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COMMENTARIES ON DISEASES OF THE KIDNEYS. :PART I I I . By ARTHUR W'~NNE FOOT~ ~[.D.~ Univ. Dubl. ; Senior Physician, Meath Hospital and County of Dublin Infirmary; Fellow and ex-Censor~ King and Queen's College of Physicians in Ireland; Diplomate in State Medicin% Trinity College~ Dublin; Lecturer on :Practice of Medicine in the Ledwich School of Medicine a~ld Surgery; Fellow~ Royal Geological Society of Ireland~ &c. [Conti~puedfrom page .~65, VoI. LXVIL]. TEE SECOND TYPE OF BRIGHT'S DISEASE.--Synonyms : the contracted, granular, small red kidney--the gouty or saturnine kidney--interstitial nephritis--renal cirrhosis--renal sclerosis--granular atrophy of the kidney. Theory of the unity (Continental), or of the multiplicity (English) of Bright's diseases. Charcot's epitome of the history and progress of the granular kidney. Insidious nature of the disease--proofs--latency of its earliest stages. Polyuria an initial symptom-- nocturnal rather than diurnal--mistaken sometimes for diabetes. Quantity of urine excreted--its colour--specific gravity--albumen, characteristic but variable in amount, and inconstant, l~ecessity of frequent and repeated urinary examina- tions. Low percentage of urea in granular kidney--character of sediment-- scanty. Form of tube-casts. The cardiac changes--their frequency and diagnos- tic significance. Cardiac complications sometimes the first indications of the disease. Bright's explanation of the cardiac hypertrophy. Traube's view--Gull and Sutton's--arterio-capillary fibrosis. The cardiac hypertrophy, an explanation of (1) the polyuria~ (2) long absence of ursemia, (3) albuminuria, (4) liability to apoplexy. Frequency of epistaxis. :Retinal lesions. Postmoo'tern appearances in granular kidney. ~VE have already discussed one of the forms or types of Bright's diseases--namely~ that whose anatomical character is ~ the large white kidoey~" and which, from a pathological point of view~ is usually spoken of as ~parenchymatous nephritis.'" We now come to the consideration of another type~ which is spoken of anatomically as the contracted kidney~ the gronular ].:idt~ey~ the small red kid~ey, and also occasionally as the gouty ]~idney~ or even as the saturnine kidney. In the opinion of the greater part of French and German physiclans~ the various alterations of the kidney discovered in autopsies of such subjects as~ during life~ have suffered from albuminuria and anasarca~ correspond to the various successive phases of the sam% or to one~ morbid process. This doctrine a The text of the essays of Professor Carl Barrels, of Kiel, and Professor Wilhelm :Ebstein, of Goettingen, in u XV. of the "Cyclopeedia of the Practice of Medi- cine," edited by Dr. H. Yon Ziemssen, has been followed as closely as possible, with additional notes from all the best authorities on the subject.--A. W. FooT.

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C O M M E N T A R I E S O N D I S E A S E S O F T H E K I D N E Y S . �9

:PART I I I .

By ARTHUR W'~NNE FOOT~ ~[.D.~ Univ. Dubl. ; Senior Physician, Meath Hospi tal and County of Dublin Inf i rmary; Fe l low and ex-Censor~ King and Queen's College of Physicians in I r e l and ; Diplomate in State Medicin% Tr in i ty College~ Dub l in ; Lec turer on :Practice of Medicine in the Ledwich School of Medicine a~ld S u r g e r y ; Fellow~ Royal Geological Society of Ireland~ &c.

[Conti~pued from page .~65, VoI. LXVIL].

TEE SECOND TYPE OF BRIGHT'S DISEASE.--Synonyms : the contracted, granular, small red kidney--the gouty or saturnine kidney--interstitial nephritis--renal cirrhosis--renal sclerosis--granular atrophy of the kidney. Theory of the unity (Continental), or of the multiplicity (English) of Bright's diseases. Charcot's epitome of the history and progress of the granular kidney. Insidious nature of the disease--proofs--latency of its earliest stages. Polyuria an initial symptom-- nocturnal rather than diurnal--mistaken sometimes for diabetes. Quantity of urine excreted--its colour--specific gravity--albumen, characteristic but variable in amount, and inconstant, l~ecessity of frequent and repeated urinary examina- tions. Low percentage of urea in granular kidney--character of sediment-- scanty. Form of tube-casts. The cardiac changes--their frequency and diagnos- tic significance. Cardiac complications sometimes the first indications of the disease. Bright's explanation of the cardiac hypertrophy. Traube's view--Gull and Sutton's--arterio-capillary fibrosis. The cardiac hypertrophy, an explanation of (1) the polyuria~ (2) long absence of ursemia, (3) albuminuria, (4) liability to apoplexy. Frequency of epistaxis. :Retinal lesions. Post moo'tern appearances in granular kidney.

~VE have already discussed one of the forms or types of Br ight ' s diseases--namely~ that whose anatomical character is ~ the large white kidoey~" and which, from a pathological point of view~ is usually spoken of as ~parenchymatous nephritis. '" W e now come to the consideration of another type~ which is spoken of anatomically as the contracted kidney~ the gronular ].:idt~ey~ the small red kid~ey, and also occasionally as the gouty ]~idney~ or even as the saturnine kidney. In the opinion of the greater part of F rench and German physiclans~ the various alterations of the kidney discovered in autopsies of such subjects as~ dur ing life~ have suffered from albuminuria and anasarca~ correspond to the various successive phases of the sam% or to one~ morbid process. This doctrine

a The text of the essays of Professor Carl Barrels, of Kiel, and Professor Wilhelm :Ebstein, of Goettingen, in u XV. of the "Cyclopeedia of the Practice of Medi- cine," edited by Dr. H. Yon Ziemssen, has been followed as closely as possible, with additional notes from all the best authorities on the subject.--A. W. FooT.

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may be termed the theor U of the utdt!! of Bright's disease. According to another view, which may be termed the theor.y of the multi]~licit?] of the forms of Bright's disease, the various forms of renal alteration revealed by the autopsy represent not the successive phases of the same process, but so many distinct anatomical states, with which are connected during life so many distinct clinical histories. This doctrine may be called the English theory, since it is espeeially in England that it has for twenty years been sustained and developed. To this doctrine Prof. Charcot says he has long been a convert ; and, in his opinion, "Bright 's disease is a class comprising several distinct species, not only f~om an anatomo- pathological point of view, but as regards etiology and symptomatology." Bright himself gave this matter consideration, but seems not to have arrived at any final conclusion. " I have been led to believe," he says, " t h a t the kidney in renal dropsies is affected by various forms of disease ; " but elsewhere he says, " I am not certMn that these views are correct," and adds that the three forms he has described a~e perhaps only modifications or stages, more or less advanced, of one and the same disease. The doctrine of the multiplicity of the forms of Bright's disease counts in England among its ablest supporters Goodfellow, Dickinson, and Grainger-Stewart, while on the Continent almost all the recen~ authorities, of which a list is given below, ~ concur in this view. G. Johnson was one of the first to reject the generally received theory of the unity of Bright's disease, advancing against it an argument of the greatest weight derived from clinical experience. ~' There are very few exceptions to the rule," says Johnson,b " tha t patients dying with the large Bright's kidney have had dropsy, in a greater or less degree, at some period of their history; whereas the majority of those who die with ~ contracted kidney have not suffered from dropsy in any form or degree." He also gives statistics which show that in twenty-six cases of the large white kidney, twenty-four were affeote~ with dropsy, which is, so to speak, the rule in that form characterised by the large white kidney; while out of thirty-three cases of contracted kidney, it occurred only fourteen times, and, even in these cases, ~as scarcely per- ceptiblc.

Charcot c tersely cpitom~ses the life-history and p~thology of this form of Bright's disease--viz., the granular or contracted kidney (interstitial nephritis).

Lecorch~--Trait6 des Maladies du Rein. Lancere~ux--article Rein in the Dic- tionnaire Encyclop~dique des Sciences MSdieales, 1875. Bartels--Cyclop. of 1)ract. of Medicine, H. yon Ziemssen, Vol. XV. Edward Bull--Klinische Studien tiber chronische Bright'sche Krankheit, Christiania, 1875. Labadie-Lagrave--Rev. des Sei. Med., 4th year, Vol. VIII., 2nd fascicule, 1876.

b Med.-Chir. Trans., 1859. u XL[I., p. 156. Bright's Disease of the Kidneys. 1879. P. 37.

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Etiology.--Subjects affected by it succumb between the age of fifty and sixty ; etiological conditions but little known ; the influence of gout, lead-poisoning, and alcoholism appear, however, to be well demonstrated.

Evolution very gradual ; the disease always of a chronic character; may last several years ten years, for example.

Symptoms.--(Edema is absent in more than half the cases ; often it is scarcely appreciable. Urine abundant, at least in the first stage ; some- times real polyuria ; it is clear, pale, of a feeble specific gravity ; albu- minutia slightly marked, and may be absent from time to t ime; the urine contains but few casts. A t an advanced period, however, (edema supervenes, or augments if it previously existed, and the albumen may be found in the urine in greater quantities.

Complications quite frequent, constituting one of the most important characteristics of this form ; hypertrophy of the left heart, without van vular lesion ; albuminous retinitis, almost peculiar to this form ; hmmor- rhages from various passages; frequent arterial a theroma; visceral inflammations, pneumonia, pericarditis, &e. This class of cases gene- ral ly terminates in urvemia.

Anatomical Characters. Kidney small, being only half its normal weight ; the capsule is closely adherent; the surface of the kidney is of a reddish tint, and has a sandy, granulated appearance ; the granulations small, nearly uniform in size, are regularly disseminated over the surface of the kidney, which presents bere and there small cysts. Section shows that the atrophy affects the cortical substance, wbich may be reduced to a thin layer.

Histologically we have to d'eal with a genuine cirrhosis of the k i d n e y ~ the connective tissue is primarily affected, the epithelium being affected only consecutively. I t is then an interstit ial nephritis.

A more detailed consideration of the clinical history of interstitial nephritis, or renal cirrhosis, will show that genuine contracting kidney may have existed for a considerable tim% and may have reached a serious degree of development before the patient becomes aware, by any kind of symptom, that his health is no longer as good as it used to be. In proof nf this fact there is on the one hand the no small number of cases in which tile kidneys have been found in a state of advanced atrophy in persons who, up to the date of their death, had both fancied themselves and been regarded by their friends as perfectly healthy. On the other hand, it still oftener happens that patients die either suddenly of the immediate results of their renal malady, or after a short illness of such an indistinct kind and trifling nature that they disdain to smnmon medical advice. I t is probable that the actual first beginning of this disease (granular kidney) always eludes diagnosis-- the symptoms which accom- pany the development and progress of the affeetion~ at least in its earlier stages, are not calculated to direct the patient 's own atten:ion to the

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kidneys as the part at fault. The only thing which disturbs these patients is the frequent desire to pass water, which is principally apparent at night, and they are apt to attribute their other sensations of malaise to the effect of taking cold, which they suppose they must have been exposed to in getting up to make water during the night. Neither pain nor any other discomfort in the renal region appears to attend the affection at any period of its course. In the well-marked cases, however, the deviation of the renal functions from their normal standard is so characteristic that the affection can be recognised by examination of the urine alone, and this although no other symptom may seem to point to this malady. In the first place the quantity of urine excreted during the twenty-four hours is always remarkably increased, so that these patients urinate far more abundantly than sound persons of similar form and build, unless they be excessive drinkers. I t is self-evident that a patient who passes a great deal of urine must repair this loss by the ingestion of a large quantity of fluid. Hence arises the very common mistake of these patients supposing that they have diabetes, because of their thirst and excessively frequent micturition. The most exteme instance of polyuria with which Bartels has met was in the case of a gentleman~ forty years of age. He succeeded in measuring the entire quantity of urine which he passed during a night of twelve hours' duration--i.e., from 8 p.m. to 8 a.m. This consisted of 6,000 c.c. (211 ft. ozs.), it had a specific gravity of 1,004, and contained albumen. In a private case in which he estimated the entire quantity of urine passed for a whole month, the patient excreted on an average 3,350 c.c. (117 ft. ozs.) daily. In another case, treated in hospital, the daily mean average amount of observations extending over six months, and involving seventy-six measurements, was 2,200 c.c. (77 ft. ozs.) per diem. a So profuse an excretion as this, of course, compels the patient to urinate frequently, and it is a remarkable fact that the patients are invariably more tormented with the desire to pass water by night than by day. One of Bartels' patients, for example, who throughout his day's work, from 9 a.m. to 4 p.m., had no call to empty his bladder, was forced to get up three or four times every night to urinate. I t appears that this greater frequency of the desire to micturate at night is founded upon the more abundant secretion that takes place at this time. Exact observations in renal cirrhosis have shown that a much larger quantity of water is secreted by the kidneys by night than during the day, but this difference in the functional activity of the kidney during different periods of the twenty-four hours is not invariable in granular atrophy, because some cases, tested in this particular direction, show the same behaviour of the

a According to Vogel the mean average daily urine excretion ("individual urinary capacity") for a thoroughly sound adult may be reckoned at from 1.200 to 1,400 cubic centimetres (42 to 49 ft. ozs.) for those who drink moderately, and from 1,400 to 1,600 cubic centimetres (49 to 56 ft. ozs.) for persons who drink freely.

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kidney as in healthy individuals--namely, that more water is secreted by day than by night. The colour of the urine, corresponding with its large amount, is, as a rule, pale yellow, or more often yellowish-green. Generally it is clear, and in most cases it deposits no sediment. I ts specific gravity is, as a rule, low, and corresponds to the amount of fluid passed--for months and even years it may fluctuate daily between 1,004 and 1,012. Although albumen in the urine forms one of the character- istic symptoms of the disease (interstit.ml nephritis) yet it is no constant symptom in this affection. Albumen may be entirely absent from the urine throughout the whole progress of the case, but more commonly it alternately appears and disappears, a phenomenon which seems to depend upon the patients moving about or remaining at rest in bed - - i n other words, upon the amount of muscular exercise they take. Under all circumstances, however, the amount of albumen contained in the urine in the course of genuine contracting kidney is insignificant in comparison with the high percentage furnished in inflammatory processes affecting the same organ. The quantity of albumen furnished by a contracting kidney fluctuates between a scarcely perceptible cloudiness on boiling and an amount of five parts by weight of dry albumen to 1,000 parts by weight of reinc. The daily loss of albamen sustained by patients in this disease reduces itself, in spite of the ordinarily profuse urinary secretion in most cases, to an extremely small sum per diem. In no other disease of the kidneys is the amount of albumen contained in the m'ine of one and the same individual subjec~ to such great variations according to the mode of life, the food, and the general state of nutrition. Although the most important evidence of coutracting kidney we can obtain is derived from accurate exambtation of the urin G yet, as Bartels forcibly urges, one must not fancy that this information is to be obtained by the analysis of single samples of urine. There exists, he continues, no renal malady in which the danger of deceiving oneself is so great, if only a few, and these incomplete, examinations of the nrine are insti tuted; for it is just in these very cases of genuine contracting kidney that urine is occasionally and temporarily excreted, which is in no way to be distinguished from that secreted by healthy kidneys.

Corresponding to the low specific gravity of the urine in contracting kidney, its percentage of solid constituents, and especially of urea, is abnormally small. As a rule, in well-marked cases, the percentage of urea. stands between 1 and 2 per cent., and occasionally even falls below 1 per cent. The urine in this disease usually deposits very little sediment, and often absolutely none at all. Great care must be taken in collecting any sediment which may be present for microscopic examination, on account of its very minute quantity. In it there may be found a few scattered casts, together with some crystals of uric acid or oxalate of lime. Many specimens must be put up, and long search be made before dis-

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covering even a few of the casts, which are generally of the narrow variety, and perfectly hyaline.

Cardiac cs are so frequent, and of such a constant character in contracting or granular kidney (interstitial nephritis), that their presence adds the strongest presumptive evidence to the diagnosis of this form of renal alteration. Dickinson ~ says that, in fact, he has got to regard simple cardiac hypertrophy as one of the most important diagnostic sigas of renal fibrosis, while Traube observes that one can recognise the renal disease by the pulse. This hypertrophy of the left ventricle without valvular lesion, which so often accompanies interstitial nephritis, is the more worthy of mention as it is ahnost never seen in cases of parenehy- matous nephritis (the large white kidney). In interstitial nephritis, on the contrary, Dickinson met with it in thirty-one out of sixty-eight cases. According to Traube it is found in ninety-three cases out of one hundred, and according to Grainger-Stewart b it is present in almost every advanced case.

In this most insidious malady--the cirrhotic or contracting form of Bright's disease---it is not uncommon for the renal affection to be detected only when the complications have drawn attention to it. When the initial manifestations of the disease proceed from the heart~ the patients often complain of occasional attacks of palpitation, accompanied sometimes with vertigo. More often they occur with a sense of great uneasiness~ or with a feeling of suffocation or want of bre~h. The radial pulse is remarkably tense and bou.nding. Then~ upon carefully examining the chest, the objective signs of enlargement of the heart are dis- covered. Any hypertrophy of the left ventricle, without valvular lesion of the heart to explain its occurrence~ ought to direct attention to this renal malady as possibly existing. Dickinson ~ speaks of it as a clinical landmark of no small value, and says that it may be taken as a practical rule to which there are few exceptions~ that, if the cardiac hypertrophy is marked, the kidneys have either primarily or secondarily undergone fibroid change-- in other words~ if the heart be hypertrophied (always excluding other obvious causes), the kidneys are the seat of grave and, probably ~ intractable disease. Bartels states that he has never failed to observe the signs of hypertrophy of the left ventricle in any of his cases of genuine contracting kidney, or to confirm the fact in every post raortem made upon their bodies. I t sometimes happens that the cardiac state may not attract notice by its symptoms, though it is at once evident to auscultation.

Bright was acquainted with the fact that hypertrophy of the heart occurs in a very large proportion of cases of contracted kidney when the

Diseases of the Kidney. :1877. P. 410. Bright's Diseases of the Kidneys. 1868. P. 131. 0p. cit. P. 556.

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disease has reached an advanced stage, and he suggested as a probable explanat ion that " t he altered quality of blood so affects tile minute and capillary circulation as to render greater action (of the left ventricle) necessary to force the blood through the distant subdivisions of the vascular system." J t is objected to Bright 's view that he failed to show that the blood was really already impure at the time when the heart- hypertrophy began, and modern exactness calls for chemical proof of the impm'ity of the blood or its serum before it will assent to charge it with such results. Both Frerichs and Traube also object to Bright 's explana- tion. Traube's opinion (in favour of which Bartels expresses himself most distinctly) upon the mode of origin of cardiac hypertrophy in renal atrophy is that it is the result of increased tension in the arterial sys tem-- a tension which must of necessity take place as soon as a great number of arterial branches in the kidneys, with the Malpighian tufts attached to them, become obliterated (by the proliferation of the intertubular con- nective tissue), and when the channels through which the blood of the renal artery must drain away are reduced within narrower limits. He places the consequences of renal contraction in the same category with the results which deficiencies of the mitral valve and certain diseases of the hmg exert upon the right chambers of the heart.

This hypertrophy of the heart is said to be the result of the renal obstruction. I f this, however, be the case, why is it not observed in parenchymatous nephritis (large white kidney) or in the amyloid kidney, in the former of which, at all events, the embarrassment of the circulation is strongly marked, in consequence of the vessels being compressed in the cortical substance? To this question theory answers (says Charcot ~) that persons affected by parenchymatous nephritis are debilitated subjects, in whom for various reasons, and particularly on account of the great loss of albumen, the nutrition is profoundly affected--the nutrition of the heart being equally so with the other organs. In interstitial nephritis, on the contrary, nutrition continues normal for many years, and as the disease is developed in a very gradual manner, there is all this time for the hypertrophy of the heart to be brought about. Such is not the case with parenchymatous nephritis, where, in consequence of the comparatively rapid progress, the equilibrium is quickly destroyed. Gull and Sutton deny the connexion between renal contraction and hypertrophy of the left ventricle as cause and effect, holding both events to be joint results of one general affection, "arterio-capiUary fibrosis," which they hold is extended throughout the entire arterial system, or spread over the greater part of it. Barrels observes- -" They appear to be perfectly unaware of Traube's theory - -a t all events they make no mention of it."

The consecutive hypertrophy of the heart which obtains in granular disease of the kidneys is the key towards interpreting a whole series of

Bright's Disease of the Kidneys. 1879. P. 57.

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symptoms which accompany ttle disease. Polyurla, the ordinary symptom of renal contraction, is a result of the increased blood-pressure in the aortic system. In this way the hypertrophy of the left ventricle acts as an efficient compensation for the loss of renal secreting-tissue such as the kidney contraction carries with it. As long as tile condition of the hypertrophied left ventricle is capable of maintaining the blood-pressure in the aortic system at its abnormal height, contracting kidneys which have dwindled down to more or less considerable remnants of secreting glandular-tissue not merely continue to secrete urine, but in the large proportion of cases actually furnish, in the same interval of time, a larger quantity of urine than healthy kidneys would supply. The lo,g absence of urcemia is also connected with these consecutive cardiac changes. So long as the hypertrophied heart labours energetically, no urmmic symptoms occur, for an overabundant secretion of urine is being carried on, and, in consequenc% there is sufficient rinsing and washing out of the secreting gland-cells. But directly this excess of blood-pressure fails from any cause, or the urinary secretion, in consequence of transitory or permanent weakness of the heart, is diminished~ urmmie symptoms set in, and not rarely dropsy sets in at the same time, or even before. That ur~emic symptoms depend rather on failure of the heart 's force than from wasting of the renal substance to a degree which renders them hopelessly impotent, we learn from the cases where patients survive their first acute urmmie attack for years. The albuminuria in this disease is to be entirely attributed to the increase of the blood-pressure in the vascular tufts rather than to structural changes in the kidneys themselves; and the best proof of the correctness of this proposition is its disappearance and reappearance, or its diminution and increase according as the p~tients observe conditions of rest and muscular repose, or persist in their usual avocations. The absence of a profuse drain of albumen, and the con- Stancy of the polyuria so characteristic of this disease, is the reason that no hydrmmia occurs. Hence it comes to pass that this affection, in more than one-half of all the cases, terminates fatally without the patient ever having been dropsical. The usually small loss of albumen in the urine affects the general nutrition so very little, while the organs of digestion continue to fulfil their functions regularly, that its influence is scarcely to be remarked, although it may, perhaps, have lasted for years. Hence it happens that when the renal affection is first distinctly recognised, i t i s impossible to say how long it may have already existed.

While the hypertrophy of the left ventricle must be credited with considerable compensatory advantages in granular kidney, there are certain dangers and disadvantages with which the increased arterial tension pro- duced by this hypertrophied heart threatens the patient. The evil influences of this condition are most evident in the relatively frequent occurrence of cerebral hmmorrhages in genuine contracting renal disease,

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the true explanation of which no one, surely (says Bartels), will seek elsewhere than in the notoriously abnormal high pressure maintained in the arteries, inasmuch as cerebral apoplexy in renal disease may attack persons who are comparatively young, and whose arterial walls are quite healthy. However, the influence in these intracranial hmmorrhages of alterations in the vessels cannot be wholly ignored. Chronic endarteritis or arterial atheroma is one of the lesions most frequently met with in those who succumb to interstitial nephritis (granular kidney), partly in consequence of the circulation of morbid blood, partly as a result of the unusual strain and pressure to which they are subjected. At length in the struggle between the propelling hypertrophied left ventricle and the resisting arterioles, a brittle vessel, gives way, and a fatal h~emorrhage occurs2 In reference to the unexpected nature of the attack, Dickinsonb observes that those who die of apoplexy (in this disease) are apt to be struck, not in the wards of a hospital, but while they are going about making use of what health they have. The same author remarks tl~at bleeding from the nose often happens, and sometimes proceeds to an alarming extent; it is more frequent with this than with any other form of renal disease, though very common as a consequence of lardaceous change. Rayer points out that epistaxis is often one of the phenomena which precede and announce urmmic poisoning. Epistaxis is the most common form of h~emorrhage in this disease, though bleeding from any of the mucous surfaces may occur. I ts appearance in the form of menorrhagia, as West has pointed out, may afford a clue to a correct diagnosis.

Certain retinal lesions are quite frequent in this form of Brlght 's disease, which are in a measure unknown in parenchymatous nephritis (large wl,ite kidney). These lesions, which present the appearance of white plates, variegated by small hmmorrhaglc strim, are situated in the retina, particularly in the neighbourhood of the papilla. So characteristic are these alterations, when well developed, that they are sufficient of themselves to establish the diagnosis of intersti t ial nephritis. Although this is not infrequently the first sign of the disease to be recognised, Dickinson believes it to be always an indication of an advanced stage of the disorder. Both eyes are always attacked, although they may suffer in unequal degrees. I t gives grounds for a very unfavourable general prognosis. In some cases a curious symptom accompanies these tesions--metamorphopsia--crooked sight--i.e., straight lines seem bent. In general, obscurity of vision commences quite gradu- ally, showing itself as simple diminution in the acuteness of sight; and the patient, consulting an oculist for the choice of glasses, is found to have interstit ial nephritis. This disturbance of vision is quite different from the amaurosis ur~emica, of cerebral origin, in which the disorder of

a Lectures ,~n Bright's Disease. Geo..Johnson. 1873. P. 68. b Diseases of the Kidney. Part II. P. 413.

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vision commences suddenly and may as suddenly subside again, while no retinal changes are observable which serve to explain its cause.

As to the post.mortem appearances in interstitial nephritis, the genuine contracting disease affects both kidneys, and each organ equally in most instances. The result of the disease in well-marked cases is a very con- siderable reduction in the volume of the two glands, so that in extreme cases they do not appear larger than children's kidneys, and often much smaller. I t is the cortical substance which is the principal seat of the a t rophy- -an atrophy so considerable that in some cases a quite small margin of cortical substance surrounds the basis of the pyramids. From the most commonly obvious naked-eye appearance the kidneys are very fre- quently called granular. A granular kidney is one of which the surface, when the capsule has been removed, instead of being level and smooth, has upon it little projections, each of which forms the segment of a sphere, and which have been described as granulations. In kidneys which have acquired granular outsides a certain definite change has invariably taken place in the fibrous tissue by which the tubes are separated. The change is closely analogous to that which produces cirrhosis of the liver. A morbid increase in the intertubul'tr tissue of the organ begins at certain points upon the surface and extends inwards. The new growth contracts as it is formed, and, in contracting, not only encloses and compresses such parts of the gland as are in its path, but draws in ~he surface at its point of origin. This intraction taking place at regular intervals results in Mternate elevations and depressions--or, in other words, in granula t ion-- the size of the granules being regulated by the distance between the starting points of the new formation. The first change which can be recognised as a result of the disease is unevenness of surface. The cap- sule is more adherent and thicker than natura l ; on removing it, some part of the surface has lost its even curve and is beset with little half- formed projections of small size and almost inappreciable prominence. In an early stage of granular degeneration the organ is not much altered in bulk; in texture it is, perhaps, harder than natural. In a section of such a kidney, examined under the microscope, smkll fibrous processes may be found start ing inwards from the depressions upon the surface. In an advanced and well-marked condition of granular degeneration the kidneys are much reduced in size, so much so that a kidney which should weigh five or six ounces may weigh only two or three. The longer the disease lasts the smaller the kidneys become. When the disease progresses more in one kidney than in the other there is an inequality of size. In advanced cases, when the thickened and opaque capsule is stripped off, the exposed surface is found studded with prominent hemispherical granulations, often about one-sixteenth of an inch in diameter, though they may be larger or smaller than this. These granules usually have a bright colour like that of parched peas, while the depressed spaces between

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are tinted with vascularity, so as to have a purplish or faint red colour. The superficial vessels are only seen in these intermediate spaces where an irregular network often exists~ forming a contrast with the pro- minences, which are always bloodless. Cysts are often conspicuous on the surface. Upon a section through the centre of the gland the cortical part appears to have undergone most alteration. Often the portion lying between the cones and the capsule is reduced to the thinness of a shilling.

[2'0 be continued.]

TANNATE OF P E L L E T I E R I N E AS A T~ENIAFUGE.

TIIE active principle of the bark of the punica granatum, discovered by M. Tauter, and described by him under the name of pelletierine, has been used with success as a remedy for t~enia. I t is given in tile form of the tannate, in the dose of 50 centigrammes, followed in two hours by 30 grammes of castor oil. Dr. Laudrieu describe~ its action as follows : - - In the two cases observed neither colic nor headache was occasioned. In the first the patient had been prepared by dieting, and a single dose sufficed to expel the tmnla entire. In the second one dose did not suffice~ it is true, but the patient was not weakened by the treatment. The patients did not exhibit that repugnance so constantly shown to the administration of kousso or the pomegranate bark. In a third case the administration of a dose of the chlorhydrate of pelletierine brought away 15 metres of worm, the only phenomena observed being diplopia and a slight tendency to syncope, both of which quickly passed off. The pulse and temperature were not influenced by this medicine; nor were the kidneys in any way affected. The medicine seemed to have an elective and toxic action, operating solely on the tmnia.--Jour, de .~ldd. de Bordeaux, June 28, and IV. Y. ~led. Rec., Sept. 67 1879.

SALICYLIC ACID IN THE TREATMENT OF L U P U S .

DR. AMEGLIO reports a case of ulcerative lupus of the face, of five years' duration, in which he employed salicylic acid locally, after all the usual applications had proved ineffective. The ulcerating surface was painted three times a day with a solution of six parts salicylic acid in twenty parts glycerine. After a few days the readily bleeding vegetations withered, and the floor of the ulcer took on a healthy appearance ; at the end of the month cicatrisatlon was completed. The patient at the same time took arsenic internally.--Gaz, degli Ospedali, June, and N. Y. l~[ed. tgecord~ Sept. 6, 1879.