
 This view of the situation distinctly indicates the necessity of keeping 
 the tubules well washed out in all forms of renal disease,, in which 
 there is a tendency to the formation of oasts. 
 
 It is the belief of some that the hyaline material undergoes degen- 
 eration, and in this way they explain the various forms of granular 
 casts. A close examination, however, of a hyaline cast, which appears 
 to be a little granular, will almost always, with a good high-power 
 lens, show the incomplete and faint outline of what once was an epi- 
 thelial cell. This tends to sustain the former view, and to disprove 
 the latter. 
 
 The waxy cast of some writers is not included in this classification 
 as its existence is extremely doubtful. 
 
 It occasionally happens that the various crystals of the urine adhere 
 to these hyaline plugs, or to a cast, and these might be termed crystal 
 casts. They are, however, more likely to be seen in sections made 
 from the kidneys than in the urine. 
 
 The distinguishing character of all casts is that they have uniformly 
 parallel sides, and usually at least one rounded end, occasionally the 
 other end is broken at a right angle, or a little irregularly, but they 
 never terminate in imperceptible lines, as is the case with bands or 
 streaks of mucus. Casts and strings of mucus are often confounded; 
 but by remembering the above-stated facts, the one should never be 
 mistaken for the other. If the observer will compare the diagrams 
 of casts as seen in the books with specimens of ropy mucus from the 
 bladder, the difference is at once apparent. 
 
 Casts are very important aids in diagnosis. They are found in 
 acute and chronic parenchymatous metamorphosis of the kidneys, in 
 acute diffuse nephritis, and in the chronic diffuse varieties. They are 
 rarely found iu the sclerotic, gouty, and waxy kidneys when uncom- 
 plicated. 
 
 Small casts of the hyaline, epithelial, nuclear, and finely granular 
 variety are found in the acute lesions, and in the early stage of the 
 more chronic forms. Large hyaline, coarsely granular, and fatty 
 casts indicate an advanced lesion. 
 
 By a careful microscopic study of the size and the amount of retro- 
 grade metamorphosis in the casts, a very accurate knowledge of the 
 extent of retrograde change in the uriniferous tubules will be ob- 
 tained. In this way an accurate prognosis can be given. 
 
PRESERVING CASTS. 32< 
 
 PRESERVING CASTS. 
 
 It is difficult to preserve casts, more especially if alkaline fermenta- 
 tion has occurred. Various methods have boon proposed. The three 
 which have been found most serviceable are: 
 
 First, by adding a 2 r /, solution of salicylic acid to the sample con- 
 taining the casts. In one case, they were woli preserved eighteen 
 months after the acid had been added. 
 
 A second method, or that employed t>y Dr. G. R. Elliott in the 
 laboratory of the New York Post-Graduate Medical (School, has been 
 found even better than the former. It is as follows: First, allow 
 fresh urine to settle in a conical glass for twenty-four hours. Second, 
 decant, i. e., pour off the supernatant fluid. Third, add to the resi- 
 due eight ounces of pure water and pour this mixture into a long and 
 narrow graduate. Fourth, add to the solution number three one 
 
 Fig. 86.— Conical, Receptacle for Collecting Sediment. 
 
 drachm of a saturated alcoholic solution of picric acid and mix. 
 Fifth, allow solution number four to stand four days. Sixth, decant 
 the supernatant fluid and wash the residue by adding pure water and 
 allow the mixture to stand twenty-four hours. Seventh, decant and 
 add to the residue one ounce each of glycerin and pure water. 
 
 This plan has been found quite satisfactory, the casts retaining their 
 microscopic features quite distinctly for many months. When pre- 
 pared in this way, they are quite serviceable for class demonstration. 
 The only objection is that they are misguiding, being much plainer 
 than when ordinarily seen in urine. 
 
 Another very good way to keep them a few days is to add half a 
 drachm of an alcoholic solution of eosin. This not only perserves 
 the casts, but it stains all the organic matter, and consequently renders 
 the casts more plainly visible. 
 
 The great objection to staining casts is that it may not always be 
 convenient to do so, and unless the examiner becomes perfectly familiar 
 with them in their natural medium, it may lead to gross errors. 
 
CHAPTER XIII. 
 
 SEDIMENTS OF DOUBTFUL ORIGIN; LIME CARBONATE; FATTY 
 
 MATTERS: CHOLESTERIN; CYSTIN; LEUCIN; TYROSIN; 
 
 XANTHIN. 
 
 SEDIMENTS OF DOUBTFUL IMPORTANCE. 
 
 There are a number of substances occasionally found in the urine, 
 some of which are indicative of a morbid condition of the body, 
 while others are purely of extraneous origin. But from the frequency 
 with which some of them are found in microscopic work, it is neces- 
 sary to speak of them, and it is also absolutely essential to be thor- 
 oughly familiar with their appearances. Many samples are found to 
 contain more extraneous matter than substances of intrinsic impor- 
 tance, and unless this point be fully appreciated, many a gross error 
 may easily be made. 
 
 LIME CARBONATE. 
 
 This substance is rarely, if ever, found in the human urine, 
 although it is one of the constituents of the body. It is always pres- 
 ent in large quantities, however, in urine taken from horses. Lime 
 carbonate from the lower animals occurs as spherical masses with 
 fine lines radiating from the centre; it has the same characteristics 
 when found in the human urine. 
 
 Some of the crystals of the urate of ammonium are said to closely 
 resemble those of lime carbonate, and the question arises which of 
 the two are present in the urine of the human species. 
 
 The carbonate of lime is recognized by its effervescing when brought 
 in contact with acetic acid. 
 
 If urine becomes alkaline from the presence of ammonium carbon- 
 ate, lime carbonate may be precipitated in the amorphous state along 
 with the earthy phosphates, but occasionally it assumes the crystalline 
 form. 
 
 The lime carbonate is found as an ingredient of urinary calculi 
 when developed iu the human system, but this form of calculus is 
 
FATTY MATTERS. .'525 
 
 about as infrequent as the crystals themselves. Practically speaking, 
 this salt may be said never to occur in the urine of the human being, 
 while it is almost constantly present in the herbivoia. 
 
 FATTY MATTERS. 
 
 Fat may occur in the urine as spherical droplets or globules of a 
 high refracting power or in the form of acicular crystals. 
 
 The characteristic microscopic appearance of fat globules is their 
 very high refracting power. They may present themselves as minute 
 droplets or as large and easily recognized globules. They have a cir- 
 cular form and sharply-defined marginal outline. They may or may 
 not have an amber color, and always act as double convex lenses, the 
 result of which is that they have a very bright centre and a dark and 
 rather broad peripheral band, which sometimes is almost black. As 
 the lens of the instrument is drawn away from the globule, its centre 
 increases in brightness and the margin becomes darker until finally 
 it is lost. 
 
 Fat may occur in the urine free and in large quantities, in the dis- 
 ease called chyluria, and occasionally from eating too much oily food. 
 It also occurs free, but in small quantities, in renal lesions in which 
 there is disintegration of the epithelial cells of the uriniferous tubules, 
 or it may be imbedded in the protoplasm of a desquamated cell or 
 in the form of a fatty cast. 
 
 Free oil globules are quite common in the urine from the fact that 
 patients do not sufficiently realize the necessity of using perfectly- 
 clean bottles. It is often collected in bottles which have previously 
 contained hair-oil, etc., and in this way much of the fat found in the 
 urine may be accounted for. 
 
 Fat crystals are occasionally found, either in the form of a stearate 
 or palmate. The two varieties have nearly the same form, i. e., fine 
 needle-like crystals. These and the crystals of leucin somewhat, 
 resemble each other. The fat crystals, however, are produced directly 
 from the oil itself, while the leucin is dependent upon an impaired 
 hepatic digestion and an incomplete proteid metabolism. 
 
 The microscopic mirror and the fat globule, which acts as a double; 
 convex lens, will often reproduce some object within the rays of re- 
 flection, such as the window, so that it is distinctly visible to the 
 examining eye. The image appears to be located in the fat globule. 
 
32i> 
 
 ( rSTIN. 
 
 CHOLESTERIN. 
 
 Those crystals are occasionally found in the urine in attacks of 
 jaundice and in connection with chronic suppurative nephritis. 
 
 Roberts records one case only, and quotes another by Murchison. 
 The author has also seen one case in which there was an abundance of 
 cholesterin in the urine, and the necropsy revealed a suppurative 
 nephritis. 
 
 The crystals are always easy of recognition, composed, as they are, 
 of thin, white and transparent plates which have a Bquare jsiece miss- 
 in g at one corner. They often pile themselves up in masses, the 
 notched corner of one plate always lying near the notched corner of 
 the opposed crystal. 
 
 The tests for cholesterin are: (1) Add to some crystals strong sul- 
 phuric acid with a little iodine or zinc chloride; they acquire a tint 
 which varies from greenish-blue to violet. (2) Put a drop of con- 
 centrated nitric acid on a crystal in a porcelain capsule, and evapo- 
 rate to dryness at a gentle heat; touch the residue with a drop of 
 ammonia. A deep-red color is produced. (3) Rub up cholesterin 
 with strong sulphuric acid, and add chloroform. A solution varying 
 in color from blood- red to purple is produced, which, after changing 
 successively into violet, blue, and green, finally disappears. 
 
 CTSTIX. 
 
 This substance is rarely met with in the urine, and is only of im- 
 portance from the fact that it is considered as an originator of calculi. 
 
 Fig. 87.— Cystix 
 
 It is also said to be peculiar from its presence in the urine of succes- 
 sive generations. It is a highly sulphurous body containing twenty- 
 
LEUCIN. 
 
 327 
 
 six per cent of sulphur, and is apparently closely allied to taurin, 
 although nothing is known of its origin. 
 
 Under the microscope, it is seen to be composed of hexagonal crys- 
 tals which often form aggregated masses, which may become the 
 nucleus of a calculus. When rapidly crystallized from an ammoniacal 
 solution, six-sided tablets and square prisms are formed. The former 
 closely resemble uric acid. Oystin crystals are distinguished from 
 uric acid by being soluble in ammonia, from which they form perfect 
 crystals upon evaporation; but the uric acid forms ammonia urates, 
 and is not recrystallized. The murexide reaction is not obtained with 
 cystin. 
 
 LEUCIN. 
 
 This is one of the intermediate products resulting from the trans- 
 formation of the proteids. From it urea is supposed to be produced, 
 which is the final product of a perfect and complete metabolism. 
 
 Fig. 88.— Lbucin Spheres. 
 
 The microscopic test for this substance is quite uncertain, for the 
 reason that many other substances have the same appearance, and 
 ■consequently errors are constantly being made by mistaking them 
 for it, and vice versa. 
 
 Unless the patient is suffering from some of the diseases previously 
 mentioned (p. 268), the diagnosis of its presence is extremely 
 doubtful. 
 
 It usually appears as highly refracting spheres, often tinged yellow, 
 and might easily he mistaken for fat globules. Leucin also forms 
 slender white glistening plates, or occurs in very thin plates grouped 
 
32S 
 
 X A Ml I I.N. 
 
 in a radiating 1'ashion. They differ from the urates, which are not 
 strongly refracting bodies. The chemical tests have been given 
 on p. 208. 
 
 TYKOSIX. 
 
 The statements regarding the former substance are equally applicable 
 
 to this, the two always being together, and have the same causes. 
 
 Tyrosin crystallizes in delicate needle-like forms, which often 
 arrange themselves in sheaves or bundles, and appear as such under 
 
 Fig. 89.— Tyrosin. 
 
 the microscope. They may be mistaken for the acicular crystals of the 
 fats, but can be distinguished by the chemical tests given on p. 269. 
 
 XAXTIIIX. 
 
 Whetstone crystals of this substance have been described as occur- 
 
 
 No. 90.— "Whetstone-shaped Crystals of Xanthin. 
 6, Crystals formed after adding hydrochloric acid. (Neubauer and Vogel.) 
 
 ring in the urine, but there appears to be some doubt in relation to 
 
FOREIGN MATTEB. 
 
 320 
 
 them, as they are so closely resembled by some of the uric acid crys- 
 tals. The question naturally arises, are they not the white crystals 
 
 Fig. 91.— Hydrochlorate of xanthin. 
 
 of uric acid which have been mistaken for the xanthin ? Hydro- 
 chlorate of xanthin is more diagnostic in its crystalline form. 
 
 FOREIGN MATTER. 
 
 There are quite a number of extraneous substances, wholly foreign 
 to the urine, with which the examiner should make himself thoroughly 
 familiar. The reasons for this are that these substances almost invari- 
 ably get into the urine and have often led to serious mistakes in diag- 
 nosis. 
 
 (a) Human hair appears under the microscope as large shafts of 
 considerable length, and varying in color. Human hair has a longi- 
 tudinal striation and at places the centre is darker and more granular 
 than the periphery. The distal extremity is striated and granular, 
 but near the root distinct interlacing lines are readily seen which in- 
 dicate the outline of the cell covering. 
 
 (b) Cat's hairs. — These also are quite common in urine and differ- 
 from the former in this, that their centre is very dark in color, sur- 
 rounded by a narrow transparent band, and on the surface the cell 
 markings are even more distinct than on human hairs. 
 
 (a) Muscle fibres. — Occasionally we find meat fibres in the urine, 
 and they are generally of the striated variety. Owing to a partial 
 disintegration, the transverse and longitudinal striations are only 
 faintly marked, but are sufficiently distinct to be recognized as muscle 
 tissue. 
 
 (d) Oil-globules. — Fat is not infrequently found as a foreign ele- 
 ment in urine (see p. 325). 
 
 (e) Air-bubbles. — These are found in almost every sample mounted. 
 
330 
 
 FoKKK.N MATTKK. 
 
 They are usually spherical, but may assume almost any form. They 
 have a bright and vacant centre with a dark peripheral margin, in the 
 centre of which there is a very narrow white circle. 
 
 (/) Feathers or fragments of them coming from the bedding or 
 dust brushes are frequently found. If a single shaft is examined, it 
 is knobbed and resembles a series of fish-hooks broken off at their bases 
 ami joined point to base. In the feather, the point is attached to the 
 common stalk and bhe base is the free extremity. The fragment of a 
 stem and a few attached branches may occasionally be seen under the 
 microscope. 
 
 (g) Cotton fibres appear at first as small fibres with nearly parallel 
 outlines and longitudinal striations, but by following along its course 
 it will be found to twist upon itself so that the right border will 
 
 Fig. 92. 
 
 a, Human hair; 6, cat's hair; c, flax fibre; d, cotton fibre; e, feather; /, knotted portion of 
 shaft; g, wool fibre; h, silk fibre; j, wood fibre; k, starch granule; 1, fat; m, air -bubble. 
 
 become the left, or vice versa. A piece of tape twisted upon itself 
 represents how this twisting is produced. 
 
 (h) Woollen fibres closely resemble hair, but as a rule are smaller 
 and not so dark in color. The irregular surface markings represent- 
 ing the ensheathing cells is very distinct, but they have no granular 
 centre. 
 
 (/) Flax or linen fibres resemble cotton, but do not twist upon 
 themselves. They are striated longitudinally and crossed at short 
 intervals by dark transparent lines, and are broken with an irregular 
 fracture similar to a round pencil broken sharply. These fibres are 
 usually round. 
 
 {j ) Silk fibres are small and glistening, with fine irregular Ion- 
 
FOREIGN MATTER. 331 
 
 gitudinal markings and break nearly at a right angle similar to linen. 
 Their glistening appearance, however, is the chief point of difference 
 from linen. 
 
 All these fibres may be tinged blue by the indican of the urine, but 
 this is especially noticeable in the cotton fibres. 
 
 (k) Starch granules are frequently found in the urine when starch 
 powder has been dusted upon the genitals, as is frequently the case in 
 young children. They are readily recognized by their elevated por- 
 tion or hilum, and the surrounding dark and light-colored rings. 
 The application of a little iodine will turn them blue. 
 
 (I) Tea-leaves also find their way into the urine and appear as 
 irregular masses, having two or three light spots with a dark centre 
 from which a spiral thread springs, looking like a partially uncoiled 
 wire spring or the simple spiral may be all that will be found. There 
 are, however, many other vegetable substances that have this spiral 
 appearance. 
 
 (m) Wood and vegetable. — Small fragments of wood fibres and all 
 kinds of vegetable substances occasionally find their way into the 
 urine. 
 
 (n) Finger markings are not of infrequent occurrence upon the 
 glass circles and are often thought to be indicative of some urinary 
 change until they are recognized as foreign elements. 
 
 Out of the preceding list the substances which are most commonly 
 found in connection with urinary analysis are air, oil, hair, cotton, 
 wood, linen, and feathers. The substances most frequently mistaken 
 for casts are hair, wool, cotton, linen, and dirt. Therefore, these are 
 the foreign bodies which every examiner should become as familiar 
 with as those of intrinsic origin. 
 
CHAPTER XV. 
 
 ANIMAL ORGANISMS. 
 
 Echinococcus; Filaria Sanguinis Hominis; Bilharzia ILema- 
 tobia; Trachin^e Cystica; Eustrongylus seu Strongylus 
 gigas; Tetrastoma Eenalis; Spurious Entozoa; Pediculus 
 Pubis. 
 
 animal organisms. 
 
 There are only a few parasites which infest the human body and 
 make their escape by the urinary channel, and there are a few that 
 may get in the nrina from the outside after it has been voided. 
 
 Ecchinococcus. — The scolices and booklets of this parasite may oc- 
 
 FlG. 93.— HOOKLETS FROM SCOLEX OF T.ENIA ECHINOCOCCUS. X 750. 
 
 (Delafleld and Prudden, " Handbook of Pathological Anatomy and Histology.") 
 
 casionally find their way out of the body with the urine. Such cases 
 are recorded, and are probably due to the rupture of an hydatid cyst 
 in the kidney. When viewed under the microscope with a low power, 
 the scolices appear to be about the size of a millet seed, and are either 
 round or oval, and have at one end a dark colored zone or disk. The 
 body is small and granular, upon one extremity of which minute 
 suckers can be made out; with a higher power, their circle of hook- 
 lets can be seen, and the four suckers placed laterally and behind the 
 hooklets are now distinctly visible. Free hooklets are often found in 
 the urine at the same time. 
 
 (b) Filaria sanguinis hominis, F. Bancrofti. — In the embryonic 
 
ANIMAL ORGANISMS. 666 
 
 state, they are about yfg- of an inch (G mm.) long, pointed at one 
 end and blunt at the opposite. When fully developed, they are hair- 
 like and from three to four inches (7 to 10 centimetres) in length. 
 
 They vary in width from -gfar ( 8 mm -) to rfo of an incn ( 4 mm -)- 
 
 Their growth and development is quite peculiar. The parent 
 worm lives in the lymphatics; the embryo escapes from the uterus of 
 the mature worm, and finds its way along the lymphatic channels to 
 the thoracic duct, and in this way ultimately reaches the blood- 
 vessels. They originate more frequently in the lymphatics of the 
 scrotum and leg, and appear in the blood most abundantly in the 
 evening and up to midnight; after this hour, they gradually disappear 
 until 8 or 9 o'clock a.m., when they are entirely absent from the blood 
 for the remainder of that day. 
 
 Fig. 94.— Scolices op T-enia Echinococcus. X 60. 
 
 In one, the rosteUum is projected, in the others it is withdrawn. (Delafield and Prudden, 
 1 Handbook of Pathological Anatomy and Histology.") 
 
 "This phenomenal filarial periodicity is apparently an adapta- 
 tion of the habits of the parasite to those of the female of a peculiar 
 species of mosquito, which preys on the blood at night, and thus 
 imbibes the young filaria, to which it acts as an intermediate host. 
 Having entered the stomach of the mosquito, the filaria undergoes a 
 metamorphosis, eventuating in'its becoming possessed of an alimentary 
 canal, rudimentary organs of generation, increased size, great activity, 
 and a circumoval crown of papillae. The latter is the boaring appa- 
 ratus, which enables the animal to leave the body of the mosquito 
 when this insect dies, after depositing her eggs on the water, and 
 to traverse the ^human tissues to which it gains access, probably by 
 being swallowed in drinking water." This history is probably more 
 ingenious than real. 
 
334 
 
 AN1NAI. ORGANISMS. 
 
 The tilaria has been found in the blood, however, in cases of chy- 
 luria. nevoid elephantiasis, <>r lympho-sarcoma, varicose and indu- 
 rated groin glands, galactocele, ascites with milky fluid, craw-craw, 
 
 lymphatic fever, and certain kinds of lymphatic abfi - - 
 
 It has been found in the urine in connection with chvluria and 
 nevoid elephantiasis. It may possibly find its way into the urine of 
 
 Fig. 95.— Filaria Sanguinis Hosirxis or Bancrofti. 
 
 a. Female (natural size i : b. head and neck ( X •">."> diam. : <•'. t ail : il. free embryo X 400 iliam. : 
 e. egg containing embryo; /, egg showing the yolk. After Cobbold. (London Lancet, Octo- 
 oer6th. 1877, p. 49E 
 
 the other enumerated diseases, but, up to the present time, has not 
 been so recorded. 
 
 (c) Bilharzia hmmatobia. — This name was given to this parasite 
 bv Professor Cobbold in 1851, from the fact that Dr. Bilharz, 
 
ANIMAL OPJJANIKMS. 
 
 335 
 
 of Cairo, was the first to discover the entozoon. The worm was 
 first found in the portal vein of a man, next in the corresponding 
 vein of a monkey, and at first was supposed to be a distoma, but it is 
 now generally known as the Bilharzia hmmatobia. Later on, it 
 was found in the mesenteric and vesical veins, and also in other 
 parts of the body, producing formidable diseases, and, finally, the 
 parasitic hematuria. 
 
 Dr. John Harley next discovered that a form of epidemic hasma- 
 turia at the Cape of Good Hope was due to a parasite which he con- 
 sidered a new species. Later researches, however, go to prove that 
 it was the same Bilharzia described by Dr. Bilharz, and this conclu- 
 sion is now pretty generally accepted. But the researches of Dr. 
 
 Fig. 96.— Filaria'in Human Blood. 
 After a photograph published by Dr. MacKenzie. 
 
 Harley showed a much wider geographical range for this parasite than 
 had previously been supposed. 
 
 It differs from all the varieties of flukes in having separate sexes. 
 The female is a very slender worm resembling filaria-form nematoids. 
 
 During copulation, the female is lodged in a long slit-like grove or 
 gynEecophoric canal with which the male is furnished. The ova mea- 
 sure from 1 | 1J to y^q of an inch in length, and are sharply pointed at 
 one end. They are a form of ciliated embryo, and an extended de- 
 scription will be found by Dr. Cobbold, British Medical Journal, 
 1872. 
 
 Both the mature worm and ova are found in the urine in this pecu- 
 liar form of hematuria. 
 
 (d) TrachincB cystica of Dr. Saulsbury. — In this case, the exact 
 
336 
 
 ANIMAL ORGANISMS. 
 
 species have not been fully determined, having been met with in only 
 a few cases. By some it is thought to be identical with the filaria 
 piscam; by others, the spiroptera hominis. 
 
 Fig. 97.— Bilharzia ILsmotobia. X about 15 times. 
 
 a, b, and c, the female, partly placed in the gynaecophorous canal of the male; a, anterior 
 extremity; c, posterior extremity; rf, body seen within the canal; c, /, g, h, and i, the male; e,/» 
 gynaecophorous canal, from which the female has been partly extracted; i, buccal sucker; k, 
 ventral sucker; between t and fc, the trunk; after fc, the tail. After Bilharz. 
 
 (e) Eustrongylus or Strongylus gigas. — This form of entozoa is 
 more frequent in lower animals than in man. The worm is commonly 
 
 Fig. 
 
 -Strongylus sea Eustrongylus Gigas. 
 
 found in the kidney or pelvis, and may possibly find its way down the 
 ureter, and in this way make its escape from the body through the 
 urethra. 
 
 Tetrastoma renalis. — This entozoon was found in the urine in one 
 case by Lucarella, and described by Dellechiaji. 
 
ANIMAL ORGANISMS. 
 
 337 
 
 SPURIOUS ENTOZOOA. 
 
 There are a number of animal organisms which may find their way 
 into the urine from the outside, such as the vorticella, the amoeba, 
 and various forms of the infusoria. 
 
 Under this heading may also be included the spiroptera hominis of 
 Eudolphi, the disposoma crenata of Farre, and the dtctylius aeuleatus 
 of Curling. 
 
 PEDICULUS PUBIS. 
 
 The pediculus pubis also finds its way into the urine, as illustrated 
 
 Fig. 99.— Pediculus Pubis found in Urine. X 125. 
 
 by a drawing from one found in the urine. 
 
 23 
 
CHAPTER XVI. 
 
 ANALYSIS OF THE CASE. INDICATIONS AS TO DIAGNOSIS AND 
 
 TREATMENT. 
 
 ANALYSIS OF THE CASE. 
 
 A careful review of each sample examined, in conjunction with the 
 clinical history, will usually make the diagnosis clear and positive. 
 This is especially true in reference to the lesions so long grouped 
 together under "the common term Bright's disease. It is positively 
 affirmed that, by a close observance of the laws already advanced in 
 reference to the methods of production and the rules given for diag- 
 nosis, the existing lesions can in every instance be diagnosticated with 
 great accuracy. It may be argued that such precision in diagnosis 
 does not materially change the method of treatment; in which there 
 is perhaps much truth, but it enables a more positive prognosis to be 
 made and renders the treatment less empirical, and offers a far more 
 certain prospect for recovery by a proper selection of remedial agents. 
 
 By reviewing closely the clinical history and the urinary findings, 
 both at the bedside and at the necropsy, in over a hundred cases, an 
 accurate diagnosis has resulted in every instance. A striking case in 
 point is recalled where, by the application of these rules to the urinary 
 analysis alone, an accurate diagnosis was made without seeing the 
 patient until the necrops}', which fully confirmed the opinion pre- 
 viously expressed. This instance was an accidental injury in which 
 no renal lesion was suspected, and was apparently developed as the re- 
 sult of the surgical accident, and caused the death of the patient. 
 
 This case is cited to show what accuracy in diagnosis can be at- 
 tained, and how often an unobserved renal lesion may be a prominent 
 factor in reference to prognosis. 
 
 To accomplish this accuracy in diagnosis, the examiner must make 
 himself thoroughly familiar with the microscopic histological changes 
 wrought in the kidneys and liver in connection with the different renal 
 lesions. He must also be thoroughly familiar with the microscopic 
 appearances of the urine, as it is by this careful microscopic examina- 
 
ANALYSIS OF THE CASE. \Y,V.\ 
 
 tion, and a proper interpretation of what is formd, that lie is enabled 
 to determine with positiveness the existing renal lesion. 
 
 A chemical examination alone yields comparatively little informa- 
 tion in relation to the physiological phenomena of the body and their 
 abnormal workings; but in conjunction with the microscopic results, a. 
 wonderful degree of precision is obtained, not only in connection with 
 diseases of the kidneys, but in all diseases, and especially in con- 
 nection with those originating in a faulty physiological function of 
 the liver. 
 
 INDICATIONS AS TO DIAGNOSIS AND TKEATMENT. 
 
 A thorough study of urinary analysis, and especially the microscopic 
 part, will often make a diagnosis sure, which otherwise would remain 
 obscure. This is true not alone in reference to renal lesions, but 
 equally so in hepatic diseases. 
 
 Having obtained an accurate diagnosis, with a clear conception of 
 the pathological processes and the interrupted or modified physiologi- 
 cal phenomena, a critical study of the clinical symptoms will enable 
 the examiner to prognosticate with a wonderful degree of accuracy. 
 
 Treatment based upon such knowledge enables the prescriber to 
 anticipate pathological processes, to strengthen the enfeebled physio, 
 logical functions, and in many instances enable or cause the system 
 to completely repair the damage, thus effecting a cure where other- 
 wise a fatal issue would be the result. 
 
 Treatment now becomes a fixed principle; a cause to be removed,, 
 and an abnormal and enfeebled system to be placed in a position to 
 restore its damaged tissues and organs to their normal state. Having" 
 fully comprehended these principles, a specific virus, drug, or mineral 
 water cannot be expected to cure these complex physiological and. 
 pathological problems. It must be clear to every one that this is im- 
 possible. The main object should be to discover where the physio- 
 logical action is most at fault, and rectify it if possible. In this way 
 each faulty action can be treated and removed in the order of its 
 importance, and many permanent cures will be effected which other- 
 wise would terminate in an early and untimely death. 
 
INDEX. 
 
 Acid, benzoic, 268 
 fermentation, 210 
 hippuric, 269 
 kinurenic, 267 
 phenolic, 269 
 uric, 263, 294 
 Acidity of urine, 208 
 Acute atrophy of the kidneys, 132 
 
 definition of, 132 
 
 diagnosis of, 133 
 
 etiology of, 132 
 
 microscoDic examination of, 
 132 
 
 pathological anatomy of, 132 
 
 prognosis of, 133 
 
 symptoms of, 133 
 
 treatment of, 133 
 congestion or hyperaamia of the 
 
 kidneys, 111 
 diffuse nephritis, 45 
 
 definition of, 45 
 
 diagnosis of, 49 
 
 etiology of, 45 
 
 microscopic anatomy of, 47 
 
 pathological anatomy of, 46 
 
 prognosis of, 49 
 
 symptoms of, 47 
 
 treatment of, 49 
 parenchymatous metamorphosis 
 of the kidneys, 17 
 
 diagnosis of, 22 
 
 etiology of, 17 
 
 macroscopic appearances of, 
 19 
 
 microscopic appearances of, 
 19 
 
 prognosis of, 22 
 
 symptoms of, 21 
 
 treatment of, S3 
 
 urinary symptoms of, 22 
 sclerosis of the kidneys, 92 
 Adenoma of the kidneys, 151 
 
 definition of, 151 
 
 diagnosis of, 152 
 
 etiology of, 151 
 
 pathological anatomy of, 151 
 
 symptoms of, 152 
 
 Adventitious coloring matters of the 
 
 urine, 279 
 Air bubhles, 329 
 Alantoin, 267 
 Albumin, 221 
 
 clinical significance of, 2S2 
 precautions in testing for, 221 
 tests for (see Tests), 222 
 Albuminoid kidneys, 98 
 Albuminuria, adventitious, 217 
 intrinsic, 217 
 prognosis of, 232 
 treatment of, 232 
 Alcohol, 24 
 
 Alkaline fermentation, 210 
 Alkalinity of urine, 208 
 Ammonio-magnesium phosphate, 211 
 Amphoterous urine. 213 
 Amyloid kidneys, 98 
 Anaemia of the kidneys, 109 
 definition of, 109 
 etiology of, 110 
 macroscopic anatomy of, 110 
 microscopic anatomy of, 110 
 symptoms of, 110 
 treatment of, 110 
 Analysis of the urine, introductory- 
 remarks on, 194 
 of the case, 338 
 Anatomy of the kidneys, 1 
 Aneurisms, 62 
 
 Angioma of the kidneys, 153 
 Animal organisms, 332 
 Apoplexy, 64 
 Arcade of Flint, 10 
 Arteriaa recta?, 10 
 Arteries, intertubular, 10 
 Ascaris renalis, 163 
 Ascending limb of tubule, 5 
 Ascites, 62 
 
 Atrophy of the kidneys, chronic, 138 
 definition of, 133 
 etiology of, 133 
 pathological anatomy of, 138 
 
 Bacillus tuberculosis, 311 
 
342 iM'i:.\. 
 
 Bacillus tuberculosis, method of Casts, nucleated, 319 
 
 staining, 138 preserving of, 328 
 
 Bacteria, micro or simple, 310 tubular. 331 
 
 sphero, 808 waxy. 322 
 
 desmo, 311 Cathartics in parenchymatous meta- 
 
 Balance, Mohr-Westphal, 215 morphosis of the kidneys, 37 
 
 Bancroft! iilaria. 332 Causes of diminished pressure in the 
 
 Bath, hut-air. 36 glomeruli, 13 
 
 Bathing the bick, 24 of increased pressure in the 
 
 Benzoic acid. 268 glomeruli, 13 
 
 Bertini, ducts of, 7 of increased temperature, 26 
 Bile pigments in urine. 280 Cells, epithelial, 302 
 
 tests for, 280 Chlorides, 276 
 
 Bilharzia hssmatobia, 160, 334 clinical significance, 277 
 
 definition of, 160 clinical symptoms of, 277 
 
 diagnosis of, 162 tests for. 27(5 
 etiology of, 160 Cholesterin, 326 
 microscopic examination of, Chronic atrophy, 133 
 
 162 definition of. 133 
 
 pathological anatomy of, 161 etiology of, 133 
 
 prognosis. 162 pathology of, 133 
 
 symptoms, 162 diffuse nephritis, first variety, 51 
 
 treatment, 162 introductory remarks on, 51 
 
 Blank for urinary analysis, 198 definition of, 51 
 
 Blindness, uremic, 87 etiology of. 52 
 
 Blood-corpuscles, 287 microscopic examination of, 
 
 haemoglobin, 283 52 
 
 supply of kidneys, 10 pathological anatomy of, 52 
 
 Bowman's capsule, 7 prognosis of, 54 
 
 Bronchitis. 66 symptoms of, 53 
 
 Bubbles, air, 329 treatment of, 55 
 
 urinary symptoms of, 54 
 
 Calculi, renal, 129 second variety, 55 
 
 Calices, 4 etiology of, 55 
 
 Capsules, 3 microscopic anatomy of, 56 
 
 Bowman's, 7 pathological anatomy of, 56 
 
 layers of. 5 prognosis of, 58 
 
 Malpighian, 7 symptoms of, 58 
 
 microscopic appearances of, 5 treatment of, 58 
 
 Mxiller's, 7 third variety, 58 
 
 Carbonate of lime, 324 definition of, 59 
 
 Carcinoma of the kidneys, 149 diagnosis of, 60 
 
 definition of, 149 etiology of, 58 
 
 diagnosis of, 150 microscopic examination of, 
 
 etiology of, 149 59 
 
 microscopic examination of, pathological anatomy of, 58 
 
 150 symptoms of, 60 
 
 pathological anatomy of, 149 prognosis of, 60 
 
 prognosis of, 150 treatment of, 87 
 
 symptoms of, 150 dieting in, 89 
 
 treatment of, 150 parenchymatous metamorphosis 
 
 Carnin, 267 of the kidneys, 27 
 
 Case, analysis of, 338 cathartics, 37 
 
 Casts, 317 definition of, 27 
 
 blood, 317 diagnosis of, 32 
 
 coarsely granular, 321 diaphoretics in, 35 
 
 corkscrew, 321 * diuretics in, 35 
 
 distinguishing characters, 322 etiology of, 27 
 
 epithelial, 318 microscopic examination of, 
 
 fatty, 321 29 
 
 finely granular, 320 pathological anatomy of, 29 
 
 hyaline, 317 prognosis of, 33 
 
INDEX. 
 
 343 
 
 Chronic parenchymatous metamor- 
 phosis of the kidneys 
 
 symptoms of, 31 
 
 treatment of, 33 
 
 urinary examination of, 32 
 sclerosis of the kidneys, 92 
 Chemical composition of urine, 190 
 
 examination of urine, 202 
 Clinical significance of bile pigments 
 in urine, 281 
 
 of blood-corpuscles in urine, 
 289 
 
 of blood-haemoglobin in urine, 
 283 
 
 of coloring-matters, 280 
 
 of fatty matter in urine, 283 
 
 of glycocholic acid, 270 
 
 of hippuric acid, 269 
 
 of indican, 271 
 
 of indigo, 271 
 
 of indol, 271 
 
 of leucocytes, 290 
 
 of oxalates, 296 
 
 of phosphates, 275 
 
 of taurocholic acid, 270 
 
 of tyrosin, 269 
 
 of urates, 274 
 
 of urea, 261 
 Coloring-matters of the urine, adven- 
 titious, 279 
 Color of urine, 204 
 Coma, diabetic, 185 
 Complications of renal lesions, 62 
 
 ascites, 62 
 
 aneurism, 62 
 
 apoplexy, 64 
 
 asthma, 65 
 
 bronchitis, 66 
 
 cardiac lesions, 67 
 
 cirrhosis of liver, 69 
 
 constipation, 69 
 
 diarrhoea, 69 
 
 eczema, 70 
 
 emphysema, 70 
 
 endarteritis, 64 
 
 endocarditis, 70 
 
 erysipelas, 70 
 
 gangrene, 71 
 
 gastric affections, 71 
 
 haemorrhage, 72 
 
 hepatic disease, 72 
 
 hydropericardium, 73 
 
 headache, 73 
 
 hydrosemia, 76 
 
 hydrothorax, 74 
 
 intestinal catarrh, 74 
 
 jaundice, 74 
 
 meningitis, 75 
 
 neuro-retinitis, 75 
 
 oedema, 76 
 
 oedema glottidis, 75 
 oedema of lungs, 75 
 
 Complications of renal lesions, peri- 
 carditis, 76 
 
 peril, onil is, 76 
 
 phthisis, 80 
 
 pleurisy, 81 
 
 pneumonia, 81 
 
 retina] lesions, 81 
 
 treatment of, 86 
 
 uraemia, 82 
 
 uraemic blindness, 87 
 Congenital rhabdo-sarcoma, 153 
 Congestion, acute, of kidneys, 111 
 
 definition of, 1 1 1 
 
 etiology of, 111 
 
 macroscopic appearance of, 
 112 
 
 microscopic examination of, 
 112 
 
 prognosis of, 113 
 
 symptoms of, 113 
 
 treatment of, 113 
 
 urinary examination of, 113 
 chronic, of kidneys, 114 
 
 definition of, 114 
 
 diagnosis of, 116 
 
 etiology of, 114 
 
 microscopic examination of, 
 115 
 
 pathological anatomy of, 145 
 
 prognosis of. 116 
 
 symptoms of, 115 
 
 treatment of, 117 
 Convoluted tubes of first order, 5 
 
 second order, 6 
 Corpuscles, 285 
 
 Malpighian, 5 
 Cortical arch, 5 
 layer, 5 
 markings, 3 
 Cotton fibres, 330 
 Crystals of uric acid, 212 
 Cysts, echinococcus, 157 
 
 renal, 134 
 Cystin, 268 
 Cystica trichinae, 335 
 
 Daily quantity of urine, 203 
 
 Desmo-bacteria, 311 
 
 Descending loop of tubule, 5 
 
 Diabetes mellitus, 165 
 
 Diarrhoea, 69 
 
 Diathesis, uric acid, 265 
 
 Dieting in chronic diffuse nephritis, 89 
 
 in glycosuria, 193 
 Digitalis, 25 
 
 Distinguishing character of casts, 322 
 Diaphoretics, 35 
 Diuretics, 36 
 
 medicinal, 35 
 Ducts of Bertini, 7 
 
 Echinococcus, 332 
 
344 
 
 INDEX. 
 
 Echinococcus cysts. 157 
 definition of, 157 
 diagnosis of, 160 
 
 etiology of, 157 
 
 pathological anatomy of, 157 
 
 prognosis of, 160 
 
 symptoms of, 159 
 
 treatment of, 160 
 Eczema. 70 
 Elaterium, 37 
 Emboli, pysemic, 1-45 
 Embolism, fat, of the kidneys, 143 
 
 renal, 141 
 Emphysema, 70 
 Endarteritis, (14 
 Endocarditis, 70 
 Entozoa, spurious, 337 
 Epithelial cells. 302 
 Epithelium, function of, 15 
 Erysipelas, 70 
 Eustrongylus gigas, 336 
 Excretory nitrogenous substances, 254 
 Experiments of Heidenhain, 15 
 of Nussbaum, 17 
 
 Fat embolism of the kidneys, 143 
 
 definition of, 143 
 
 diagnosis, 144 
 
 etiology, 143 
 
 microscopic examination, 143 
 
 pathological anatomy, 143 
 
 prognosis, 144 
 
 symptoms, 144 
 
 treatment, 145 
 Fatty matter, 325 
 
 in urine, 282 
 Faveola, 7 
 Feathers, 330 
 Fel bovis inspissatum, 26 
 Fermentation, acid, 210 
 
 alkaline, 210 
 Ferrein, pyramids of, 3 
 Fibres, cotton, 330 
 flax, 330 
 muscle, 329 
 silk, 330 
 woollen, 330 
 Fibroma of the kidneys, 153 
 Filaria sanguinis hominis, 332 
 Finger markings, 331 
 First form of large white kidney, 27 
 Flint, arcade of, 10 
 Floating kidney, 2 
 Foetal markings of the kidneys, 2 
 Foreign matter. 329 
 Fourth form of large white kidney, 51 
 
 of small kidney, 97 
 Fungi, 315 
 
 Gangrene, 71 
 Gastric affections, 71 
 Gigas Eustrongylus, 336 
 
 Glycosuria, 165 
 
 circulatory symptoms in, 185 
 
 clinical history of, 183 
 
 definition of, 165 
 
 diabetic coma, 185 
 
 diagnosis of, 188 
 
 diet in, 190 
 
 etiology of, 165 
 
 falling out of nails in, 187 
 
 gangrene in, 187 
 
 integumental lesion and symp- 
 toms. 186 
 
 nervous symptoms, 185 
 
 ocular symptoms in, 186 
 
 oedema in, 187 
 
 pathological anatomy of, 169 
 
 pathological considerations of, 
 167 
 
 physiological considerations of, 
 167 
 
 prognosis of, 188 
 
 respiratory symptoms in, 185 
 
 thrombosis in, 187 
 
 treatment of, 188 
 
 urinary symptoms, 187 
 Globules, oil, 329 
 
 Glomeruli, causes of diminished pres- 
 sure in, 13 
 
 causes of increased pressure in, 
 13 
 
 physiological action of, 12 
 Glomerulus, 8 
 Glottis, oedema of, 75 
 Glucose in urine, 235 
 
 experiments in testing for, 235 
 
 quantitative analysis of, 292 
 
 quantitative tests for, 244 
 
 tests for (see Tests), 234 
 Glycin. 268 
 Glycocholic acid, 270 
 
 clinical significance of, 270 
 Gonococcus, 311 
 Gouty nephritis, 97 
 
 definition of, 97 
 Granules, starch, 331 
 Gravity, specific, 214 
 Guanin, 267 
 Gummata of kidneys, 155 
 
 Haemoglobin, 283 
 Haamatobia Bilharzia, 334 
 Hasmatoglobinuria, 106 
 
 definition of, 106 
 
 etiology of, 106 
 
 microscopic examination of, 108 
 
 pathological anatomy of, 107 
 
 prognosis of, 109 
 
 symptoms of, 108 
 
 treatment of, Id!) 
 Haemorrhage, 72, 105 
 Hair, cat's, 329 
 
 human, 329 
 
INDEX. 
 
 545 
 
 Headache, 73 
 
 Heidenhain, experiments of, 15 
 
 rods of, 8 
 Hepatic disease, 72 
 Hilum, 34 
 Hippuric acid, 269 
 Horse-shoe kidney, 2 
 Hot-air bath, 36 
 How to use the microscope, 285 
 Hyaline kidneys, 98 
 
 definition of, 98 
 diagnosis of, 101 
 etiology of, 98 
 
 macroscopic anatomy of, 99 
 microscopic anatomy of, 99 
 prognosis of, 101 
 symptoms of, 101 
 treatment of, 101 
 Hydatids of the kidney, 157 
 Hydrosemia, 66 
 Hydronephrosis, 127 
 diagnosis of, 128 
 definition of, 127 
 etiology of, 127 
 pathological anatomy of, 127 
 prognosis of. 128 
 symptoms of, 128 
 treatment of, 128 
 Hydropericardium, 173 
 Hydrothorax, 74 
 Hyperaemia of the kidneys, 111 
 acute, 111 
 chi'onic, 111 
 Hypertrophies of the kidneys, 134 
 definition of, 134 
 etiology of, 134 
 physical examination of, 134 
 symptoms of, 134 
 Hypoxanthin, 267 
 
 Increased temperature, causes of, 26 
 Indican, 271 
 
 Indications for diagnosis and treat- 
 ment, 339 
 Indigo, 271 
 Indol, 271 
 Infarction of the kidneys, 141 
 
 definition of, 141 
 
 diagnosis of, 143 
 
 etiology of, 141 
 
 pathological anatomy of, 141 
 
 prognosis of, 143 
 
 symptoms of, 142 
 
 treatment of, 143 
 Inflammation, 16 
 Infundibnla, 4 
 Intercalated tubes, 6 
 Intertubular arteries, 10 
 plexuses, 11 
 veins, 10 
 Intestinal catarrh^ 74 
 Intrinsic albuminuria, 217 
 
 Jaborandi and its alkaloids, 24, 85 
 Jaundice, 74 
 Junctional tubes, 6 
 
 Kidneys, 132 
 
 acute atrophy of, 132 
 
 congestion of, 111 
 
 hyperaemia of, 111 
 
 parenchymatous metamor- 
 phosis of, 17 
 
 sclerosis of, 92 
 adenoma of, 151 
 albuminoid, 98 
 amyloid, 98 
 anaemia of, 109 
 angioma of, 153 
 blood supply of, 10 
 carcinoma of, 149 
 chronic atrophy of, 133 
 
 congestion of, 114 
 
 parenchymatous metamor- 
 phosis of, 27 
 
 sclerosis of, 92 
 congenital rhabdo-sarcomaof, 153 
 cysts of, 134 
 fat embolism of, 143 
 fibroma of, 153 
 first form of large white, 27 
 
 small red, 92 
 fourth form of small, 97 
 gouty, 97 
 
 gummy tumors of, 155 
 hyaline, 98 
 hydatids of, 157 
 hyperaemia of, 114 
 hypertrophy of, 134 
 infarction of, 141 
 lardaceous. 98 
 large red, 98 
 lipoma of, 153 
 lobules of, 7 
 lymphatics of, 11 
 lymphomata of, 154 
 microscopic appearances of, 5 
 nerves of, 11 
 number of, 1 
 osseous tumors of, 155 
 physiology of, 12 
 sarcomata of, 146 
 second form of large white, 38 
 
 small white, 55 
 size of, 1 
 situation of, 1 
 specific gravity of, 1 
 stroma of, 11 
 
 summary of lesions of, .101 
 third form of large white, 41 
 
 small white, 58 
 tubercular, 136 
 variations in, 2 
 veins of, 10 
 waxy, 98 
 
346 
 
 INDEX. 
 
 Kidneys, weight of, 1 
 Keratin, 266 
 Keratinin, 366 
 Kynurenio acid, 267 
 
 1 ,;il>\ rintli, Litdwig's, 98 
 Lardaceous kidneys, 98 
 Large red kidney, 98 
 
 white kidney, first form of, 27 
 
 fourth form of, 27 
 
 second form of, 38 
 
 third form of, 38 
 Leptothrix. M 1 
 Lesions, cardiac, 67 
 
 retinal. 81 
 Leucin, 268, 327 
 Leucocytes, 290 
 Lime, carbonate of, 324 
 
 oxalate, 295 
 Linen libres, 330 
 Lipoma, 153 
 Liver, cirrhosis of, 69 
 Lobules of the kidney, 17 
 Loop of tubule, 5 
 Looped tube of Heule, 5 
 Lungs, cedema of, 75 
 Lymphatics of the kidneys, 11 
 Lymphomata, 154 
 
 Macroscopic appearance of the kid- 
 neys, 2 
 Malpighian pyramids, 4 
 
 capsule, 7 
 
 corpuscle, 5 
 Markings, finger, 331 
 
 of the cortex, 3 
 Matter, fatty, 325 
 
 foreign, 329 
 Muscle fibres, 329 
 Medicinal diuretics, 25 
 Medullary substance, 3 
 Meningitis, 75 
 
 Method for staining bacillus tubercu- 
 losis, 138 
 Micro- bacteria, 311 
 Micrococci, 308 
 Microscope, how to use, 385 
 Microscopic appearance of capsule, 5 
 of kidneys, 5 
 
 pigments, 300 
 Mohr-Westphal balance, 215 
 Mucus, 282, 292 
 Muller's capsule, 7 
 Murexide test, 265 
 
 Neck of tubule, 5 
 Nephritis, acute diffuse, 45 
 dieting in, 39 
 
 chronic diffuse, first variety, 51 
 second variety, 55 
 third variety, 58 
 
 Nephritis, gouty, 97 
 
 suppurative, 118 
 Nerves, section of the renal. 13 
 
 of the kidney, 11 
 Neuro-retinitis, 75 
 
 Nitrogenous excretory substances, 254 
 Nussbaum's experiments, 17 
 
 Odor of urine, 208 
 
 (Edema, 76 
 
 glottidis, 76 
 of lungs, 75 
 treatment of, 37 
 
 Oil globules, 329 
 
 Opening of ureter into bladder, 3 
 
 Opiates in renal lesions, 25 
 
 Organisms, animal, 332 
 
 bilharzia hsematobia, 332 
 echinococcus, 332 
 filaria sanguinis hominis, 332 
 pediculus pubis, 337 
 spurious entozoa, 330 
 strongylus gigas, 336 
 tetrastorna renalis, 336 
 trichinae cystica, 335 
 vegetable, 308 
 
 Osseous tumors of the kidneys, 155 
 
 Oxalate of lime. 295 
 
 Papillae of the kidney, 4 
 Parenchymatous infiltration meta- 
 morphosis of the kidneys 
 with wasting diseases, 41 
 
 definition, 41 
 
 etiology, 41 
 
 microscopic examination of, 
 42 
 
 pathological anatomy, 42 
 
 prognosis, 43 
 
 symptoms, 43 
 
 treatment, 43 
 metamorphosis of the kidneys, 
 acute, 17 
 
 chronic, 27 
 
 with pregnancy, 38 
 
 etiology of, 38 
 
 microscopic examination of, 
 38 
 
 pathological anatomy of, 38 
 
 prognosis of, 39 
 
 symptoms of, 38 
 
 treatment of, 40 
 Parasites, 157, 332, 336, 337 
 Pelvis of kidney, 4 
 Penicillium glaucum, 315 
 Pericarditis, 76 
 Peritonitis, 76 
 Pettenkofer's test, 270 
 Phenolic acid, 269 
 Phosphates, 274, 298 
 Phosphate, ammonio-magnesium, 211 
 
 clinical importance of, 275 
 
JNDJOX. 
 
 •'517 
 
 I'hosphate, stellar, of lime, 300 
 treatment of, 276 
 triple, 211, 299 
 Phthisis, 80 
 
 renalis, 156 
 Physiology of the kidney, 12 
 Physiological action of the glomeruli, 
 
 12 
 Picnometer, 215 
 Pigments, bile, in urine, 280 
 
 microscopic, 300 
 Pleurisy, 81 
 
 Plexuses, intertubular, 11 
 Pneumonia, 81 
 Potassium salts, 25 
 Precautions in testing for albumin, 
 
 321 
 Preserving casts, 323 
 
 Elliott's method, 323 
 
 eosine method, 323 
 
 salicylic acid method, 323 
 Pyaemic emboli, 145 
 
 definition, 145 
 
 diagnosis, 145 
 
 etiology, 145 
 
 pathological anatomy, 145 
 
 prognosis, 145 
 
 symptoms, 145 
 
 treatment, 145 
 Pyelitis, 121 
 
 definition, 129 
 
 diagnosis, 123 
 
 etiology, 121 
 
 pathological anatomy, 121 
 
 prognosis, 124 
 
 symptoms, 122 
 
 treatment, 124 
 
 urinary examination, 122 
 Pyelo-nephritis, 118 
 
 definition, 118 
 
 etiology, 118 
 
 microscopic examination, 119 
 
 pathological anatomy, 118 
 
 prognosis, 120 
 
 symptoms, 120 
 
 treatment, 120 
 
 urinary changes, 130 
 Pyonephrosis, 126 
 
 definition, 126 
 
 diagnosis, 126 
 
 etiology, 126 
 
 pathological anatomy, 126 
 
 prognosis, 126 
 
 symptoms, 126 
 
 treatment, 126 
 Pyramids of Fei'rein, 4 
 of Malpighi, 4 
 
 Quantitative analysis of glucose in 
 urine, 254 
 tests for glucose, 244 
 Quantity, daily, of urine, 203 
 
 Reaction of urine, 208 
 
 Regional relations and topography of 
 
 the kidney, 1 
 Relation between parenchymatous 
 change and inflammation, 18 
 of vessels and ureter in the 
 hilum, '■) 
 Renal artery, 10 
 calculi, 129 
 
 definition of, 129 
 etiology of, 129 
 pathological anatomy of, 129 
 prognosis of, 130 
 symptoms of, 130 
 treatment of, 130 
 cysts, 134 
 
 definition of, 134 
 diagnosis of, 135 
 etiology of, 134 
 pathological anatomy of, 134 
 prognosis of, 135 
 symptoms of, 135 
 treatment of, 135 
 haemorrhage, 105 
 etiology of, 105 
 pathological anatomy of, 105 
 prognosis of, 106 
 symptoms of, 105 
 treatment of, 106 
 lesions resulting from surgical 
 injuries, 77 
 complications of, 62 
 phthisis, 136 
 veins, 10 
 Retinal lesions, 81 
 Rods of Heidenhain, 8 
 
 Saccharomyces cerevisiae, 316 
 
 Sarcinas, 309 
 
 Sarcosin, 267 
 
 Sarcomata of the kidneys, 146 
 
 definition of, 146 
 
 diagnosis of, 148 
 
 etiology of, 146 
 
 microscopic examination of, 
 146 
 
 pathological anatomy of, 148 
 
 prognosis of, 148 
 
 symptoms of, 148 
 Scrofulosis of the kidneys, 136 
 Sclerosis of the kidneys, acute, 92 
 chronic, 192 
 
 diagnosis of, 96 
 
 etiology of, 92 
 
 macroscopic anatomy of, 94 
 
 microscopic anatomy of, 94 
 
 prognosis of, 96 
 
 symptoms of, 95 
 
 treatment, 96 
 Second form of large white kidney, 38 
 
 form of small kidneys, 55 
 Section of the renal nerve, 13 
 
34S 
 
 INDKX. 
 
 Sediment in urine, 213 
 Sediments of doubtful importance, 324 
 Septa vel columns Bertini. 5 
 Sick, bathing of, 04 
 Silk fibres, 330 
 Sinus renalis,.:; 
 Size of the kidneys, 1 
 Specific gravity of kidneys, 1 
 Spermatozoa, 307 
 Starch granules, 331 
 Stars of Verheyen. 11 
 Stellated veins of Verhej'en, 11 
 Straight collecting tubules, 7 
 Strassburgh test, 270 
 Striations of pyramid, 4 
 Stroma of kidney, 11 
 Strongylus seu Eustrongylus gigas, 
 163 
 
 definition of, 163 
 
 etiology of, 163 
 
 microscopic examination of, 
 163 
 
 pathological anatomy of, 163 
 
 symptoms of, 164 
 
 treatment of, 164 
 Substances, excretory nitrogenous, 254 
 Sugar, 234 
 
 Summary of kidney lesions, 101 
 Suppurative nephritis, 118 
 Surgical injuries, renal lesions result- 
 ing from, 77 
 Surgical kidneys, 118 
 
 Table of urinary changes, 104 
 
 Taurin, 268 
 
 Taurocholic acid, 270 
 
 Tea leaves, 331 
 
 Tests for albumin, 222 
 
 Abbott's, 227 
 
 acetic acid and sodium sul- 
 phate, 225 
 
 acidulated potassic ferro- 
 cyanide, 225 
 
 Pavey's test pellets, 230 
 
 carbolic acid, 231 
 
 caustic potash and copper, 225 
 
 heat, 224 
 
 Hellers or nitric acid test, 226 
 
 Millon's reaction, 226 
 
 Oliver's or sodium tungstate, 
 230 
 
 picric acid, 2o8 
 
 Porter's 227 
 
 Robert's acid brine, 228 
 
 Tanret's, or potassio-mercuric 
 iodide, 229 
 
 test papers, 230 
 
 xanthoproteic 225 
 for bile pigment in urine, 280 
 
 Brucke's, 281 
 
 Gmelin's, 281 
 
 Huppert's, 281 
 
 Tests for bile pigment, Ultzmann's, 281 
 for chlorides, 27(1 
 for cholesterin, 326 
 for fat in urine, 282 
 for haemoglobin, 283 
 
 guaiac, 283 
 Heller's, 283 
 
 spectroscopic, 283 
 for indican, 271 
 for indigo, 271 
 for indol, 271 
 for leucin, 268 
 for mucus in urine, 282 
 
 acetic acid, 282 
 
 iodine, 282 
 
 tartaric acid, 282 
 for phosphates, 274 
 for sugar in urine, 234 
 
 Bailey's, 238 
 
 Boettger's, 239 
 
 Brucke's, 240 
 
 Cappezzuole, 234 
 
 caustic potash and alcohol, 
 241 
 
 Cruckshank's, 241 
 
 Fehling's, 237 
 
 fermentation, 241 
 
 Flint's, 238 
 
 Heinzinga, 241 
 
 Httnafeld's, 242 
 
 Lowe's, 240 
 
 Maumene's tin, 240 
 
 Moore's or Heller's, 234 
 
 Mulder's, 240 
 
 Piffard's, 239 
 
 polarization, 240 
 
 quicklime, 241 
 
 Runger's, 241 
 
 silver, 241 
 
 Squibb's, 239 
 
 Trommer's, 234 
 for ty rosin, 269 
 for urates, 273 
 for urea, 256 
 
 Davey's, 258 
 
 Doremus', 259 
 
 Fowler's, 258 
 
 Liebig's, 258 
 
 Russfll and West's, 256 
 for uric acid, 265 
 Third form of small white kidneys, 58 
 Tincture of the chloride of iron, 25 
 Topography and regional relations, 1 
 Torula cerevisia?, :'.l 5 
 Translucency of urine, 208 
 Triple phosphates, 211, 299 
 Tubercular kidneys, 136 
 
 definition of, 136 
 
 diagnosis of, 139 
 
 etiology of, 136 
 
 microscopic examination, 137 
 
 pathological anatomy, 136 
 
INDEX. 
 
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 Tubercular kidneys, symptoms of, 137 
 
 treatment of, 140 
 Tuberculosis bacillus, 311 
 Tubes, convoluted of first order, 55 
 second order, 6 
 
 intercalated, G 
 
 junctional, 6 
 
 straight or collecting, 7 
 Tubules, ascending limb of, 5 
 
 descending limb of, 5 
 
 loop, 5 
 
 looped of Henle, 5 
 
 neck of, 5 
 
 uriniferous, 5 
 Tunica adiposa, 1 
 Ty rosin, 268, 338 
 
 Uraemia, 82 
 
 treatment of, 86 
 Ursemic blindness, 87 
 Urates, 273, 297 
 Urea, 255 
 
 clinical significance of, 261 
 tests for, 256 
 Ureter, 3 
 
 opening of, into bladder, 3 
 Uric acid, 263, 294 
 crystals, 212 
 diagnosis of, 265 
 diathesis, 265 
 prognosis, 265 
 tests for, 265 
 treatment of, 265 
 Urinary analysis, introductory re- 
 marks on. 195 
 blanks, 198 
 changes, table of, 194 
 
 Urine, acid fermentation of, 210 
 
 adventitious coloring matter of, 
 279 
 
 alkaline fermentation of, 210 
 
 amphoterous, 318 
 
 chemical composition of, 196 
 examination of, 202 
 
 color of, 204 
 
 daily quantity of, 203 
 
 odor of, 208 
 
 reaction of, 208 
 
 quantitative analysis of, 242 
 
 sediment in, 213 
 
 specific gravity of, 214 
 
 translucency of, 208 
 Uriniferous tubules, 5 
 Urinometer, 215 
 
 Variations in form of kidneys, 2 
 
 in number of kidneys, 2 
 
 in position of kidneys, 2 
 
 in size of kidneys, 2 
 Vegetable organisms, 308 
 Veins, interlobular, 10 
 
 stellated, of Verheyen, 11 
 Verheyen, stars of, 11 
 
 stellated veins of, 11 
 Vibriones, 311 
 
 Waxy kidney, 98 
 Weight of kidney, 1 
 Wood, fragments of, 331 
 Woollen fibres, 330 
 
 Xanthin, 267, 328 
 
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