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 ii^Biwaissy^gji^Mgag'gggyw^'y^g^w'- _ 
 
THE RELATIONS 
 
 CARDIAC HYPERTROPHY 
 
 RENAL DISEASE. 
 
 BY 
 
 EGBERT SAUNDBY, M.D. EDIN., M.R.C.P. LOND., 
 
 ASSISTANT PHYSICIAN TO THE GENERAL HOSPITAL, BIRMINGHAM. 
 
 REPRINTED FROM THE BIRMINGHAM MEDICAL REVIEW, 
 January, 1880. 
 
 Birmingham : 
 Hall and English, Printers, High .Street. 
 
i^2 
 
THE EELATIONS OF 
 CAEDIAC HYPEETEOPHY TO EENAL DISEASE. 
 
 The coincidence of cardiac hypertrophy with renal 
 disease, more especially with granular degeneration of 
 the kidneys, is so frequent, and so often wanting in any 
 local mechanical explanation, that it has always attracted 
 considerable attention, and, although the discussion has 
 not yet arrived at a very definite settlement of the 
 question, it has been the cause of a thorough examination 
 of the entire pathological relations of Bright's disease, 
 which has produced results of the highest practical 
 importance. 
 
 The frequency of this coincidence seems to be in about 
 one-half of the cases. It cannot be admitted that its 
 absence is due to the renal disease being not far enough 
 advanced. Doubtless the coincidence would be very much 
 more complete were all the cases of hypertrophy included 
 in the statistics, but those explicable by valvular or 
 vascular disease have been excluded. Some authorities 
 give a much larger proportion than one-half, and, 
 perhaps, it is difficult to determine who is right ; but 
 this we do know, that the heart is not always hyper- 
 trophied even when the kidneys are very contracted. In 
 
the other forms of Bright's disease, hypertrophy, though 
 common, is certainly less frequent. 
 
 Bright,* in recording the various organic changes in 
 lOO cases of renal disease, says, "The obvious structural 
 changes in the heart have consisted chiefly of hyper- 
 trophy, with or without valvular disease ; and what is 
 most striking, out of fifty-two cases of hypertrophy, no 
 valvular disease whatsoever could be detected in thirty- 
 four ; but in eleven of these thirty-four, more or less 
 disease existed in the coats of the aorta ; still, however, 
 leaving twenty-two without any probable organic cause 
 for the marked hypertrophy generally affecting the left 
 ventricle. This naturally leads us to look for some less 
 local cause for the unusual efforts to which the heart has 
 been impelled ; and the two most ready solutions appear 
 to be, either that the altered quality of the blood affords 
 irregular and unwonted stimulus to the organ immediately, 
 or, that it so affects the minute and capillary circulation 
 as to render greater action necessary to force the blood 
 through the distant sub-divisions of the vascular system." 
 In the next paragraph, he says, " It is observable that the 
 hypertrophy of the heart seems, in some degree, to have 
 kept pace with the advance of disease in the kidneys ; 
 for in the majority of cases where the muscular power of 
 the heart was increased, the hardness and contraction of 
 the kidney bespoke the probability of a long continuance 
 of the disease." 
 
 In this table Bright had included not only granular 
 kidney, but all forms of renal disease with albuminuria. 
 It will be found that the pendulum of modern opinion is 
 now again oscillating between these two explanations in 
 spite of forty years of discussion and observation with 
 
 * Cases of Renal Disease accompanied with Albuminous Urine. Guy's 
 Hospital Reports, vol. i., p. 397. 
 
the aid which the modern use of the microscope has lent 
 to pathological researches. Thus Prof. Senator* of 
 Berlin, in a recent communication suggests that in chronic 
 parenchymatous nephritis the heart is excentrically 
 hypertrophied, and that this is probably attributable to 
 the increased capillary resistance while, in interstitial 
 nephritis, the hypertrophy is concentric, and is due to 
 direct irritation of the heart, either from some nervous 
 disorder, as in Basedow's disease, or, as is more likely, 
 from the blood dyscrasia. 
 
 Since the time of Bright there have been four original 
 explanations brought forward and all other writers on the 
 subject have adopted some one, or a combination, of these 
 
 various theories. 
 
 Traube,towhomweowe the observation of the hard pulse 
 of Bright's disease, regarded the destructionof alarge capil- 
 lary area in the kidneys as necessarily causing so much ob- 
 struction to the circulation that, aided by the imperfect 
 elimination of water, the blood pressure in the aortic system 
 must rise and cardiac hypertrophy follow. Bamberger ob- 
 jected to this that the hypertrophy begins in the earlier 
 stages of Bright's disease ; moreover it is present in chronic 
 parenchymatous nephritis in which no destruction of 
 capillaries has occurred. Ludwig and his pupils have 
 shown that ligature of both renal arteries, or of even larger 
 arteries, does not raise the blood pressure in the aorta, 
 while it is well known that in granular kidney the 
 elimination of water is rather in excess of the normal 
 yet it is specially in this affection that cardiac 
 hypertrophy occurs. It is, therefore, not without reason 
 that this hypothesis has been generally abandoned, 
 
 *Beitrage zur Pathologie der Nieren und des Hams Ueber die 
 Beziehungen der Herzhypertrophie zu Nierenleiden. Virchow's Archiv. 
 Bd. 4. Ixxiii. Heft 3, p. S^S- 
 
although in recent times it received the support of- so 
 eminent an authority as Bartels. 
 
 The next original explanation was that given by 
 Dr. George Johnson, which has undergone at least 
 two modifications. In the first place Dr. Johnson 
 pointed out the excessive thickening of the niuscular 
 walls of the renal arterioles, and suggested that 
 the obstruction to the circulation offered by a state of 
 tonic spasm in these vessels, would explain their own 
 alterations, the rise of blood pressure and the cardiac 
 hypertrophy. But having been able to discover similar 
 changes in the vessels of the pia mater and mesentery, he 
 enlarged his hypothesis and imagined a state of tonic 
 spasm of the whole systemic arterioles which he attributed 
 at first to direct irritation by the impure blood, and later 
 on to stimulation of the vaso-motor centre. According 
 to his present views he regards the condition as analogous 
 to asphyxia, in which unoxygenated blood going to 
 the brain stimulates the vaso-motor centre in the 
 medulla, and causes contraction of the arterioles 
 throughout the body with consequent increase of 
 the arterial blood pressure. The great , objection 
 to this theory of general constriction of the vascular 
 system is that, under such circumstances, the urinary 
 secretion would be diminished or suppressed, as indeed 
 occurs in asphyxia ; whereas, in granular kidney, as is well 
 known, the rise in blood pressure is accompanied by an 
 increase in the flow of urine. Moreover, Grutzner 
 (Pfliiger's Archiv Bd. xi., s. 370) has shown that the 
 diuresis excited by the intravascular injection of salts 
 such as nitrate of potash is arrested during suspension of 
 the respiration, unless the nerves to the kidney are divided. 
 This failure in the analogy has always appeared to us a 
 very weak point in the theory, but recently further light 
 
5 
 
 has been thrown on the question. MM. Dastre and 
 Moret* have communicated to the Societe de Biologie 
 the results of their investigations into the state of the 
 circulation in asphyxia. They have determined that the 
 vessels of the skin in an asphyxiated animal are dilated 
 to five or ten times their normal diameters, but that the 
 vessels of the intestines and viscera are at the same time 
 contracted, this antagonism holding good in the reverse 
 condition, when the skin vessels are contracted those of 
 the internal organs are dilated. 
 
 As the depression of the cutaneous circulation and 
 functions are as prominent features of granular kidney 
 as the increase in the renal secretion, it seems probable 
 that if any vaso-motor action does occur it must be 
 contraction of the vessels of the skin and dilatation of the 
 vessels of the internal organs. Under such circumstances 
 this vaso-motor action may play some part in the rise 
 of blood pressure. 
 
 The third original explanation is that which we owe to 
 Sir William Gull and Dr. Sutton.-|- They rediscovered 
 the vascular changes described by Dr. Johnson, but drew 
 attention more especially to the thickening of the fibroid 
 tissues. They regard these vascular changes as primary 
 and essential, the increased blood pressure and cardiac 
 hypertrophy being their consequences while the kidney 
 disease is but a local expression of a general degeneration 
 of the arterioles and capillaries attended by atrophy of the 
 adjacent tissues. Although we may admit that when estab- 
 lished these vascular changes do obstruct the circulation, 
 and thus might be determining causes of cardiac hyper- 
 trophy, according to Thoma ;|: the fibroid thickening occurs 
 
 * Influence du Sang Asphyxique siir* la Circulation. Societe de 
 Biologie. Seance du 8 Novembre. Le Progres Medical, Nov. 15th 
 
 f Medico-Chir. Trans. Second Series. Vol. xxxvii., p. 273. 
 
 J Zur Kentniss der Circulationsstorung in der Nieren bei chronischer 
 interstitieller Nephritis. Virchow's Archiv Bd. Ixxi. Heft i & 2. 
 
in dilated vessels so that the normal calibre is only excep- 
 tionally reduced. But in addition we have the fact that in a 
 considerable proportion of cases of granular kidney cardiac 
 hypertrophy is found unaccompanied by the vascular 
 changes. According to Ewald* this occurred in 4 out of 20 
 cases, and we have been able to confirm the statement in 
 about the same proportion of cases (2 out 10). Finally in 
 chronic parenchymatous nephritis the occurrence of 
 cardiac hypertrophy is not infrequent, but the vascular 
 changes are quite exceptional. Therefore, although there 
 is much in the view taken of Bright's disease by these 
 authors with which we cordially agree, we must regard 
 their explanation of the cardiac hypertrophy as failing to 
 square with all the facts of the case. 
 
 The latest explanation we owe to v. Buhl.-|- He 
 believes the cardiac and renal changes proceed pari 
 passu, the hypertrophy is to be attributed to the self- 
 increased activity (Selbsteigene Thatigkeit) of the heart. 
 Myocarditis occurs very early, which may cause no 
 alteration, or atrophy or hypertrophy of the organ. 
 Most frequently it causes hypertrophy. As the in- 
 flammatory process comes to an end the cardiac 
 muscle hypertrophies from excess of nutrition, and to 
 overcome the increased work of the dilated ventricle. In 
 addition he regards the fact as 'quite new,' that a relative 
 stenosis of the aorta is present. The rise of blood pressure 
 in the aortic system is due to the hypertrophy of the 
 ventricle and the narrowing of the aorta. 
 
 The relative frequency of myocarditis in renal disease 
 is an undoubted fact, and this process plays an important 
 
 * Ueber die Verauderungen kleiner Gefasse bei Morbus Brightii und die 
 darauf Bezuglichlen Theorien. Virchow's Archiv Bd. Ixxi. Heft 4. 
 
 t Ueber Bright's Granularschwund der Nieren und die damit zusammen- 
 hangende Herzhypertrophie. Mittheilungen aus dem pathol. Institut zu 
 Munchen, 1878. S. 38. 
 
part in many cases, but there is no warrant in the 
 assumption that it has occurred in all cases. Buhl is not 
 at all clear as to the cause upon which the self increased 
 activity of the heart or the myocarditis depends. He 
 cannot claim novelty for the fact that the aorta is in some 
 cases relatively stenosed as Bamberger* adduced it as 
 opposed to Traube's hypothesis. With regard to its 
 frequency in granular kidney Ewald has measured the 
 circumference of the aorta above the valves in 12 cases, 
 and found it to vary between 12.1 and 5.7 cm., the average 
 being ^.6 cm., while the normal circumference according to 
 Bouillaud is 6.3 cm., so that we cannot attach very much 
 importance to it as a cause of cardiac hypertrophy. 
 
 Having failed to find any of these explanations quite 
 satisfactory we return to Bright's suggestions, that either 
 the altered quality of the blood affords irregular and 
 unwonted stimulus to the heart immediately ; or that it 
 so affects the capillary circulation as to render greater 
 action necessary to force the blood through the distant 
 subdivisipns of the vascular system. Both these explan- 
 ations rest upon the supposed impure state of the blood. 
 In the acute and chronic stages of parenchymatous 
 nephritis the condition of the blood was investigated 
 many years ago by Bostock, Gregoiy, and Christison.-j- 
 According to the latter, urea was always found in 
 considerable quantity in the blood whenever the excretion 
 of urine was diminished, the density of the blood 
 serum was always less, and the fibrine was frequently 
 increased. Nothing of importance has been added to 
 this observation in modern times ; but experiments with 
 animals have shown that urea, extractive matters of the 
 blood, creatine and leucin, accumulate in large quantities 
 
 * Quoted by Niemeyer. Text Book of ^Practical Medicine. Vol. I., 
 p. 300. 
 f Granular Degeneration of the Kidney. 1839. P. 58 et seq. 
 
in the blood and tissues after nephrotomy ; and it does ^ 
 not require much argument to convince anyone that 
 during the abeyance of the renal function the blood 
 depurating process must be more or less incomplete. 
 
 But in granular kidney, as we understand it, the 
 density of the serum is normal, or increased, according 
 to Christison ; the proportion of salts and albumen 
 may be very high, and the fibrine is normal ; the most 
 striking characteristic being a rapid reduction of the 
 blood pigment or hsematin. Bartels has published some 
 observations, but none of them bearing on the state of 
 the blood in the earlier stages ; in the latter stages, when 
 dropsy was present, the density of the blood serum was 
 low ; a certain amount of urea was found in many cases, 
 in others it was absent. 
 
 But there are other reasons for believing that blood 
 impurities are early and important phenomena in granular 
 kidney.' Dr. Todd first pointed out the frequent 
 co-existence of this form of renal disease with gout, 
 hence the name Gouty Kidney ; Ollivier has drawn 
 attention to its frequent occurrence among workers in 
 lead. Dr. Johnson states that the disease is common in 
 persons who " eat and drink to excess, or who, not being 
 intemperate in food or drink suffer from certain forms 
 of dyspepsia, without the complication of gouty 
 paroxysms." He says, that "renal degeneration is 
 probably a consequence of the long-continued elimination 
 of products of faulty digestion through the kidneys." 
 The late Dr. Murchison was persuaded of the relation 
 borne by contracted kidney to persistent lithaemia. 
 Prof Semmola,* of Naples, maintains the view that 
 Bright's disease is a consequence of the blood dyscrasia 
 
 *Brit. Med. Journal, 1879, II., p., 501. Report of Sixth Amsterdam 
 International Congress of Medical Science. 
 
resulting from suppression of the respiratory function of 
 the skin. Our own observations indicate the probability 
 that prolonged and habitual dyspepsia is in many cases a 
 precursor of this disease. 
 
 Therefore, although during the greater part of its 
 course this affection does not lead to any diminution 
 of the renal secretion, there is ground for believing in a 
 blood dyscrasia depending upon other causes. 
 
 The next point for enquiry is whether such blood 
 impurity as may arise from defective elimination or 
 perverted digestive functions can be shown under any 
 conditions to obstruct the capillary circulation. Heiden- 
 hain* speaks of copious diuresis occurring after the 
 injection of urea in spite of the blood pressure remaming 
 below normal, or not being proportionately ijicreased. 
 
 Ustimowitsch and Grutznerf determined a certain 
 constant rise in blood pressure after injecting urea into 
 the blood accompanied by increased flow of urine. 
 
 Dr. Rendu \ in his inaugural thesis quotes M. Potain 
 as having noticed that although injections of urea into the 
 blood do not modify the mechanical conditions of the 
 circulation, yet if a mixture of urea and blood serum be \ , ' r 
 allowed to stand some hours, and be then injected, the | ^pcAA.^-^^ 
 arterial tension rises to an unexpected degree. 
 
 Drs. Paul Grawitz and Oscar Israel || found that neither 
 unilateral artificial nephritis nor extirpation of one 
 kidney, although followed by hypertrophy of the heart, 
 effected any rise in the blood pressure. Their experi- 
 
 * Pfliiger's Archiv, IX., p. i., quoted by Foster. Text book of Physio- 
 logy, p. 283. 
 
 t Quoted by Ewald. Op. cit. 
 
 X Quoted by Hanot. Contribution a I'etude de I'hypertrophie concen- 
 trique du ventricule gauche dans la nephrite interstitielle. Arch. Gen. de 
 Med. 1878, p. 172. ■ 
 
 II Experimentelle Untersuchungen iiber den Zusanimenhang Zwischen. 
 Nierenkrankung und Herzhypertrophie. Virchow's Archiv. Bd, Ixxvii.v 
 s- 315- 
 
10 
 
 ments are so interesting in relation to the present 
 enquiry, that a further account of them is necessary. 
 By taking strict antiseptic precautions they were able to 
 clamp either of the renal arteries of a rabbit without any 
 unfavourable surgical result. One and a half to two 
 hours afterwards the clamp was removed. In half an 
 hour after the operation the urine became bloody, and, in 
 from one to two hours the organ if examined was found to 
 be grayish red and opaque. If the clamp was allowed to 
 remain on longer the kidney became of a dirty yellowish 
 grey colour, indicating commencing gangrene. The effect 
 of this operation was to cause intense acute parenchy- 
 matous nephritis with fatty degeneration of the epithelium 
 of the tubules. This passed into either granular atrophy 
 or the large white kidney. In the former, microscopical 
 examination showed no trace of nuclear prolification, the 
 substance of the organ consisting simply of wasted tubules. 
 In another series of experiments they extirpated one 
 kidney altogether. They found that the results of these 
 conditions varied accordingly as the animals operated on 
 were young and growing, or old, strong, and fully grown. 
 
 In the young, after 2 or 3 days, the intact kidney began 
 to increase in size to 20 or 30 per cent, more than its 
 normal weight. .As the contraction of the other icidney 
 went on the intact organ continued to increase until it 
 equalled the weight ofthe two kidneys of an animal of the 
 same size. At the same time they ascertained by ab- 
 dominal section that the other kidney still secreted a 
 watery urine of low specific gravity, but in small quantity. 
 
 In the old animals the intact kidney also increased a 
 little, the greatest being in one case of nephrotomy, where 
 the extirpated right kidney weighed 7.7 grms., and the 
 left, after 82 days, weighed 11.3 grms. The hypertrophy 
 of the kidney consisted in a true hyperplasia of the renal 
 
II 
 
 elements, at least the enlargement was certainly not due 
 to increase in the diameters of the tubules. The con- 
 sequence of the imperfect compensation by hypertrophy 
 of the other kidney caused in some cases death by acute 
 or chronic uraemia, in others the animals continued to 
 live, but were ill nourished until the deficit was covered 
 by hypertrophy of the left ventricle. By careful 
 estimations of the relative normal weights of the heart 
 and kidneys, and comparison of these data with the 
 weights of the altered organs, they were able to determine 
 that the cardiac hypertrophy bore a definite proportion 
 to the loss of renal substance, and therefore was truly 
 compensatory for the renal defect. As a rule, the heart 
 was not dilated, in many the ventricle was in a state of 
 spasmodic contraction, and they were unable to obtain 
 any confirmation of Senator's views already quoted 
 relative to the pathogenesis of excentric and concentric 
 hypertrophy. In those cases where cardiac dilatation oc- 
 curred, the symptoms during life indicated a primarily 
 defective or later destroyed compensation, the animals 
 died with acute or chronic dropsy, and the weight proved 
 imperfect compensation. In the case of. a large black 
 doe, which died with dropsy of all the serous cavities lo 
 days after the operation, the cardiac muscle was intensely 
 granular, even after the addition of soda solution. They 
 regard this as evidence of the occasional occurrence of 
 primary myocarditis. Much more frequently the myocar- 
 ditis was secondary,' but whichever it was it produced the 
 appearance of " excentric hypertrophy." They were never 
 able to obtain evidence of any increased blood pressure, 
 but by careful measurements they determined a constant 
 increase in the velocity of the circulation. Injections of 
 urea also failed to produce a rise of blood pressure, but 
 stinmlated the hearts action and quickened the blood 
 stream. 
 
12 
 
 Here we have the explanation of the "self increased 
 activity " of the heart, to which Buhl refers, and also of 
 the myocarditis. The impure state of the blood acts as 
 Bright suggested, by affording an unwonted stimulus to 
 the heart immediately, and this leads to a hypertrophy 
 proportionately compensatory for the loss of renal secret- 
 ing substance. Myocarditis is the cause of dilatation and 
 the subsequent hypertrophy takes place as Buhl indicates 
 from over nutrition, and increased work from the greater 
 capacity of the ventricle. The rise in blood pressure is 
 not a cause of the cardiac hypertrophy; moreover, in these 
 experiments neither the state of the heart, nor the renal 
 condition nor the blood impurity combined, were able to 
 effect any increase in the tension of the aortic system. 
 
 But the high pressure pulse of Bright's disease* is a con- 
 stant and now universally admitted fact. Traube asserted, 
 not without reason, that he could diagnose granular kidney 
 by the pulse alone, and Galabin * has shown that the same 
 condition is present in the other forms of Bright's disease. 
 But a great step was taken when Mahomed -f proved that 
 this rise in the blood pressure precedes the occurrence of 
 albuminuria, the development of which he watched at the 
 termination of scarlatina. Here there is no question of 
 structural change in the heart or arterioles, the sole con- 
 dition present is that of faulty elimination due to 
 the morbid state of the skin. When to this con- 
 stipation is added, the blood pressure rises, blood 
 crystalloids appear in the urine, and if not averted 
 by a sharp purge, albuminuria follows. Moreover, 
 Dr. Mahomed:): has recorded cases of high arterial 
 
 * On the Connection of Bright's Disease with changes in the Vascular 
 System. 
 
 f The Etiology of Bright's Disease and the pre-albuminuric Stage. Med. 
 Chir. Trans. Second Series. Vol. xxxix., p. 197. 
 
 X Clinical Aspects of Chronic Bright's Disease. Guy's Hosp. Reports, 
 vol. xxiv. 
 
 MsfJM^Mr^°WI~, 
 
13 
 
 tension, sometimes accompanied by albuminuria in young 
 dyspeptic patients free from cardiac hypertrophy ; and 
 we have published similar cases * In both, it is suggested 
 that in these young persons, we may have to do with the 
 condition which gives rise to granular kidney later in life. 
 In this place it is of interest to quote the following 
 passage from Dr. Murchison's Cronian lectures on 
 " Functional derangements of the liver." He says, " so 
 often have I observed albuminuria associated with 
 hepatic disorder, which has disappeared completely and 
 permanently when this has been set to rights, that I have 
 little doubt that we have in the liver a cause of albumin- 
 uria to which attention has not hitherto been sufficiently 
 directed. The pathology of the albuminuria in these 
 cases may be similar to that of certain cases of diabetes 
 already referred to, the liver having too much work to do, 
 and permitting some albumen to pass through in a form 
 which cannot be assimilated ; or possibly there may be 
 some defect in the destructive functions of the liver in 
 consequence of which the albuminous matter, instead of 
 being converted into urea, does not even reach the stage 
 of lithic acid. It is possible that in many- of the cases 
 now referred to the albiiminiiria may indicate an early 
 stage, not yet described, of the contracted or gonty kidney, 
 yet it is certain that the symptoms may persist or recnr 
 during many years without any other symptom of renal 
 disease, and with but little impairment of the general 
 health." It is especially to the latter part of this passage, 
 which we print in italics, that attention is directed. 
 When we recall the known connection between persistent 
 lithaemia and contracted kidney, and recollect that in 
 these cases we find high arterial tension, retinal haemor- 
 rhages, occasional hyaline casts, albuminuria, and 
 
 The Functional Stage of Granular Kidney. Birm. Med. Rev., Oct., 1879. 
 
lithuria, there is warrant for believing that such an 
 early stage of granular kidney, as Murchison here 
 alluded to, has been recognised clinically. 
 
 To return to the matter in hand, if the rise in pressure 
 precedes all structural change it must be due to increased 
 energy in the cardiac contractions, or to obstruction 
 in the distant parts of the vascular system, or to both 
 combined. Most modern writers, Grainger Stewart, 
 Broadbent, Mahomed, Ewald, and others, regard the 
 obstruction as seated in the capillaries, and the cardiac 
 hypertrophy as the consequence of this impediment to 
 the circulation. But we have seen that the cardiac 
 hypertrophy must be regarded as directly dependent on 
 the state of the blood, and therefore is rather to be re- 
 garded as a cause than an effect of the rise in blood 
 pressure. 
 
 But Israel and Grawitz appear to have proved that the 
 cardiac hypertrophy per se does not raise the blood 
 pressure, nor does the state of the blood which manifests 
 itself by the stimulus to the heart's action seem to suffice 
 to produce any peripheral obstruction great enough to 
 cause this result. We are compelled therefore to seek 
 some other factor, or to believe that in some respect the 
 conditions of these experiments differ from those of 
 patients suffering from Bright's disease. Such a differ- 
 ence plainly existed in the intact state of one kidney, and 
 it may be that the increased functional activity of the 
 heart In these animals sufficed to maintain elimination ; 
 the rise of blood pressure, with which we- are clinically 
 familiar, being the result of a higher degree of toxaemia 
 than that present in these experiments. 
 
 As the rise in blood pressure precedes all structural 
 changes, and as the theory of vaso-motor action is incon- 
 sistent with the augmented secretion of urine, we may 
 
15 
 
 assume an increase in the capillary resistance as the other 
 factor, which, combined with the augmented cardiac 
 energy, determines the characteristic pulse of Bright's 
 disease. How far Dr. Johnson's theory, modified in 
 accordance with Dastre and Moret's observations, may 
 be accepted as assisting the above named factors, we can 
 not determine, but we are unwilling to exclude it altogether 
 from some share in this partnership, in which one other 
 participator has only a hypothetical existence. 
 
 These conclusions, which have been arrived at by com- 
 bining and comparing pathological, clinical, and experi- 
 mental data, suggest certain practical conclusions. 
 
 1. In chronic Bright's disease the augmentation of the 
 cardiac function is compensatory to the renal defect. 
 This view confirms the propriety of the practice of ad- 
 ministering digitalis in these cases. But as far as possible, 
 elimination should be favoured by the skin and bowels, 
 while the diet should consist of elements containing as 
 small an amount of urea-forming substances as the general 
 condition of the patient may warrant. 
 
 2. The high tension pulse indicates a high degree of 
 toxaemia and relative failure of the kidneys. As the 
 toxic material in the blood stimulates the heart (Israel 
 and Grawitz) and probably the kidneys (Heidenhain.) 
 without raising the blood pressure, polyuria or even 
 albuminuria may precede any change in the state of the 
 pulse. Careful examination of the urine is therefore of 
 the greatest importance for detecting the earlier stages of 
 the condition which leads to granular degeneration of the 
 kidneys. 
 
 ROBERT SAUNDBY. 
 
MMMiiMMHHMI 
 
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