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 Chronic I fit erst it ia I Nephritis and 
 Arteriosclerosis 
 
 BY 
 
 OSKAR KI.OTZ, M.D., CM. 
 
 Pr-T«BlHiiH, PA. 
 
 FROM THE 
 
 AMKKU AN JOl RN.Al. OK THK MKDICAI. SCIENCKS 
 
 DecenibtT, 191.S No. 6, vol. cl, p ^i'l 
 
n.- 
 
Eitni -ted from th>' American Journal ol the MmlUal Sp=ence», 
 IV<«'nil)cr, 1U15, N'li, »l, vol. el, p. »27. 
 
 CHROmC INTEESTITIAL NEPHRITIS AND 
 ARTERIOSCLEROSIS. 
 
 By Oskar Klotz, M.D., CM., 
 
 PITTBBUHQH. PA. 
 
 (From the Pathologiral Luborotoricg, University o. 'ittsburgh.) 
 
 No agreement has as yet been reached as to the nature of and 
 the progressive changes leading up to the granular kidney. Almost 
 all the factors having to do with the carrying out of the normal 
 kidney function, as well as the known factors giving rise to pro- 
 cesses' of fibrosis in c*her organs, have been mentioned as the incit- 
 ing cause of renal sclerosis. Particular weight has been placed 
 upon certain of these factors, because of their presence diiriiiL. one 
 stage of the disease; but the opportunity of weighing their impor- 
 tance as an active cause for the contracted kidney hps not been 
 sufficiently good to direct a knowing finger at them. No one has 
 yet been able to describe in a single instance the sequence of events 
 from the beginning to the fully developed chronic interstitial 
 nephritis. Thus, opportunity has remained open for wide specu- 
 lation on the interpretation of the pathological processes involved. 
 
 Some attempt has been made to link up the clinical and urinary 
 findings with the successive changes that are taking place in 
 the tissues of the kidney. These, however, have added little to 
 our understanding of the process. True it is, that with the fully 
 developed disease, certain manifestations make their appearance, 
 and we believe that some light has been thrown upon the correla- 
 tion of the urinary character with the altered functional capacity 
 due to renal sclerosis. But as for saying that the clinical manifes- 
 tations bear any relation to the ructural change of the kidney 
 prior to the stage of granular coi paction or, better, that we can 
 forecast the outcome or even suggest the past processes in the 
 kidney by clinical analyses we have no definite evidence. 
 
 Thus the problem has been left in the realms of conjecture and 
 in the absence of incontestable proof by experiment, our knowledge 
 concerning the development of the granular kidney has not mate- 
 riallv advanced since the days of Gull and Sutton. In the face of 
 
2 KLOTZ: IvrilRHllUAL NEPHBITW AND ARTERIOHCLF.nOHlS 
 
 this we do not wish to minimize the value ot the many observations 
 whicli have jjiven us a clearer unfierstHndinK of some of the fan'-r 
 reactions in the kidney sul)stan(e; l.ut it wouKl ai)i>ear that the 
 minutia- t some of tiiese observations iiave led us astray froin the 
 broad aM,ects of tU proMm. That Jores should Knd a splitting 
 of the internal elastic latnuia of the renal arterioles, and from this 
 finding discuss the importance of those still indefinite factors indue- 
 infc :>rteriosclerosis as of prime imiwrtame for kitlney di-ienso, is, 
 it seems to me. quite aside from the main issue. 
 
 For the main part, as was brought before the Association of 
 American Phvsicians last year, studies upon the pathologu'al 
 nature of chronic interstitial nephritis have been made upon the 
 ach ance<l form of the disease. The criterion fo' the recognition of 
 the important tvpe of the «lisease is still based upon the description 
 of the kidnev as given by Richard H ' -ht. «f we a.lhere clos; . 
 these described characters, we will finu acre is a general similu. v 
 grouping them into one class, (iradually, however, our attentioi. 
 has been drawn to the fact that there are other forms of renal sc e- 
 rosis differing to a greater or less degree from the type here under 
 discussion ami readily recognized by careful observatum and 
 supplemented bv the microscope. Thus we have kidnev hbroses 
 associated with hydronephrosis, ascending infection of ureter and 
 bladder, hematogenous infection (pyogenic), infarcts, thromboses, 
 amyloid disease, syphilis and other infective granulomata. and 
 arteriosclerosis. But when we are speaking of the small, contractcil 
 or granular kidnev we have in mind a diseased condition of the 
 kidnev which is different from each of these. It is different not 
 only in the structural changes induced, but it is different also in its 
 progress and in the distant systemic responses. The small, granular 
 kidney is recognized bv its small size, the thickening of its capsu.e 
 with 'adherence to the underlying cortex. The kidne.v substance 
 when strippeil of its capsule is distinctly granular, each granule being 
 surrounded bv a depression from which fibrous tissue radiates par- 
 allel with the ascending vessels. The kidney substance may appear 
 red, but, on the other hand, may be quite pale with not a few ot its 
 granules as vellow as the adrenal cortex. The cc rtex is most markedly 
 altered, and is commonly only half the thickness of the normal 
 structure. Within it are found many fine wedge-like sclerotic 
 areas which occupv the positif)ns between the granules observed on 
 the surface. Alternating with these areas of fibrosis a fairly norinal 
 kidney .issue is observed. Along the patch of these radiating 
 fibroses the tubules and Malpighian corpuscles become inv()lved. 
 The medulla is less altered, although a hyaline fibrosis not intre- 
 quentlv surrounds the excretory tubules. As in other regions 
 subject to progressive fibrosis a considerable adipose tissue (le\ elops 
 in the surrounding structures, particularly about the pelvis. 
 At the present time, opinion as to the development of this torm 
 
KLOTZ: INTERCTITIAI. NK-IIHiriH AM> AHTKItlOHl I.KIU w|H 3 
 
 of the interstitial nephritis h«s Im>»'h ilividwl rnuiniy iMtwwii i o 
 schools: the one fonsiders it the outeoine of a h>w ariulv hut pnn 
 gressive inHanimation, while the other l»elie\es it the re-*uit of n 
 primary cireuhitory distnrhnnce with u seeondury atrophy ami 
 replacement fihrosik Unfortunately the issue has In-en somewhat 
 eonfnse«l hy the further intro<hi< tion of the terms primary and 
 seeontlary interstitial nephritis. Kach jjroup clainis that their 
 explanution is adecpiate for the so-calle*! >t«"'>iii"ie eoiitraet»-<l kid- 
 ney. We would do well to drop such irrelevant terms and leave 
 the apjilication of a new nomenclature to him who clearly indieates 
 the ptttholoKicul secpietice of events coneerne<l in chronic interstitial 
 nephritis. 
 
 Ciull and Sutton considered the relationship of the arteries to 
 the diseiiMS of the kidneys as a peculiarly intimate ojie in which 
 the arterial processes pre<-ede«l and determined the interstitial 
 nephritis. No agreement was reachetl hy suhsecpient workers of 
 the actual nature of the arterial disease, some vicwiu); it as an 
 endarteritis (Thoma), others as an hypertrojjhy (Johnson, Kwald, 
 Fricdmann), while the suhsecpient work hy I'rym n-id .lores drew 
 attention to the arterial lesion as a true arteriosclerosis, .lores, 
 furthennore, contended that the asscM-iated a.terial changes in 
 other organs, as was ilescrihed h\ nany, was also an arteriosclerotic 
 process. The differentiation of tlii ))r(K-ess rested upon the finding 
 of deep arterial dejtenerations associated with a splitting of the 
 internal elastic liner. As Jores, however, ohservcnl, arteriosclerosis 
 may occur in the arteries of other organs in the ahsence of sclerosis 
 of the renal vessels. 
 
 While the ahovc authors were contending the ilcpendence of 
 chronic nephritis ui)on disease of the hlovMlves.sels. Zieglcr main- 
 ta' -ed the differentiation of types of chronic nephritis into iiroups 
 associated or nTi,.s.sociated with arteriosclerosis. Those kidney 
 lesions resulting from nrterio.sclerosi- he hclieved to he individual 
 and of a ])urely degenerative character, and designated them the 
 arteriosclerotic kidney. 
 
 Both Jores and his pupils repeatedly remarked that dironic nucr- 
 stitial nephritis is a disease most frecpiently encountered in advanced 
 life, a period when arteriosclerosis is also most prevalent. Never- 
 theless, they remark upon the finding of occasional cases in which 
 they have been able to demonstrate ar'vanced renal sclerosis unac- 
 companied by arteriosclerosis within the kidney. This agrv s with 
 the finding c.f Orth, who believes that in chronic interstitial nephritis 
 the vascular changes are not essential because their Vc-'iety does 
 not correspond with the extent of the lesions. Roth dt rihed a 
 number of cases in which renal sclerosis was advanced, but in 
 which the arteries did not show the type of sclerosis defined by -lores 
 as arteriosclerosis. He did, however, find that the arteries were 
 affacted I a connective-tissue thickening of the intima with 
 
4 KUrrZ: INTERKriTIAL NKPIIRITIB AND ARTERlOSCtEROSW 
 
 splitting of the elastic lamina. As. however. |.n.ces8e9 of (WiMieni- 
 tion were wanting, he refuse<l to call it arteriosclenwis. Me Mim'-ts 
 that the <■ vessels might »uhse«,uently show artcrioscler«)tic cluuiKf 
 Fron. his obsenati.ms we can only comliule that the kidiM y lesions 
 have advance«l with greater rapidity than those m tin intima of 
 the renal vessels, and his casts illustrate tht point we wish to nrnke 
 that the narrowlv definecl Umn of arteri()s«leros\s as given Jores 
 is not an essential factor in brinKing out snl.sequent n»terstitia! 
 
 "Tloth de8cril>e<l 3 cases of chronic interstitial rephritis without 
 arteritwclerosis. In the kidneys, however, endarteritis was present 
 in the small arteries. The cases were of relatively yc.ung individ- 
 uals and all of tl.em had definite chronic or recurrent lieart aii<l 
 arterial discuses. Yet with it all neither .lores nor his pupil s.m's 
 anv direct relationship insofar as a common causative fuct.jr is 
 .•..luerned in the simultaneous ami progr. 4ve lesions -u these three 
 organs These authors lav much stress on the finding of a single 
 stlemscd arteriole or the mildest beginning of intimal degeneration 
 as indicative of the influence of arteriosclerosis uiwn the kidney. 
 N(. recognition is given to the fact expressed Im their own cases 
 that the fibrosis of the kidney wa" marke<liy advanced, and in the 
 late stages of contraction, while the arteriosclerosis xyas only 
 iH-ginning. We can in no way follow the conclusion of tins author 
 as illustrated by his own cases that the chronic interstitial nephritis 
 was the result of the early endarteritis demonstrated. 
 
 In the admirable work of Councilman (!Sn7) the part playc( 
 bv the inflammatory process in bringing alwut the interstitial 
 lesions of the cortex of the kidney was well demonstrated, in part, 
 the cii^es studied included some of scarlet fever, diphtheria, pneu- 
 monia, and other infections, and the lesions described wrre ot 
 the nature of diffuse non-suppurative interstitial nephritis or t.vi)es 
 of glomerulonephritis. Of the latter, two fonn were distinguished: 
 a non-suppurative exudative form and a proliferate e type. -No 
 clear distinction can b«> made between the etiological factors present 
 in these two tvpes. and it would sc.m that both may arise from the 
 same causativ^ factor. At the time of carrying out his work, bac- 
 teriological methods were not available to ma ke a <listinction between 
 the various forms of streptococci, and we find the author siu-aking 
 of the organisms isolated from cases of he«-^ disease as pncumococci. 
 I believe we will be correct in interpreting these results as indicating 
 the presence of the Streptococcus viridans group. These organ- 
 isms were found in cases of glomerulonephritis in large percentage, 
 but the author's descriptions of the lesions indicate a transition 
 between the glomerulonephritis and the diffuse, interstitial type. 
 The work of Wagner bears out these findings, particularly in 
 indicating the importance of the inflammatory process of scarlet 
 fever and other infections in bringing about permanent interstitial 
 change. 
 
Muyn: intebhtitui. nephmitw and \kt»' 
 
 MIHIW 
 
 The work of CouncilniHti is atnoiiK tlic (vw in wiiioli it stmly of 
 the progressive lesiutis of the kidnt-y was areuinpanieil hv ha«'terio- 
 logical examination. (M this he suys: "Various forms of ili.scast> 
 of «)ther organs, particularly of the heart, are often ass<Kiutetl with 
 them, and Iwcteriohtgical investigatiuti has fre<pieiitly shown in 
 mm y cases the presence of .-rtain organisms in the kidneys. In 
 mo>f cases the bu«teriii are found in sunie other lesion and in the 
 bl«HKl, and their presence in the kidneys is but a part of a general 
 septicemia. Moreover, the same ctmditimis in the kiilneys may Ih: 
 found associated with various orgtnisms, and the same organisms 
 may be associatetl with widely different anatonii al lesions." A 
 very fertile iield awaits the routine study of the bacteriology of the 
 kidneys in conjunction with the histological examination of all 
 types of infc .>n. The wor' -vhi'-h has U-en i)erformed up to the 
 present time is very sugges of indicating the actual pres«'nce 
 of bacteria rather thru their • ns in the interstitial res|M)nsc of the 
 kidney. 
 
 Undoubtedly wh.. O'/jK-ars as complete disagreement ii the 
 persona^ • Sser\ atioi ■ . chronic nephritis lies mainly in the mcthtxls 
 and ma i I sludieu. Although the iiiuitomical classification of 
 kiihiey i..:.case has not fo'ind favor with either the clinician or the 
 pathologist, yet in the absence of a better substitute we all revert 
 to this methotl. Miiller attempted un etiological classification which 
 as yet is hardly practical, and Ilerrick, while finding the old ana- 
 tomical grouping unsatisfactory, offers nothing to replace it. 
 
 The tyiH-'s of nephritis whic"i totlay attract our attention as the 
 forerunners of the contracted kidney are the acute glomerulo- 
 nephritis and the acute non-suppurative interstitial nei)liritis. 
 Without desiring to describe the various tyi)es of gU)meruh)nepliritis, 
 as well as the variety of interesting lesions that niaj- l)e observed 
 in the Malpighian body and Bowman's capsule, there is ample 
 evidence that, in t' : human, these glomerulonephritides are infec- 
 tive lesions (Councilman, Guskeil, Baehr). The imiK)rtant feature 
 lies in the fact that the glomeruli become the centres of inflamma- 
 tory response in which a non-suppurative exudate and endothelial 
 proliferation of the capillaries and a proliferative resjionse of the 
 inner lining of the capsule is commonly observed. The occlusion of 
 the capillaries of the glomeru)"s by cellular proliferation or by 
 thrombosis is only an added complication, and the subsequent 
 degeneration that occurs in the tubules of the kidney is also to be 
 viewed as a secondary disturbance depending upon vascular change 
 rather than an injury produced by the primary factor. 
 
 A study of these i les of glomerulonephritis soon convinces one 
 of the varying picture, even during the acute stage. In some 
 thromboses of the glomeruli are common, in others rare, or the 
 lymphocytic infiltration of the glomerulus is great and confined to 
 this structure; others again, show the inflammatory reaction diffuse, 
 
6 KLOTZ: INTERSTITIAL NEPHRITIS AND ARTERIOSCLEROSIS 
 
 surrounding Bowman's capsule, infiltrating the stroma between 
 Se tubulef and following the course of the mterlobular artenes 
 and vessels of the intermediate zone. Many such cases have been 
 descriS by Councilman, Ziegler, and others. In fact, the p'cture 
 nresented by those kidneys in which the mflammation is more 
 diffuse simulates more closely the type of acute mterstit.al non- 
 suppurative nephritis. This latter type, which was originally 
 diSsed as a disease of the kidneys found after scarlet fever 
 measles, and sometimes smallpox, is .. v being incorporated ..ith 
 the glomerulonephritis, mainly because a certain amount of glomer- 
 ular disturbance is always present. Fahr finds the streptococcus and 
 pneumococcus most frequently associated with acute interstitia 
 nephritis, and finds also that the same organisms are the chief 
 cause of glomerulonephritis. , i • j 
 
 In short, although there are variations of glomerular lesions and 
 we encounter forms of inflammation of the kidney stroma, there 
 does not appear to be any difference in the causative agent, most 
 frequently the Streptococcus viridans. We must, however, point 
 out that the bacterial infection reaches the kidney under different 
 circumstances, and in a somewhat different form, in the various 
 ™emic diseases in which it is met. It is the bacterial clusters 
 or small infective thrombotic masses which are liberated in he. rt 
 disease that give rise to a type of glomerular infarction, in 
 this wav particular structures in the kidney are more intensely 
 involved than others. So. too, in cases of bacteriemia, by organ- 
 isms of low virulence, the kidney, as well as other organs, becomes 
 a local focus of infection and this is particularly tnie in the bacterie- 
 mia of acute rheumatic fever in which the heart and bloodvessels 
 are also affected. In these infections the heart may be involved 
 in a variety of ways, and when the endocarditis becomes well- 
 marked the kidney may be subject to embolic processes m its glo- 
 meruli, so that both the acute interstitial and the glomerulonephritis 
 are simultaneously prominent. Hence it is obvious that to state 
 that a definite tvTC of kidney lesion is constantly to be found as a 
 disease associate with infection of other organs is only voicing a 
 rule with prominent exceptions. 
 
 The frequency with which acute interstitial and glomerulo- 
 nephritis are present with infective heart disease is known to all 
 who have observed these cases at autopsy and studied the tissues. 
 It is, furthermore, easy to demonstrate the fate of the early mflani- 
 matorv process. Fibroses of the glomeruli, of Bowman s capsules, 
 and of the intertubular stroma may be demonstrated in all stages 
 of formation, and recurrent attacks of these infective processes give 
 rise to combinations of inflammatory responses in the kidney tissues. 
 The question immediately arises whether the localization of these 
 inflammatory processes gives us definite types w^hereby their 
 futur" scars mav be recognized. In answer to this the best reference 
 
KLOTZ: INTERSTITIAL NEPHRITIS AND ARTERIOSCLEROSIS 7 
 
 is made to a few experimental results. In these it has been shown 
 that inflammatory reactions in the kidney due to bacterial agents 
 are prone to follow and surround the course of the bloodvessels 
 particularly the interlobular vessels, and the ascending cortical 
 branches as well as the afferent arteries of the glomeruli. Asso- 
 ciated with these inflammatory responses there are not infrequently 
 glomerular reactions, infiltrative, proliferative, or thrombotic. 
 The progress of these lesions is similar to that in the human kidney 
 and the end-result is a process of fibrosis radiating in its character 
 with shrinking and granulation of the cortex and contraction of 
 the entire kidney. Such lesions were reproduced in animals by the 
 use of organisms (various members of the Streptococcus viridans 
 group) isolated from infective heart disease, and the responses in 
 the kidney were found to be accompanied by a myocarditis, at 
 times an endocarditis, and in a few cases pericarditis. In only a 
 few instances were systemic intimal arterial lesions obtained, 
 although the perivascular response was always noted. Here, then, 
 we have evidence of the development of the various stages of the 
 contracted kidney in the presence of chronic infection and in the 
 absence of primary arterial lesions. 
 
 These findings are in accord with the observations on human 
 material and explain the occurrence of the contracted kidney in the 
 first half of life as well as its greater frequency in the later years. 
 L'We all chronic diseases, the frequency of chronic interstitial 
 nephritis is greatest in the late decades, and it is also a rather 
 depressing outlook when we find that the incidence of these chronic 
 diseases shall increase with the saving of more lives in childhood 
 from death from scarlet fever, acute rheumatic fever, chorea, and 
 other Streptococcus viridans infection. We must also equally 
 appreciate that the heart and arteries suffer, sometimes much, at 
 other times less, by invasion of these bacteria. In the arteries an 
 endarteritis, a mesarteritis, and a periarteritis have all been r<ipeat- 
 edly demonstrated in these infections during the early years of life. 
 Of the heart lesions, we need make no other comment than rei'erence 
 to Aschoff's studies upon focal myocarditis, and of the f -equent 
 presence of endocarditis in the human and in experimental infec- 
 tions. 
 
 What, then, is the relation of renal arteriosclerosis to chronic 
 interstitial nephritis? Before one can answer this we :r " have 
 a clear understanding of the nature and genesis of arteriosclerosis. 
 It is not enough to boldly speak of general arteriosclerosis as of 
 common type and constant origin. Nor is this true v.ithin the 
 kidney itself. There are arterial lesions within the kidney whose 
 origin is widely different and which vary in their character. 
 
 Ziegler has long ago demonstrated the peculiar renal fibrosis 
 resulting from peripheral arteriosclerosis. In old age, where it is 
 not uncommon to have various arterial tracts severely involved in 
 
 PA:^^^£r-^.\^&:->~ 
 
 1:<S««~te3^5< 
 
8 KLOTZ: IXTERSTITIAL NEPHBITIS AND ARTERIOSCLEROSIS 
 
 sclerosis and in which the lumina of the vessels are ftinMy 
 imSd, atrophic changes result in the area supplied. It is 
 Kous hat the amount of sclerosis varies greatly and is bound to 
 S out limited areas. The kidney tissues which suffer from the 
 &atory disturbances undergo atrophy, and even complete 
 ™ Sthout. however, necessarily showing evidence of intra^- 
 u ar degeneration (fat), as is otherwise so commonly encountered. 
 S kidney Aows ar.:;s of sharp depressions scattered irregulariy 
 ov?r its surface so thai .ts structure and shape are distorted. The 
 indTv durdepressions simulate those of infarct, bu microscopic- 
 aUv may at times be distinguished from these in that the involved 
 areas contain some of the parenchymatous structures not com- 
 Sly de troyed . Furthermore, the kidney capsule is rarely adher- 
 er.' and the cortical surface between the areas of depression is 
 
 tuSe^eSons are the result of the obliteration of Mrly la^ge 
 vessels within the kidney. At times, it may be. smaller vessels 
 invdvlng more restricted portions of the kidney are affected 
 This then, leads to a local fibrosis of the glomeruli supplied by this 
 ciSation Under these conditions the process, both m he glom- 
 eridi and tubules, is one of slow and progressive degeneration with 
 a secondary replacement fibrosis. It is unusual to observe under 
 these conditions any evidence of an inflammatory reaction. 
 
 Smp ed with the gr« alar contracted kidney these changes 
 in trarteriosclerotic kid, y are quite different. It is inconceiv- 
 able that a process of arteriosclerosis could so ""'"^ ^^f * ^^ 
 manv arterioles of a constant caliber to give the character found 
 Tthe uniformly granular kidney. A comparable picture is to be 
 ob erved n n'^ part of the body, and we are wdl a^va^e how uncer- 
 tain is the distribution of arteriosclerosis. As the fibrosis fol owing 
 upon processes of degeneration in the atrophies of vascular scleroses 
 
 b'wXut inflammatory response, one -\--.-^*-^^,fXe:fn 
 of a granulation tissue and subsequent adhesions The absence of 
 the' e is noted in the freedom of the kidney capsule and in the lack 
 of vnechi.^ about the glomerulus. Frequently too, Bowmans 
 capsule shows no thickening. Ziegler truly calls this the .enile 
 
 '"Itb," however, not common to meet with a clear-cut and uncom- 
 plicated case. The vascular scleroses of the kidney are most com- 
 monlv the result of the same influence which has produced a pri- 
 ma?v inflammatory lesion in the kidney stroma. Hence, the devel- 
 opment of scar tissue in the renal siructures goes hand in hand 
 S lal arter.osclerosis. Here, however, in the early stage, as 
 well as during the years of progressive involvement the kulnej 
 tissue and arteries show the presence of inflammation. These 
 nflammatory deposits are easily recogmzed, and obvious y vary 
 in amount at the different stages. Jores has seen them in his inter- 
 
KLOTZ: INTERSTITLVL NEPHRITIS AND ARTERIOSCLEROSIS 9 
 
 stitial nephritis, but has taken the view that no relation l.etween 
 the arterial disease and the inflammation can be determmed. Like 
 the resuhs of the Streptococcus viridans infection upon the heart, 
 giving rise to inflammatory processes differently disposed, so too, 
 ?his Ime infection, which is so frequently at the bottom of the 
 fibrosis of the contracted kidney, brings about inflammatory 
 reactions of varying intensity in different portions of its structur^ 
 The arteries appear to form the centre of distribution for the^ 
 reactions, and much of the response is spent in the tissue surround- 
 ing the small vessels coursing through the cortex To a certain 
 e^rtent, however, intimal reactions are also found. The latter, 
 however, arise somewhat later in the course of the kidney disease 
 so that examples are not difficult to demonstrate in which intimal 
 sclerosis is wanting while a non-suppurative inflammation is active 
 about the vessel. Later, however, the picture is reversed and the 
 intimal sclerosis attracts our eye. This is now the stage w^n 
 appearances suggest that a close relation of cause and effect exists 
 between the intimal arteriosclerosis and the renal fibrosis. 
 
 The intimal disease of the arteries most commonly met with 
 in the late stages of chronic interstitial nephritis consists of a 
 chronic endarteritis with deep, fatty change. The presence of a 
 true hyperplasia of the musculo-elastic layer ^ylth secondary 
 degeneration of the inner muscle bundle has never been met with 
 bv us nor have its advocates ever clearly demonstrated its pres- 
 ence. The finding of splitting of the internal elastic lamina is 
 now found to have no specific bearing on the problem of arterio- 
 sclerosis. McMeans (of our laboratory) has shown that sucli 
 splitting is the common occurrence during inflammatory reactions 
 
 of the intima. , . i ■ u i i +„ +1,0 
 
 Granted, therefore, that the early reactions which lead to the 
 granular contracted kidney, simultaneously involve portions ^ the 
 kidney parenchj-ma and its arteries, it is often extremely difficidt 
 to distinguish in the late stages of the disease exactly how much of 
 the scar tissue has resulted through inflammation or as replacement 
 fibrosis following arteriosclerotic atrophy. We should, howeNer 
 continue to distinguish clearly the arteriosclerotic kidney of Ziegier 
 from the granular interstitial nephritis, the former giving rise to 
 true atrophic processes in the parenchyma v,jth replacement fibrosis 
 the latter having an inflammatory basis for the development of 
 connective tissue variously distributed about the important 
 structures of the organ. 
 
I».'.-,.T 
 
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