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 LELAND STANFORD JUNIOR UNIVERSITY PUBLICATIONS 
 UNIVERSITY SERIES 
 
 TheJPathology of Nephritis 
 
 as illustrated by thirty-two consecutive cases 
 
 BY 
 
 WILLIAM [OPHULS 
 
 Professor of Pathology 
 
 From the Division of Pathology 
 Stanford University Medical School 
 
 STANFORD UNIVERSITY, CALIFORNIA 
 
 PUBLISHED BY THE UNIVERSITY 
 
 1916
 
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 571ti 
 
 LELAND STANFORi:) JUNIOR UNIVHRSITY PUBLICATIONS 
 UNIVHRSITV SHRIES 
 
 The Pathology of Nephritis 
 
 as illustrated bv thirtN'-two consecutive cases 
 
 WILLIAM OfHULS 
 
 Professor of Pathology 
 
 From tlie Division of Pathology 
 Stanford University Medical School 
 
 STANFORD UN'IVERSITY, CALIFORNIA 
 
 PUBLISHED BY THE UNIVERSITY 
 
 1916
 
 Stanford University 
 Pkess
 
 353 
 
 TO ALL THOSE WHO CONTRIBUTED 
 IN THE COLLECTION OF THE CLIN- 
 ICAL DATA UTILIZED RY THE AUTHOR 
 
 7n(;n^D
 
 THE PATHOLOGY OF NHPHRIUS 
 
 AS II.I.DSTRATED BY 
 miR I'lTWO CONSECUTIVE CASES 
 
 It may seem ]iresum|ilii(iii> mi the ipatt cil' a |)alli()Iii,i;i>t to atlempl 
 to write a treatise on the I'atholoj^y of W-iili litis inchi(lin|L;- a resume of 
 tlie symptomatology of the disease, hecause the evidence collected from 
 the histories of tlie patients i^ necessarily second-hand and incomjilete 
 and the author i> not iraiiud in the interpretation and evaluation of 
 clinical phenomena. It may Ijc coiiteiuled. however, that the careful 
 judicious contemplation of a clinical liistory liy some one not connected 
 with the case and not interested in the matter of clinical diaifnosis — 
 ])rovided he has the necessary knowledge of .Medicine in general — may 
 bring out the salient points in the biology of the disease with greater 
 clearness. 1 lowever that may be. since it became necessary to consult 
 the records in trying to solve the etiological (|iiestions involved, an at- 
 tempt has been made to give an outline of the progress of the disease in 
 each individual case as brielly as i)ossible. without entering into aii\ of 
 the many details that are chiefly of clinical importance. 
 
 The aim has been to collect in each case all relevant data which 
 migiit have any bearing on the etiology, progress and termination of the 
 disease.' To this was added an abstract of all autoi)sy findings which 
 might be of interest, and an esjjecially careful descri])tion of the findings 
 in the kidneys, both in the gross and microscopically. Since no mere 
 descri])tion in words can convey an adec|uale conception of the fmdings. 
 photograjihs of the gross specimens have been added wherever feasible, 
 and in all cases photomicrograjihs of the diseased kidneys. The latter, 
 of course, reproduce only a very small area of the tissues e.xamined ; 
 but an attempt has been made to show as much as ])ossible without 
 
 • The results of functional tests li.ivc not hci-n considered, vvilli the exception 
 (jf an occasional reference to the phenolsulphone-plitlialein lest. 'I his has been 
 done, not because their great scientilic interest and practical value is not fully 
 recognized, but because many cases antedated the use of such functional tests, so 
 that the evidence in the few recent cases is hardly sufticieiit to warr.uit any <leduc- 
 tions. .\n attempt to go into this question, in vvhicli all clinical workers at present 
 are deeply interested, would also h.ive i>pened up such a large field for <liscHssion 
 that it seemed wise to refrain from discussing it altogether.
 
 6 Tin-: i'ATii()i.()(;v of nkimiritis 
 
 losing all detail, and lo select for rcjirodiiction as representative ]ilaccs 
 as possible in the sections. The tissues were hardened in ()rth"s mix- 
 ture and stained with haematoxylin-eosin, or according to van Gieson's 
 method. In each case several sections were also stained with W'eigert's 
 stain for elastic fibers, and with Giemsa's stain for bacteria, and in order 
 to bring out the characteristic granulations of the various leucocytes. 
 
 All photographs and photomicrographs are comparable with one 
 another, since all jjhotograi^hs have been taken at about one-half normal 
 size, and all photomicrographs at the same magnification ( ^~ times nat- 
 ural size). 
 
 It is hoped that the cases as represented will s[)eak for themselves. 
 The comments which precede them serve the [)urpose of presenting some 
 of the main facts in a readable manner, and also to draw such conclu- 
 sions from them as may seem warranted. 
 
 The cases, in the opinion of the author, are all cases of true iliffuse 
 glomerulo-nephritis, and represent all such cases that were encountered 
 in a consecutive series of about nine himdred necropsies. They are the 
 same cases which were used in i)rei)aring the author's previous publica- 
 tion in the Journal of the American Medical Association in 1915. where 
 a summary of the findings is given under the headings of acute, subacute, 
 and chronic glomerulo-nephritis. It is unlikely that any case of import- 
 ance escaped detection, because microscopic sections of the kidneys were 
 examined in all nine hundred cases, and in the vast majority of instances 
 personally by the writer. All cases of chronic parenchymatous nephritis 
 with amyloid disease have been excluded, as also all cases in which the 
 renal lesions were evidently of minor im])ortance as compared with co- 
 existing arterial disease. 
 
 For convenience' sake the main data of each case have been gathered 
 in one large table, which is placed at the end of the volume. 
 
 A historical review of the subject is purposely omitted, because to 
 cover this part of the subject adequately would consume much space — 
 unnecessarily, it would seem, because the subject has been dealt with ex- 
 tensively and adequately by other writers. Since the author has pre- 
 viously attempted to present what api)eared to him the main facts in the 
 historical development of the subject, and has attempted to give due 
 credit for previous work, he hopes to escape the imputation that he 
 attempts to assume more credit than is due for his own efforts. In fact, 
 the author specifically disclaims all credit to himself except that which 
 may be due to the careful presentation of a series of case-reports. His 
 comments are merely expressions of his personal opinion, and are based, 
 naturally, not only on his own observations, but upon the splendid work
 
 INIKlllHl TION 7 
 
 done liy luimerdiis invostiiiators rcccntlv and diirinL; llio course of the 
 last century. 
 
 Since in teacliini; it is necessary always to i;o hack to tiie sources of 
 orif.;inal information, a series of com|)lete case-re])orts of one particular 
 disease should be of ^;reat benefit to teacher and student. It would 
 be especially ijratifyinsj to the author if thi> little xohinie should jirove 
 to be useful for teacliin_a; purposes.
 
 THE I'ATIIOI.OCV Ul- NHI'IIKITIS 
 
 I. Acute Glomerulo-Xephritis (Cases 1-4). 
 
 The first two patients were males of over 50 years of age. with old 
 infectious endocarditis of the aortic orifice. According to the histories, 
 and also according to the anatomical findings, the original infection 
 dated back many years ; in the first case, at least eight, and in the second 
 altogether twenty years. The course of the disease in both cases was 
 quite the usual one for chronic endocarditis, and the patients died in one 
 of the exacerbations. 
 
 The nephritis in both cases was terminal and incidental to the main 
 disease. In the first case it revealed itself clinically by \ery definite 
 urinary findings, and by a slowing of the phenolsulphone-phthalein secre- 
 tion. In the second case the urinary changes were very slight — so much 
 so that the condition might very well have been overlooked clinically. 
 
 In both cases diplostreptococci were found in the lesions in the 
 heart valves, and in the first case also in the urine, and in the spleen at 
 necropsy. 
 
 The kidneys in these two cases were not as yet very much swollen : 
 the cortex was somewhat opaque, the seat of petechial haemorrhages. 
 The glomeruli showed the very earliest lesions: hyaline necroses of some 
 of the loops, and a very marked infiltration with neutrophilic leucocytes. 
 In case 2 there was some extra-capillary proliferation in the glomeruli, 
 and a slight infiltration of the adjoining connecti\e tissue with neutro- 
 philic leucocytes. There had been much bleeding irom the diseased 
 glomeruli, and also escape of some leucocytes into the tubules. There 
 were as yet few casts, and the epithelium was nearly unaltered. 
 
 In the case ( i ) in which the bacteria were found in the urine, no 
 bacteria were found in sections of the kidneys either in the glomeruli or 
 in the tubules ; but there were many capillary diplostreptococcic emboli 
 between the tubules, some with beginning suppuration about them. This 
 is one of the cases which so strongly suggest that in glomerulo-nephritis 
 coccus embolism does take place in the glomeruli, but that in these struc- 
 tures the bacteria are rapidly dissolved, in this way causing the hyaline 
 thrombosis and necrosis of the vascular loops. 
 
 It is interesting to note that in both of these cases there were quite 
 a few small foci of old focal nephritis, such as have been described in 
 diplostrei)tococcus endocarditis by previous observers. This was also 
 the case in observation 3. Evidently for many years the kidneys with- 
 stood the effect of continued bacterial embolism fairly well, until in the 
 end they more or less suddenly gave way. It is difficult to say whether
 
 ACl'TK C.I.OMKKri.O-MCI'HUI I l> *) 
 
 this slimilil lie ascrihcd t(i an iiurcaseil vinilfiuc on tlic ))art nf tin- in- 
 fectious organism or to tlie (K\ flopniint of a liyperscnsitivencss in the 
 organ. It appears to nie tliat mi tlie wliolc the last view is the more 
 likely one. 
 
 The third case is remarkable hecause, in spite of tiie fact that an old 
 endocarditis was found at autojjsy, there were no clinical symiitoms to 
 suggest it. The fourth case is one of cirrhosis, with the usual clinical 
 manifestations. In both of these last cases the acute nephritis devcloi)ed 
 in the last three weeks. In case 3 there was a very suggestive history 
 of a sudden breakdown, with characteristic disturbances in urination 
 three weeks before his death. The patient suddenly had to urinate very 
 frequently, and developed oedema. In case 4 there is no such detinile 
 history of the onset, but about a month before her deatii she liccame 
 much worse, this being some time after tl-.e development of se])tic ulcers 
 on her legs, which were probably the cause of her nephritis. The ne])hri- 
 tis in these cases is therefore probably about three to four weeks old. 
 Clinically it showed by the develojiment of oedema. .Some jjuffiness of 
 the face is recorded in case 4. The urine in both cases containeil much 
 albumin, many hyaline and gr.iiuilar casts, and some leucocytes. 
 
 The kidneys were greatly swollen. They were hyiwraemic and 
 oedematous. The cortex was wide, more or less yellowish, and o]ia(|ue. 
 It contained petechial haemorrhages. Histologically there was somewhat 
 more evidence of extracapillary proliferation in the glomeruli: otherwise 
 the lesions were similar to those observed in the earlier cases. Many 
 tubules were filled with blood and with neutrophilic leucocytes. The 
 epithelium was swollen, somewhat granular, and in one case fatty de- 
 generation had occurred. The interstitial tissue in both cases was heavily 
 infiltrated with neutrophilic leucocytes and with lym|)hocytes. In case 4 
 there was already evidence of a beginning jiroliferation of the connective 
 tissue cells. That this proliferation was of inflammatory origin is so 
 evident that it docs not admit of any discussion. In some of the glom- 
 eruli also a beginning organization of the necrotic material had set in. 
 In the one case in which the tissues examined were sufficiently well jire- 
 served for bacteriological examination no bacteria were found, in sjiite 
 of long continued search with the mechanical stage through several 
 sections. 
 
 In all four cases of acute glomerulo-ncphritis the etiology was 
 clearly evident. There was streptococcic infection with bacteriaemia in 
 all, and in three the nephritis occurred in the final stages of an old dijilo- 
 streptococcic endocarditis. The death of these four patients is largely 
 attributable to their ])re-existing disease, and it was for this reason that
 
 10 Till-: rATIlnl.OG'i' OF NICPIIRITIS 
 
 there was an oppDrlunity of stiulsinn' llie alterations in tlie kidneys at 
 this early stage. 
 
 In the very beginning the lesions are practically confined to the 
 glomeruli, the initial change being a hyaline thrombosis of some of 
 the vascular loops, followed by necrosis and an infiltration of tlie entire 
 glomerulus with neutrophilic leucocytes. Naturally in ordinary sections 
 not all affected glomeruli show the necrotic loops, but my impression is 
 that in a series one can always find them in each affected glomerulus. 
 The diseased glomeruli bleed and permit of the passage of albumin and 
 leucocytes — w-hich explains the material found in the ca])sular spaces, in 
 the tubules, and in the urine. Sometimes the exudate has a tendency to 
 spontaneous coagulation in the capsular spaces and in the tubules. 
 
 \'ery soon these glomerular lesions are followed by a general hyper- 
 acmia and oedema which causes considerable enlargement of the organ. 
 Tile oedema often is very pronounced. The hyperaemic blood-vessels 
 show a marked local leucocytosis, numerous venules in the region of 
 the vasa recta being especially engorged and full of various types of 
 leucocytes. The congestion is soon followed by a general extravasation 
 of leucocytes into the tissues, the intensity of the reaction naturally 
 depending on the severity of the process. Among the leucocytes that 
 find their way into the tissues there are many neutrophilic cells, together 
 with lymphocytes and plasma cells, as can easily be seen in sections 
 stained with Giemsa's stain according to Schridde's method. The amount 
 of epithelial degeneration also naturally varies with the intensity of the 
 process. In some of our cases it is noted as slight, in others it is ciuite 
 considerable. There is no question that the disturbance in circulation 
 and the oedema as such must be important factors in the development 
 of these degenerative lesions ; still one can hardly escape recognizing 
 also the importance of a toxic factor. The possible epithelial lesions at 
 this time consist in swelling, with slight granular degeneration, fatty 
 degeneration, and scattered necroses. 
 
 As a result of the inflammatory oedema the connective tissue cells 
 of the interstitial tissue become swollen. After a few weeks, evidences 
 of proliferation may be observed on their part. As has been stated 
 above, of the inflammatory nature of this proliferation there can be no 
 doubt. 
 
 In the glomeruli also proliferative changes occur quite early in the 
 process. The capsular epithelium swells, is partly detached, and pro- 
 liferates somewhat. My impression, however, is that the majority of the 
 new cells in the glomeruli which become so plentiful in the later stages 
 are derived from the connective tissue, both of the capsule and of the
 
 ACL'Ti-; (;i.<i.mi-;kii.(i-ni:i'Mki I IS 11 
 
 stalk of tlie j^lnnuriihis. I'liu prolitcralix i- process in ihc L;loimTiili also 
 is partly <listiiu'tl\ inllamniatory ; in pari, iiowcvcr. it is in the nature of 
 an organization of the necrotic material ])roduced, or (jf ileixisits of filirin 
 which are a|)t to occur in the capsular s])ace. 
 
 Of the origin of the apparently initial hyaline tlironiliosis and necro- 
 sis of some of the vascular Ioojjs of the glomeruli, 1 have sjjoken at 
 length in m\ previous article. Suflfice it to state here that it ap|)ears 
 proliahle to me tiiat it may be due to ra])id lytic destruction c)f bacterial 
 emboli, with liberation of haemolytic and necrotizing endo-toxins. 
 
 The slight lesions in the larger arteries in the kidnevs and else- 
 where wliicii arc noted in the i>n)tocols. are naturally purely incidental. 
 
 I ni.iy state at this ])oint that for brevity's sake in the protocols I 
 ha\e \i^fd tlie terms "arteriosclerosis" and "endarteritis" in the sense of 
 Jores. employing "arteriosclerosis" when there was a notable hy|)erplasia 
 of the elastic elements of the intima. The distinction, however, is meant 
 to be a ])urely morphological one. not implying the deejier --ignificance 
 attributed to it by Jores.
 
 12 Till-; I'ATUOl.OGV 01' NICIMIRITIS 
 
 II. SuiiACUTF, (Ii.omkkulo-N'ki'iikitis (Cases 5-12). 
 
 Naturally, there exists no sharp line of division between the acute, 
 subacute, and chronic cases. Cases 5 and (\ for instance, might just as 
 well have been classified with the acute, and cases 11 and 12 with the 
 chronic types. 
 
 The beginning" and the course of the disease were very cliaracter- 
 istic in case 5. The patient's trouble commenced with an attack of 
 tonsillitis about nine months before she died. Soon symptoms of acute 
 polyarticular rheumatism made their appearance, and continued inter- 
 mittently for about six months. The severe endocarditis, which evidently 
 developed simultaneously, was overlooked until the patient entered the 
 hospital in the last stages of the disease. At that time she already 
 showed evidence of severe renal involvement. It is not apparent from 
 the history when her renal disease started. How far her oedema was as- 
 sociated with her nephritis is difficult to tell : but there are certain symp- 
 toms recorded in the history, like frequent vomiting, restlessness, drow- 
 siness, muscular twitching, which arouse the suspicion of a uraemic 
 condition. Her blood pressure, in spite of the severity of her renal com- 
 plication, was not afifected, possibly on account of the severe sejJtic in- 
 volvement of the heart muscle. Diplo-streptococci were recovered during 
 life from blood and urine, and after death from the infected heart 
 valves. 
 
 The following case (6) is an interesting one on account of the fact 
 that the infection which caused the nephritis was apparently caused by 
 colon bacilli, no evidence of streptococcus infection being discovered 
 either during life or at necropsy. On account of the fact that the child 
 had congenital syphilis, it might be suggested that the lesions in the 
 kidneys also were of syphilitic origin ; but so long as we know so little 
 of the histology of acute and subacute syphilitic nephritis, I believe we 
 would hardly be warranted in making this assumption. In other words, 
 I do not believe that the proof has yet been furnished that spirochetes 
 can produce lesions in the kidneys similar to those observed in ordinary 
 bacterial infections. 
 
 The next case (7) is a good example of how inattentive some patients 
 are to the state of their health. The first symptom that attracted this 
 patient's attention was a hemiplegia and aphasia as a result of embolism 
 from a severe diplostreptococcus endocarditis. The urinary findings 
 were unusually slight for the severe lesions in his kidneys. Except for 
 the general oedema, which of course may be attributed to his cardiac 
 disease, there were no other general symptoms of nephritis.
 
 SUUAITTK f.l.OMKKll.O-NKl'MKITIS 1.^ 
 
 Ill paiicin S. wliu liad an ohj streptococcus infection of a compound 
 iraclure of the lc,n. the urinarv tindings made the diagnosis of nephritis 
 eviilent. I "here was some oedema, but it was not very marked at any 
 time. C)ther "nephritic" symptoms were cnm])lctely absent, in s])ite of 
 \ ery severe lesions in the kidneys. 
 
 In case 9 the renal disease was only a minor incident in tlie typical 
 clinical develo])ment of a severe septic endocarditis, iirobal)ly arisinjj 
 ei,c:ht months before death from infected wounds on the lins^ers. Still, 
 the urinary tindintis were unmistakable and the phenolsulphone-phthalein 
 excrelion was distinctly slowed. Three months before his death the 
 patient liad noticed some oedema at ihe ankles, increased thirst, and in- 
 creased urination. The oedema at no time was a prominent symptom. 
 and was absent at death. 
 
 Case 10 is notewnrthy in several particulars. The patient, a nouul; 
 woman, liad h,id an unusually severe long-continued infection, develop- 
 ing from a decayed tooth about one \ear before her death. .\n abscess 
 e\entiially formed at the lower jaw which had to be drained from the 
 outside. I-'ollowing the operation the abscess healed, and at necropsy 
 a small scar only could be found at the place where it had been. Several 
 decayed teeth, however, remained in her mouth. .After the healing of 
 the abscess she was apparentlx' well until four weeks before her death, 
 when she developed a painless oedema of the legs. Ten days later the 
 right leg. which was still oedematous, became infected with streptococci, 
 from which infection she died within a short time. 
 
 The histological picture of the lesions in tlu- kidneys in this case 
 differs from that of other cases of this series by the lack of evidence of 
 actively progressive inflammation. The alterations were very extensive, 
 but ai)parently not very severe, and almost (|uiescent. .Almost all of the 
 glomeruli were diseased. They showed development of fibrous tissue 
 Iietween the vascular loops, making the tufts thick and heavy. There 
 was also some little proliferation in some of the capsules and in the 
 capsular spaces. Although so many glomeruli were diseased, one did not 
 receive the impression that theymajority were functionally badly dam- 
 aged. The newly formed fibrous tissue was found on the inside of the 
 tufts, and did not therefore apparently interfere much with the secretion 
 of the urine-water: and the vascular looi>s themselves, although some of 
 them showed a slightly thickened hyaline wall, ai)peared otherwise nor- 
 mal. Many tubules were filled with hyaline casts, and some of them 
 with neutrophilic leucocytes. The epithelial degeneration which was 
 jireseiit in the tubules was probably recent, and to be attributed, at least 
 in jiart, to the streptococcus sepsis from which the patient died. The
 
 14 Tin-; I'A'IIKll.UC'i- (IF MJMIKITIS 
 
 arteries were ])raclic:ill\ iKirmal. except the main stems of the renal ar- 
 teries, which were moderately sclerosed. On the whole, therefore, the 
 histological picture would suggest that the process was fairly well healed, 
 at any rate rather (|uiescent. Clinically, however, the evidences of 
 renal disease were well marked. Her first symptom, the oedema, was 
 evidently a "renal" oedema, because there were no signs, either clinical 
 or anatomical, of cardiac decomjjensation. There was also distinct hyper- 
 tension, and a slight but unmistakable hypertrophy of the left ventricle. 
 The urinary findings also were well marked. Although the urinary 
 production was diminished, the specific gravity was fixed at about loio; 
 there was much albumin in the urine, and many formed elements in the 
 sediment. Symptoms of uraemia, however, were altogether absent. 
 
 In the following case ( 1 1 ) we have subacute nephritis in an indi- 
 vidual suffering at the same time from old diplostreptococcic endocardi- 
 tis and syphilitic aortitis with aneurysm. The time when the diplo- 
 streptococcus infection took place cannot any more be established exactly, 
 but the patient complained of heart trouble for at least four years before 
 his death. As shown by a history of extreme polyuria half a year before 
 his end, his nephritis must have dated back before this time. The 
 polyuria in this case was a striking and constant symptom, and possibly 
 accounts for the comparative absence of oedema. His symptoms were 
 largely those of endocarditis, complicated naturally by the co-existing 
 aortic aneurysm. His blood pressure was high and rising. His heart 
 was twice normal size, an enlargement partly due to aortic regurgitation. 
 His urine, on account of the polyuria, naturally had a constant low 
 specific gravity ; it contained much albumin and many formed elements. 
 While he was at the hospital there was practically no excretion of phenol- 
 sulphone-phthalein. The pericarditis which he developed eventually was 
 due to an extension of the dijilostreptococcic infection from the heart 
 valves to the pericardium. 
 
 In the last case ( 12) the nejihritis is evidently much older than in 
 the others of this series. This patient had had numerous attacks of 
 tonsillitis from infancy. Six years before death her nephritis had been 
 first noticed. For the last five years she had had definite "uraemic" 
 symptoms (headache and vomiting), and occasionally slight oedema. 
 The most interesting feature in this patient's history was that she had 
 associated with her nephritis what appeared to be typical symptoms of 
 "Raynaud's disease," attacks of syncope and cyanosis in fingers and toes. 
 Eventually she developed an anaemic ( ?) contracture of her left arm and a 
 dry gangrene of her left foot. This symptom-complex was probably due 
 to a o-radual closing of, her peripheral arteries by lateral thrombosis and 
 endarteritis. I'n fortunately we were not permitted to verify this sup-
 
 SUUAl ITI-: (J.dMl-.Kll.lP-M-.l'IIKIllS 15 
 
 position at aiitoi)s\ ; l>ut uc lia\c I'vidiiut- that Ikt internal arteries, 
 more especially those in the heart and kidneys, were fjraduaily i>eing 
 closed hy such a process. In hotii of these ortjans. as a conse<|nence, 
 small multiple necroses resulted, which in the heart were irrei^ularly 
 scattereil, and in the kidney were situated in the pyramids, liacteria 
 were not found in the small arteries which were the seat of the throm- 
 bosis. Towards the end a similar thrombotic obstruction took ))lace in 
 some of the arteries of the sigmoid flexure, with much bleeding and ex- 
 tensive sloughing. .Ml these processes naturally at first suggested the 
 occurrence of multiple embolism: but no source of embolism was dis- 
 covered in the pulmonary vein, left heart, or the aorta: besides, tlie 
 gradual development of the conditions in the extremities speaks very 
 much against embolism as the causative factor, and favors the idea of 
 their origin by gradual thrombosis. 
 
 The case, 1 believe, is of unusual imixirtance. because it seems to 
 furnish the proof that tin- Literal thrombosis followed by endarteritis, 
 which is so frequently observid in llu- kidneys in these cases of glom- 
 erulo-nephritis (see below), may involve arteries in other parts of the 
 body, and may in this way give rise to symptoms resulting from a more 
 or less gradual obstruction of them. .\"o doubt sometimes the cerebral 
 arteries may be involved in the same way. That this i)atient, in spite of 
 the absence of an infectious endocarditis, suffered from a chronic di])lo- 
 streptococcus bacteriaemia, at least as long as she was under clinical 
 observation, seems evident. She had a septic temperature all the time. 
 Her pulse rate varied between 80 and 130, and the blood culture was 
 positive. In fact, clinically there seemed to be no doubt that the patient 
 had a septic endocarditis, and the absence of this condition at autopsy 
 was a great surprise. In fortunately, a thorough search for another 
 chronic septic focus could not be made. It is possible that in this in- 
 stance the urinary tract itself may have harbored the diplococci, because 
 there was evidence at necro])sy of a slight chronic sujipurative ])yelitis 
 and cystitis with positive finding of diplostreptococci. This, however, 
 may have been merely the conse(|uence of the constant elimination of 
 diplostrejJtococci by way of the kidneys. 
 
 This jjatient's "nephritic" complications were uiuuistakable. .She 
 had headaches and vomiting: she had albuminuric retinitis: she had 
 comparatively little oedema : she had a high blood (iressure with clinical 
 signs of excessive heart action, but without gross hyijcrtrojihy : she died 
 in uraemic coma. The urinary findings also were very well marked. She 
 had some symptoms suggesting jjolyuria. a fixed low si)ecific gravity. 
 The urine contained much albumin, and at times there were large show- 
 ers of casts. Red blood cells were also commonlv found.
 
 16 Till': ^ATll()l,(l(;^ oi' xkimikitis 
 
 To sum u|>: In all these cases of siiliaciitc nephritis, except in case 
 6, there can hardly be any question of the etiology; and in this one I am 
 inclined to believe that the nephritis was due to a colon bacillus septi- 
 caemia arising from the infected urinary tract. In the cases with endo- 
 carditis ( 5, 7, <;. Ill chronic diplostreptococcus septicaemia existed, 
 without doubt ; in case 8 a chronic streptococcus septicaemia from the 
 infected bone is also ver)- likely; and in case 12 the clinical symptoms 
 and the positive blood culture proved the existence of a chronic septi- 
 caemia, at least as long as the patient had been under clinical observation. 
 The source of the continued infection in this case was possibly in the 
 urinary tract. The only somewhat questionable case is case 10, where the 
 original septic infection was present in the region of the jaw, where, 
 however, after long treatment the lesion eventually healed. \o ])ersist- 
 ing septic focus was definitely made out, although she still had several 
 decayed teeth ; and it is possible that the histological evidence of com- 
 parative quiescence of the process in the kidneys might indicate that 
 whatever infection remained was not very active or extensive. 
 
 The clinical symptoms of nephritis were quite definite in all cases. 
 All of them had oedema at one time or another, the amount of oedema 
 and its distribution varying very much in different cases. One early case 
 (S) had somewhat indefinite symptoms of uraemia; otherwise the others 
 were free from it, except the most chronic case, which was much older 
 than the rest, in which there were observed very definite uraemic symp- 
 toms and a well marked retinitis albuminurica. 
 
 Case 8, of about six months' duration, already showed a beginning 
 hypertrophy of the left ventricle ; and the last three cases had a definite 
 rise of systolic blood pressure to between 170-200 mm. mercury, and two 
 of them a noticeable hypertrophy of the left ventricle. In the case (ill 
 with very marked hypertrophy of the heart, the hypertrophy w-as probably 
 largely due to valvular disease. 
 
 The urinary findings were striking in all cases. The urine at all 
 times contained much albumin. Casts ( hyaline, granular and epithelial ) 
 were almost just as constantly present, although sometimes they were not 
 found at all times, but in showers. Leucocytes and erythrocytes, either 
 free or as blood casts, were also commonly encountered. Two cases (9 
 and II) had a definite polyuria, which was extreme in case ir. In the 
 more chronic cases (10, 11, 12) the specific gravity was fixed at a low 
 point, not always apparently as a result of polyuria, the condition being 
 suggestive of a true hyposthenuria. 
 
 In case 9 the phenolsulphone-phthalein excretion was somewhat 
 slowed, in case 11 entirely, suppressed, and in case 12 very much delayed.
 
 si'hai r ii-. i;i.(iMKKii.i)-M;niKiris 17 
 
 III tlu- ^ross, tlu- kidiR'vs were smootli, conj^cstcil, (n.'(leiiiat>piis anil 
 swollen, or already contracted to about normal size. Tiic cortex was 
 either dilTuseJy opac|ue or contained small opaque spots. Petechial cort- 
 ical haemorrhai:jcs were often seen. They were most numerous in case 5 
 (see fig. 7). Histologically, in the more acute cases the tissues were still 
 much infiltrated with neutrojihilic leucocytes, to which were n<iw added 
 many eosinojjhilic and basophilic cells. The glomeruli in most cases 
 showed a very general intense intra- and e.xtra-capillary jiroliferation. In 
 the more chronic cases many of them had already become fibrous. The 
 tubules were full of blood. neutro|)hilic leucocytes, and casts. The 
 amount of degeneration in the epithelium of the tubules varied, being 
 intense in some cases and rather light in luiicrs. without much reference 
 to the severity of the lesions elsewhere. In all cases the interstitial 
 tissue, in addition to being infiltrated with lymphocytes and granular 
 leucocytes, showed evidence of considerai)le fairly diffuse, inflammatory 
 proliferation, which in the later stages had already commenced to en- 
 croach upon the tubides in some places. 
 
 The arteries in the kidneys were normal in cases 5, 6, 7, and 9. In 
 case 8 the slight arterial lesions were evidently purely incidental, which 
 is probablj- also true in case 10; hut in case 11 definite lesions were found 
 in some of the arterioles and larger Itlood-vessels, which must be asso- 
 ciated with the nephritis: and in case 12 the arterial involvement was 
 unusually well marked. The lesions in these last cases seem to extend 
 back from the affected glomeruli into the arterioles, and to consist in 
 lateral hyaline thrombosis, with rapid organization leading to endarter- 
 itis. In the cellular newly-formed connective tissue in the intima there 
 are practically no elastic fibers, as is well shown in fig. 18. In the larger 
 arteries, on the other hand, there is no evidence of such a process ; but 
 there is present a definite hyperplastic thickening of the elastic tissue of 
 the intima. 
 
 The arteriosclerosis found in other parts of the Ijody in cases 8, 11 
 and 12 can almost certainly be looked upon as being unconnected with 
 the renal disease. Cases 10, 11, and 12 demonstrate clearly that the 
 blood pressure rises and remains constantly elevated before there are 
 anatomical signs of general arterial disease. The rise in pressure must 
 be due to some functional disturbance in arteries and heart, which throws 
 out of action the regulatory mechanism which normally maintains tlie 
 blood pressure at such a remarkably constant level. 
 
 The anaemia which was present in all cases is in all probability to 
 be attributed to the chronic sepsis, rather than to the disease of the 
 kidneys.
 
 18 THE PATHOLOGY OF NEPHRITIS 
 
 III. Late Subacute Glomerulo-Nephritis ix Children (Cases 13-15) 
 
 The following three cases are of special interest because they show 
 the effects of continued nephritis on the youthful organism. The patients 
 were children between 6 and 10 years of age. The possibility of arter- 
 iosclerosis complicating the condition can be positively excluded in these 
 cases, and as a matter of fact no general disease of the blood-vessels was 
 observed in any of them. Whatever cardio-vascular disturbances were 
 observed in these instances must therefore be in some way associated 
 with the disease in the kidneys. 
 
 The first of these cases (13) had no history of any acute infections 
 except the milder types of diseases of childhood. The possibility of her 
 having had an attack of tonsillitis, rheumatism or scarlet fever was pos- 
 itively denied on repeated questioning, which is remarkable and shows 
 that the diplostreptococci sometimes enter without provoking severe 
 symptoms, because at necropsy it was discovered that she did suffer from 
 an old diplostreptococcic infection of the aorta. 
 
 Her first symptoms, five months before death, were of a uraemic 
 nature, of that type which gives rise to headaches, vomiting and convul- 
 sions. The convulsions in this patient were not very severe. They were 
 frequently followed by periods of amaurosis, probably due to spasm in 
 the retinal artery. 
 
 In addition to this functional and more or less transitory condition, 
 organic lesions later developed in the fundus of her eyes ; optic neuritis 
 and retinitis, and a detachment of the retina in the left eye. After a 
 while increased thirst and polyuria was noticed. She had remarkably 
 little oedema of the skin (slight puffiness of the face at one time). Her 
 polyuria with low specific gravity continued to the end. Otherwise the 
 urinary changes were not very pronounced ; the urine containing little 
 albumin, few casts, and some leucocytes. Her systolic blood pressure 
 was about 140. The clinical signs were pre-eminently those of a severe 
 sepsis (continued fever and leucocytosis), and the general findings and 
 also the local ones in the region of the heart again suggested strongly 
 endocarditis, as in case 12. Contrary to all expectations, no endocardial 
 lesion was discovered at autopsy, but an infectious aneurysm in the upper 
 part of the abdominal aorta in which there were numerous diplostrepto- 
 cocci, and a severe glomerulo-nephritis with considerable shrinkage of 
 one kidney." The cardiac hypertrophy which had been noticed clinically 
 
 2 The only clinical symptom of the aneurysm had lieen obscure pa 
 upper abdominal region.
 
 I.ATB-: SUBACUTE cr.OMERl'I.O-N'KPIl RITIS IN CIIIIIIKKX 1'' 
 
 and had been ascribed to tlie suspected endocarditis, turned out to be due 
 entirely to the "nepliritic" hypertension. In tliis case the arteries were 
 normal, grossly and microscopically, in kidneys and elsewhere, with the 
 one exception of the arterioles in the spleen. 
 
 Patient 14, a girl of 10 years, had had fre(|uent attacks of tonsillitis. 
 She had a septic temperature on a subnormal base at about 96° I', also 
 continually some leucocytosis ; but the old septic focus, which evidently 
 existed somewhere in her body, was not discovered at autopsy. The 
 first symptoms, which appeared two years before death, were more of a 
 cardiac nature (precordial pain and dyspnoea) ; and in her last attack 
 the symptoms of broken compensation were the prevailing ones. To- 
 wards the end she was very restless and in a semi-comatose condition, 
 probably as a result of true uraemia. Her blood pressure was quite high 
 (160) for a child of her ag3. and the necro])sy revealed marked hyper- 
 trophy of the heart, which was especially well developed on the left side. 
 The urine contained much allmniin and lalher few casts, also a few 
 erythrocytes occasionally. 
 
 The last one of these cases (151 showed a definite localization of the 
 septic focus in the urinary tract. The involvement of the kidneys was 
 not due to ascending infection, but it was in the nature of a true haema- 
 togenous glon-.erulo-nephritis (see fig. 27). Two years before this little 
 boy"s death a large stone was removed from his bladder. .\t that time 
 already infection of his bladder was evident, and this infection with 
 streptococci continued to his end. Cardiac and renal symptoms (poly- 
 uria) developed five months after the oi)eratii)n, and he died in uraemic 
 coma. In this case also the cardiac hypertro|)hy was well marked, more 
 especially on the left side. 
 
 In these three cases of late subacute ne])hritis in ciiildren. then, the 
 cardio-vascular disturbances were very i)rominent clinically, and the 
 cardiac hypertrophy well developed anatomically. Cases like these furn- 
 ish the best proof that the hypertension is closely associated with the dis- 
 ease in the kidneys, but does not necessarily depend upon the extent of 
 destruction of renal tissue. In case 15 the amount of functionating renal 
 tissue left is very small ; still the cardiac hypertro[)hy is quite insignificant 
 in comparison with that observed in case 13, in which the damage to the 
 kidneys is evidently much less extensive. In the growing body of a child 
 the response of the heart muscle by hypertrophy to the increased work 
 seems to be unusually rapid and extreme. That arterial spasm plays some 
 role in the production of the hypertension is strongly suggested in case 
 13, in which the tendency to spasmodic contraction was so well marked 
 in the retinal arterv and was directly observed by means of the ophthal-
 
 20 TllK rATllOI.OCV OK NEPHRITIS 
 
 moscope. 1 1. from the behavior of this one artery, one could arrive at a 
 definite conclusion as to the state of the rest of the small arteries, the 
 evidence would, of course, be more convincing; but unfortunately such 
 is not the case. 
 
 Oedema was observed in two of these three cases, but it was not a 
 prominent feature in any of them. Clinically a certain puffiness of the 
 face was practically all that was noticed. In the last case, at autopsy all 
 tissues were found to be unusually dry. In this connection it is interest- 
 ing that the existence of a polyuria is especially emphasized in the records 
 of cases 13 and 15. In case 14 it had been unfortunately impossible to 
 determine the amount of urine. In cases 13 and 14, however, ascites and 
 hydrothorax developed in the end. 
 
 In case 13 the urinary findings, apart from the polxuria, were un- 
 usually slight. Repeated examinations failed to reveal anything more 
 than a small amount of albumin and occasionally a few hyaline casts. 
 The albumin was much more plentiful in case 14, but here again the 
 number of casts was limited. In case 15 the condition of the urine is 
 unknown. 
 
 "L'raemic" symptoms were present in all three cases. The symptoms 
 of the first patient started with headache and vomiting, and there were 
 imperfectly developed convulsive attacks. Whether she eventually de- 
 veloped true uraemia and coma is unfortunately unknown. That this 
 condition was present in case 14 is very probable from the history, and 
 certain in case 15. 
 
 Whether the changes in the backgrounds of the eye which were ob- 
 served in case 13 can be included in the usual picture of retinitis albumin- 
 urica is doubtful. 
 
 The anaemia which usually accompanies chronic sepsis and nephritis 
 was present in all cases, but to a moderate degree only. 
 
 The kidneys, except for the one large kidney in case 13, were ir- 
 regularly contracted. In cases 13 and 15 they showed large, deep, irreg- 
 ular scars ; in case 14 they were more finely granular. The unusually 
 small size of the one kidney in case 14 is probably partly due to disturb- 
 ances arising from the stenosis of its ureter by a congenital fold. 
 
 The microscopical appearance of the lesions was very much that 
 which has been described in the later cases of subacute nephritis in adults, 
 only that in cases 14 and 15 in places the development of the fibrous 
 tissue was more massive and the atrophy of the tubules in these areas 
 further advanced, as is well shown in figures 25 and 28. The inflam- 
 matory character of the connective tissue proliferation was again very 
 evident in all cases. Many glomeruli were already entirely fibrous, more 
 especially in the older lesions.
 
 I. ATI-: sriiAi r I !■: <.i.(imi.i(i i o-m riii;: ris in i ii ii |)Ui:n Jl 
 
 It was case 15 wliidi first (Jcnioiistratfil to im- the lallacv of tho 
 belief tliat from tlie a|>i)earance of tlie .y;lomeriilar remnant one c<inl<l 
 determine wliether the j^lomernhis was thrown ont of function l)y arter- 
 iosclerosis or whether it was destroyed by u;lomeriilo-nei)hritis. It is true 
 that in the latter case the fibrous remnant is usually badly defined and 
 has lost all semblance to a glomerulus, whereas in arteriosclerosis the 
 vascular tufts merely collapse and are surrounded by a more or less cres- 
 cent-shaped thickened hyaline capsule. If in s^lomerulo-nephritis the 
 lesions are mostly capsular, however, a \ery similar condition to that 
 which occurs in arteriosclerosis may be observed in the end. This may 
 be very puzzling, especially when it is associated with much endarteritis, 
 as in case 15. It is for this reason, I believe, that many cases have been 
 classified as arteriosclerotic ne]>liritis which really belong; to "glomerulo- 
 nephritis. 
 
 The local condition of the arteries again xaried reiiiarkablv in this 
 short series. In case 1.^ tliey were entirely normal. In case 14 the small 
 arteries showed a well marked "endarteritis," and in some of the larger 
 ones the internal elastic membrane was split up into several thick super- 
 imposed layers. gi\ing the typical picture of a hyperplastic develojiment 
 characteristic of true arteriosclerosis according to Jores. In case 15 the 
 lesions in both small and larger arteries were in the nature of a very 
 jiroiiouuced "endarteritis."
 
 THE PATIIor.o(',^■ or NF.niRiTis 
 
 r\'. Chronic Gi.o.mkrulo-Nkphritis (Cases 16-32). 
 
 in order to avoid tedious repetition the cases of tliis last scries will 
 We taken up in a more summary fashion. 
 
 Ever since the disease has been recognized the etiology of these 
 chronic cases has been a most vexing problem. Whereas in the acute 
 and even the subacute cases the history of some septic infection can 
 usually be obtained and a persisting septic focus can often be demon- 
 strated fairly easily, in the chronic cases the history of the original in- 
 fection dates back so far that it often is entirely forgotten by the patient, 
 especially by patients who are more or less indifferent in regard to the 
 state of their health ; and the persisting focus apparently may be so 
 insignificant that an unusually careful clinical examination and even an 
 unusually carefully performed necrojisy may fail to reveal it. In these 
 cases the original infection is probably often due to organisms of a low 
 degree of virulence which provoke very slight symptoms, and the bacteri- 
 aemia also is comparatively slight and intermittent, as one would expect 
 from a comparatively insignificant and hidden focus. 
 
 In searching for the time and character of the original infection the 
 question, how far one is able to communicate with the patient and his 
 family, is of great importance; so that in patients able to speak foreign 
 languages only, especially such languages as Chinese and Japanese, it is 
 often a i)racticaliy hopeless task. Many of these patients arrive at the 
 hospital in a comatose condition, and, unless close relatives or friends are 
 accessible, very little or nothing can be made out about their ante- 
 cedents. 
 
 Among our sixteen cases there were seven (cases 16, 18, 20, 25, 27, 
 29, 32) in which for one reason or another the history is imperfect. Of 
 the other nine patients one (17) had scarlet fever as a child and rheu- 
 matism at twenty years of age. another (19) claimed to have been 
 healthy all his life. He even denied having had any diseases in child- 
 hood, which makes his statements somewhat improbable. Patient 21 
 had had a severe infection, "a touch of typhoid," as she said, at the age 
 of 22, and her symptoms dated from the time she was 23. Patient 22 had 
 had a long continued suppuration of the neck due to chronic tuberculosis, 
 necessitating twelve operations. In such a case the existence and persist- 
 ence of mixed infection with septic organisms is, of course, not at all 
 unlikely. In the history of patient 23 we read of repeated attacks of 
 tonsillitis and several attacks of polyarticular rheumatism. Patient 24 
 also has a history of rheurnatism. In case 26 we encounter once more a
 
 LllRoNK CI.O.MMUfl.o-NI'.niKms 2^ 
 
 general denial oi" all diseases except measles in infancy. In case JS also 
 there is no statement in regard to the original infection. I'aiieTit ,^o had 
 had trec|uent attacks of sore throat, and patient ,^i had had what she 
 called "l,a Grippe" as a girl and an attack of acnte api>eiidicilis nine 
 years before her death. .\ direct relation of the original infection to the 
 following nephritis is traceable only in one case (21 ) ; still the investi- 
 gation shows that in fully six of the nine cases the existence of some in- 
 fection ]5rece<ling the nephritis and iikcl\' to provoke nephritis, coidd be 
 established. 
 
 The mere ])resence of such a history docs not of course |)rove that 
 the nephritis must have been due to such infection. However, in this 
 connection we have to consider that in all acute and subacute cases the 
 relation of such infections to the nephritis is very evident: and there is 
 no reason to assume that the clironic cases of evidently the same disease 
 should be due to a different cause. Considering the difficulties, I believe 
 that the finding of a history of a suspicious infection in six out of nine 
 complete histories is (juite suggestive — all the more so, as in one of these 
 negative cases (28) in spite of the denial of all infection and in the ab- 
 sence of any symptoms observed by the |)atient. a chronic infectious en- 
 docarditis was found at autopsy. 
 
 Definitely persisting sejJtic foci were found in the sixteen cases as 
 follows: old atheromatous ulcers infected with diplococci in case 16; 
 old ]>us |)ockets in the tonsils with considerable scarring in case 20: an 
 old healed scar at the base of the aorta and an old septic infarct of the 
 spleen full of influenza bacilli in the patient (21 I who had had a "touch 
 of typhoid" thirteen years before her death : an old ulcerative endo- 
 carditis in the i)atient (231 w'ho had a history of tonsillitis and rheu- 
 matism: an old ulcerative endocarditis in case 28; an old ulcerative 
 tonsillitis and an ajJiJarently old mild suppurative pyelitis in the patient 
 (31 I who had had the attack of "La Grippe," The long continuance of 
 the rheumatic infection in case 17 is shown by the fact that many years 
 after his original trouble he developed a pleurisy, evidently on a rheimiatic 
 basis, because there was no evidence of tuberculosis found at autojisy. It 
 is also to be noted that during the last years of his life he complaineil for 
 several years of chills in the evening and night sweats. In case 32 there 
 is a history of "malaria." so frequently wrongly diagnose<l in chronic 
 sepsis: and in case 30. with a history of tonsillitis, there is a subse(|tient 
 history of repeated attacks of arthritis, which may. however, have lieen 
 gouty in character. 
 
 .Mtogether of the sixteen cases there are six only which are entirely 
 negative so far as history and autopsy findings are concerned ; and of
 
 24 Till-; I'ATIIOI.OCV OK NKl'HKITIS 
 
 these, four have imperfect histories. One of these ( Hj) had a chronic 
 suppiirative catarrh of the rectum due to diplostreptococcus infection, 
 and a diplostreptococcus sepsis at autopsy. There was no way of de- 
 termining the age of this infection, because the infection of the rectum 
 had not been noticed by the patient, but was accidentally discovered when 
 a routine examinati(«i of the rectum was made after he had entered the 
 hospital. 
 
 No really careful examination of the nose, the accessory sinuses, the 
 roots of the teeth, and other well known foci of chronic septic infection, 
 was made in these cases either clinically or anatomically : and I believe 
 the result should encourage us to search more carefully for such condi- 
 tions. Even under the most favorable circumstances we can hardly hope, 
 in a disease which often lasts twenty years and more, to definitely estab- 
 lish its relation to chronic sepsis in more than a majority of cases. My 
 impression is, that the original infection usually takes place at a compara- 
 tively early age (fifteen to twenty years and longer before death ), and, as 
 is clearly shown in several of the histories, is unfortunately not imme- 
 diately followed by clear symptoms of nephritis, the earliest symptoms 
 (possibly indicating renal disease and consisting of headache and vomit- 
 ing) having been observed about one year after the infection in case 21. 
 Otherwise the damage to the kidneys is not noticed at the time, nor the 
 persistence of the infection in some more or less hidden focus. Whether 
 a careful clinical examination at the time, with urinanalysis, etc., would 
 reveal the seriousness of the condition remains to be seen, but does not 
 seem at all unlikely. 
 
 In such an early discovery of the real seriousness of the situation 
 would consist the only hope of the patient for a permanent cure, by the 
 possible eradication of the septic focus, a general treatment directed 
 towards increased resistance to infection, and a careful symptomatic 
 treatment of the disease of the kidneys. My belief is, that the acute 
 nephritis in scarlet fever is so rarely followed by chronic nephritis, be- 
 cause in the first place the septic infection in scarlet fever is self-limited, 
 and if the patients recover, heals completely; and secondly, because the 
 patients usually are in bed under professional care and the nephritis often 
 is severe enough to be noticed easily, both of these latter circumstances 
 assuring proper treatment. In the more obscure septic infections neither 
 the original disease nor the nephritis which is associated with it may 
 attract sufiicient attention on the part of the patient, or of the physician 
 if the case happens to be brought to the attention of a professional man. 
 
 The time at which the first definite "renal" symptoms make their 
 appearance varies very much. In case 21 they seem to have followed the
 
 ClIKONIC C.l.dMllKli.o-Mll'llKI'llS J> 
 
 original inui.li(in within tin- year, hut iiMially ten years or nmrc sccni to 
 ilai)se hctort tlu'y become at all prominent. The patients most commonly 
 noticed them from two to five years before death : but in some, in which 
 tiie disease, from the ajjpearance of the kidneys, must have e.\iste<l for 
 many years, the complaints of the patients did not commence until four 
 to live months before their end (see cases 28 and 29). 
 
 In practically all of our cases the history, when complete enouj,di, 
 contains quite definite evidence of renal disease, with the one exception 
 of case 30, in which there is a fairly typical history of gout, but other- 
 wi-ic nothing suggesti\e of disease of the kidneys except the one com- 
 plaint that he had to urinate frequently and had to get up several times 
 at night. Curiously enough in this case the urinary findings also were 
 very slight: both in si)ite of the fact that the lesions in the kidneys in 
 the gross and histologically were unusually severe ( see fig. 59 ) . 
 
 There is another case ( 22 ) in which the only symptom for the last 
 three years before death was occasional nycturia.^ .\ rather common 
 initial symyitom was oedema, which in several cases commenced in the 
 face, but not so rarel\ at the ankles. The time of onset of this initial 
 symptom \aried greatly. 
 
 In case 16 oedema of the face and legs developed three years before 
 death, and since then recurred at intervals. Similarly in case 17 oedema 
 and dyspnoea made their appearance two and one-half years before the 
 end. Facial oedema was not observed until considerably later. In 
 [)atient 20 the first symptoms manifested themselves four years before he 
 died, and consisted of general oedema and ascites. In this case the 
 oedema disa])peared comjiletely, to return slightly for a short time two 
 months before death. .Ml that was left eventually was some puffiness 
 about the eyes. In case 22, as stated before, the only symptom for several 
 years was occasional nycturia. It was only ciuite late in the disease that 
 he developed marked oedema of the lower extremities, with very marked 
 dysjjuoea and cyanosis. Case 24 started in with dyspnoea and increasing 
 weakness two years before his death. The dyspnoea again was a prom- 
 inent feature in his last attack in which some facial oedema was ob- 
 served ; but there was no other oedema at any time. Patient 26 became 
 dropsical as early as five years before his death, and had another similar 
 attack four years later. In addition he complained of dyspnoea, palpita- 
 tion of the heart, jjrecordial pain, headache and jjains in the legs. Patient 
 2<) had noticed puffiness of the face, swollen legs, shortness of breath, 
 l)alpitation of the heart, and precordial |)ain for about four to five months. 
 
 •■' Tlic word "nycluria" in this paper i.s used as meaning iiriii.iiinn at iiIkIu, 
 and is not meant to refer t<) involuntary urination.
 
 26 Tlli'. l'.\Til()l,(K;V OF NEPHRITIS 
 
 There is no history of a previous attack, hut the data are incomplete. In 
 case 31 the exact nature of the renal symptoms which were first observed 
 when she was pregnant five years before death is not stated; but in her 
 subsequent history oedema is not a very prominent symptom. 
 
 In six cases, then, oedema was an early and prominent symptom. 
 
 Dyspnoea, as may be seen from the above, was often noticed very 
 early, and this symptom frequently was very severe, out of all proportion 
 to any disturbance in circulation that might have been present. In case 
 28 it was an early and apparently the most prominent clinical symptom, 
 not associated with oedema or any more definite "uraemic" manifestation. 
 It is not at all improbable that the attacks of "asthma" in case 19 which 
 preceded the end by four years were of this nature. In this patient it 
 was years later that oedema first developed, and he died, similarly to case 
 28, in extreme dyspnoea. 
 
 Palpitations of the heart were quite frequently complained of, and 
 in a few instances there was quite a little precordial distress, sometimes 
 suggesting angina pectoris. The patient in whom this symptom was most 
 prominent (17) had an unusually well marked general arteriosclerosis. 
 The right coronary artery was almost closed at one point, but there were 
 no scars in the heart muscle. In case 26, with similar symptoms, the 
 necropsy also revealed marked arteriosclerosis of the coronary arteries. 
 In cases 21 and 29, however, in which anginoid attacks were complained 
 of, there were no lesions in the coronary arteries or in the heart muscle, 
 and merely a few small yellow spots in the base of the aorta. (Jn the 
 other hand, in case 18, in which there were small scars in the musculature 
 of the left ventricle, no local symptoms were complained of. Patient 
 24, in whom the heart muscle was similarly atiected, also did not com- 
 plain of any subjective symptoms in the region of the heart, but clinical 
 examination revealed an absolute arythmia. ( It may be stated that the 
 heart muscle, like all other important organs, was examined microscopic- 
 ally in all cases. ) 
 
 In a certain number of cases "uraemic" symptoms occurred early 
 and often dominated the clinical picture. In the early stages the con- 
 vulsive form of uraemia, characterized by headache, vomiting,, and, in 
 extreme cases, convulsions, was usually encountered. Towards the end 
 the symptoms of true uraemia made their appearance, often terminating 
 in coma."" In case 17, for instance, the first symptoms two years before 
 death were headache, dizziness, loss of memory, failing eyesight, short- 
 ness of breath, progressive weakness, and frequent urination. This man 
 
 * A discussion of the different forms of uraemia cannot here be attempted, 
 and the reader is referred to the voluminous literature on this subject.
 
 ciiRoMi- (■.i.umi:ki'i.(i-.\i:i'iihi IIS 27 
 
 ni'Vi-r li;ul any dfiicma. i'xcc])l slijjlu i)iirtiiK'ss of tlu' cvditls. lie liad ;i 
 retinitis alhuminnrica. iiraemic convulsions, and died in coma. TIk- 
 symi>toiTis of patient 21 started thirteen years before her death with in- 
 tense headache and vomitintj. She liad much oedema at times, and 
 eventually develo|)ed symptoms of true uraemia. In case 23 the uraemic 
 convulsions were cvidentlv mistaken for ei)ik"])sy. When he came to the 
 hos]ntal. he comi>laineti of shortness of l)reath, increasing dimness of 
 vision, cramps in the legs, and deep jiains in the liones. He never had any 
 oedema, and died in uraemic coma. 
 
 In other cases again the uraemic symptoms were a late develojiment. 
 as in patient 20, who first had considerable oedema. Later the oedema 
 was much less marked, but he had intense headaches with vomiting. l)e- 
 came severely dyspnoeic, was intensely hyi)ersensitive all over his body, 
 esjiecially to deep pressure, and died in an attack of excessive dyspnoea. 
 The patient (22) in whom frequent urination, especially at night, was 
 the only symptom for several years, eventually develo])ed an intense 
 dyspnoea, had some oedema, and died in uraemic coma. In patient 31 
 the exact symptoms of her earlier attacks are unfortunately unknown. 
 One year before death she noticed anorexia and vomiting. Later she had 
 some attacks of violent delirium, associated w-ith complete unconscious- 
 ness. For the last seven months she had headache, much vomiting, jerk- 
 ings and cramps in legs, progressive amaurosis, and at times oedema of 
 the feet. Ophthalmological examination showed the typical picture of an 
 albuminuric retinitis. Tlie sxinjitoms of true uraemia contiiuied to her 
 death. 
 
 Retinitis albuminurica was observed in the above mentioned two cases 
 only. In case 23, in spite of the failing vision, the backgrounds were 
 normal. The retinal arteries were slightly tortuous, and the disturbance 
 may have been due to this patient's severe anaemia, associated with arter- 
 ial spasm. 
 
 .\11 iiaticnts. with few exce[)tions. suffered from severe anaemia. 
 .\bout half the normal number of erythrocytes, or less, and a correspond- 
 ing decrease in haemoglobin, was observed in cases 17. 19. 20, 23. 24, 28, 
 29, 30, 31. In several of these cases there was a marked anisocytosis. 
 Associated with the anaemia there was frec|uently observed a tendency to 
 bleeding in skin and mucous membranes, assuming at time-; the severity 
 of a haemorrhagic diathesis. 
 
 The temperature was either normal or often subnormal, with oc- 
 casional rises to 99- or 99.5° F. The pulse rate was either normal, or as 
 in case 29 rather slow (between 60 and 80). but in c|uite a number of 
 cases it varied considerablv, and occasionallv rose to icxj or e\en 120.
 
 28 rill-. :• A rii()i.()i;N- oi- xia-iiKiTis 
 
 I'licsc (listiirbanccs in pulse and temperature are ])r()lial)ly due to tlie 
 associated septic conditions, it is of some interest that in case 21. in 
 which an old septic infarct iieavily infected with influenza bacilli was 
 found in the spleen, the temjjerature was normal, hut the pulse rate 
 varied a f^reat deal and sometimes rose to 120. 
 
 in practically all, hut more especially in the uraemic cases, the tonjjue 
 in I lie last sta5.!;es of the disease was heavily coated and the breath was 
 loul. In some of them a severe pseudomembranous and ulcerative stoma- 
 titis developed eventually, which in case 16 was mistaken for ili])htheria, 
 because it started in the ref^jion of the tonsils and gave rise to the forma- 
 tion of greyish membranes. The lesions usually, however, are much more 
 widely distributed than those of diphtheria, involving gums, palate, inner 
 surface of cheeks, lower surface of tongue and floor of mouth, etc. The 
 base of these su])erficial idcerations is either exposed and then greyish 
 while, due to the necrosis of the tissues; or it is covered with thick 
 brownish crusts. The condition is so characteristic that one might speak 
 of it as a "stomatitis iii'.ii'mica." These lesions are usually directly due 
 to streptococcus infcclioii of the weakened tissues. 
 
 In the majority of the chronic cases the systolic blood pressure was 
 distinctly elevated, varying from i(m to 250. I'levations to 200 and more 
 were present in five cases ( 17, iiS, 22, 23, 2()|. As the cases are arranged 
 somewhat according to the .severity of the lesions in the kidneys, it is 
 evident from the figiu-es that the amount of destruction of kidney tissue 
 in itsilf docs not control this ])henomenon. In fact, there are more cases 
 with low pressures and small hearts among the cases with the most ex- 
 tensive destruction of renal tissue than among those with less destruction. 
 The patients with unusually high pressures were all rather strongly built 
 males between 45 and 35. Three of them had a marked general arter- 
 iosclerosis, one had fairly normal, and the last one entirely normal arteries. 
 ( )n the other hand some of the cases with the most marked and extensive 
 general arteriosclerosis had low |)ressnres and small hearts. One gets 
 the impression, thereffire, that the pressure is forced up more energetic- 
 ally in comjiaratively vigorous individuals, when the disease develops 
 com])aratively ra|)idly and leads to death before extreme changes have 
 taken i)lace in the kidneys. 
 
 The cardiac liypertroi)hy is evidently caused by the hypertension, but 
 it is b\ no means pro])ortionate to it. The largest heart (24) was found 
 
 in an in(li\i(lnal with .1 bl 1 pressure of 170, which on rest in bed came 
 
 down to I 55. ( )n the whole, the hypertro[>hy of the heart remains within 
 moderate limits, varying; from one and one-fourth to one and one-half 
 times normal size in bulk. The hypertrophy is primarily a concentric
 
 ciiKo.vit (if.oMicKii.o-Minikri IS 29 
 
 hy|)iTtr()|ihy of the left ventricle (see for instance cases i'» and 10 I. foi- 
 lowcfl by its dilatation and later sometimes l)y involvement of the rijjfht 
 heart; but the cases showing mnch dilatation on the rij^ht side and 
 marked cyanotic atrojihy of the liver, as a sij^n of chronic passive con- 
 jjfestion in the perijjheral veins, arc c|uitc small in number (see cases 19, 
 2(), 2-j ) . 
 
 Cases with low pressure^ and normal, or even small, hearts arc I)y 
 no means rare, cs|)ccially in very chronic cases with extreme contraction 
 of the kidneys ( see cases 25, 28, 29 and 2^2 ). 
 
 The relation of chronic nephritis to g'out is af:(ain brought out jirom- 
 iTiently by our series of cases. f)nly one of them (30) had a definite 
 clinical history of gouty arthritis, but gouty lesions in kidneys and else- 
 where were encountered in five cases (24, 26, 27, 29, 30), without a sys- 
 tematic search in every instance. It is reasonable to assume, therefore, 
 that actually the incidence was greater than is indicated in our records. 
 It appears especially to occur in the very chronic cases with extreme kid- 
 ney lesions (second half of this series). The recent observations of 
 Denis '' that in healthy individuals an excess of purins is rapidly excreted, 
 leaving the uric acid percentage in the blood undisturbed, whereas re- 
 tention follows early in cases with renal insufficiency, may furnish some 
 clue to the frequency of this association. 
 
 The death of the patients was either the result of terminal infection, 
 usually broncho-pneumonia (cases 16, 23, 24, 25, 27, 28, 29. 30 ), or of 
 true uraemia ( 17, 18, 19, 20, 21, 22, 26, 27, 28, 31 ). In the latter case 
 the patients often develofied uraemic coma, but some showed no disturb- 
 ance of consciousness, merely excessive dyspnoea ( 19, 20, 28). 
 
 As may be seen from the table of summary of the cases, the urinary 
 findings were fairly constant in all cases. Polyuria was a very jirominenl 
 symptom, occurring at one time or another in seven out of the thirteen 
 cases in which anything definite is known of the urine. This was com- 
 monly associated with frecpient urination at night (nycturia). The 
 amount of urine was definitely increased in about one-half of the cases. 
 \n three the quantity is designated as decreased. The sjjccific gravity was 
 generally low (loio and less). The lowest specific gravity (1002) was 
 found in the most acute case (16) of this scries. The specific gravity 
 was low, not only in the cases with polyuria, but also in some of those 
 with a decreased amount of urine, suggesting hy()Osthenuria (Schlayer). 
 ■~ec cases 22, 23 and 24. ) 
 
 With few exceptions ( 19, 29, 30 ), the urine contained much albumin 
 
 ^ Denis, "The K(Tect of itiKcstcd Piiriiis on the L'ric .Arid Conlc-nl of the 
 IJIood." Jour, nf Biol. Chcm.. IQI5, NXIH, 147.
 
 30 THE I'ATIUM.DCV OF NEI'IIKITIS 
 
 I at least a heavy cloud). The allnimimiria was moderate in cases 19 and 
 29. In case 30 no albumin was found, but the patient was at the hospital 
 for a short time and there is record of one examination only. 
 
 The finding of casts was not so constant. There were several cases 
 in which no casts were found, but repeated examination usually revealed 
 showers of casts once in a while. Frequent examinations of the urinary 
 sediment are therefore of great importance. Leucocytes and erythro- 
 cytes were discovered only occasionally. The difficulty of finding formed 
 elements in the urine at times is rather astonishing, because in sections 
 of these kidneys casts are always fairly numerous, and frequently quite 
 a few tubules are filled with blood or leucocytes (see protocols of indi- 
 vidual cases). It may be that in these later stages the contents of the 
 tubules are washed out less easily and are carried down only when there 
 is a more or less sudden flood of urine. 
 
 The phenolsulphone-phthalein test was employed in a few cases only, 
 many of them dating back before its introduction. In every instance the 
 excretion was distinctly slowed. In case 26 there was no excretion in 
 three trials. 
 
 The gross appearances of the kidneys varied considerably, except 
 that they all showed evidences of contraction. The capsule was more or 
 less thickened and adherent. The surface of the kidneys was either 
 smooth or granular, or full of large irregular scars, more or less lobu- 
 lated, according to the distribution of the newly formed connective tissue.** 
 The color was frequently mottled, purple and grey, or in other cases dark 
 red, in others again quite pale. In quite a few cases one could make out 
 small petechial haemorrhages. The number of them varied from a few 
 to a great many. In some instances the color of the organ was distinctly 
 brown on account of an abundant deposit of haematogenous pigment in 
 the epithelium. On the cut surface the cortex naturally appeared more or 
 less contracted, and on account of the great structural alterations the 
 normal markings of the cortex had disappeared to a great extent. If 
 there was much epithelial degeneration, opaque, frequent yellowish spots 
 were seen scattered through the cortex. The arteries on the cut surface 
 varied greatly. In some cases they were distinctly thickened, in others 
 they were entirely normal. The same is true of the main stems of the 
 renal arteries. 
 
 Histologically the connecting link of all cases was the inflammatory 
 lesions in the glomeruli and the inflammatory proliferation and eventual 
 fibrosis of the connective tissue. The great variety of lesions encountered 
 
 " The differences are well shown in the photographs acconipanyiii.n the inili 
 vidiial cases. Thev are all taken at nearly one-half norm.al size.
 
 riiud.vu (;i.()Mi:i<i:.(i-.\i;i'iii<i IIS 31 
 
 is well ilhislral(.'(l in tin- iiiiotumiiru^raiihs. Slill ihcy all show llit same 
 pattern. The intlaminatory character of these lesions is naturally most 
 evident in the more acute cases, but even in the very old cases typical 
 subacute lesions may be encountered in some of the t^lomcruli (sec 
 photomicrot;Tai)h of case 31 ) and in certain jiarts of the interstitial tis- 
 sue. Eventually most of the glomeruli become shrunken and fibrous. 
 The newly formed connective tissue also becomes more and more fibrous 
 and the neutrophilic leucocytes disappear from il. Inil cosin<)|)iiiIes and 
 "Mastzellen" persist for a lonaf time. 
 
 The extent of the epithelial defeneration varietl very much. In 
 some cases sjranular and fatty defeneration was \ery well marked, in 
 others there was hardly any evidence of it. 1 cannot say that it apjieared 
 as if the cases with much epithelial degeneration were more likely to 
 develop oedema, as has been suggested. It is to be considered that the 
 relation of the oedema to the epithelial degeneration may be the opposite 
 from that which is usually assumed. If there is general oedema at 
 the time of death involving the kidneys, tiie existence of this oedema in 
 the kidneys may very well favor the (level(j|)ment of degenerative changes 
 in the epithelium. 
 
 Eventually the majority of the tulmlcs collai^se, and the amount of 
 tissue destruction may continue to an astonishing degree before death 
 ensues. In those cases in which the glomerular involvement and the 
 connective tissue develoj^ment are of a i)atchy character the remaining 
 comparatively normal glomeruli and tubules often show evidences of 
 compensatory hypertrophy. These latter conditions, however, do not 
 seem to have much effect on the clinical picture. The developnunt of 
 numerous small cysts is quite common in the later stages. 
 
 Macteria w-ere found in the tissues in one early case only (case i')). 
 It w-as the most acute case of this series, a case in wliich there existed an 
 infection of old atheromatous ulcers with diplostreptococci. The diplo- 
 streptococci were found in many caf)illarics. and a few outside in the 
 inflamed connective tissue. < )nce more, no bacteria were discovered in 
 the diseased glomeruli. 
 
 This same case had acute and very marked lesions in the arterioles, 
 consisting of hyaline thrombosis which in some ])laces filled the arterioles 
 com])letely, in others formed a thick layer on the inner surface partly 
 above, i>artly below the endothelium. In other small arteries these hyaline 
 masses had been partly or com])letely organized, giving rise eventually 
 to the ]jicturc of a cellular endarteritis. In what appeared as the later 
 stages of the same |)rocess much elastic tissue had developed in tlu- 
 thickened intima, in such a way that eventually an appearance was pro-
 
 32 •ini'. i'ATiiiiL(i(,\ I)]- Mcniunis 
 
 duccd resc-mMiny tliat (Joscrihcd b\- Jores as characteristic of tlie "func- 
 tional" hyperplasia of the intima in arteriosclerosis. 
 
 In case i8 the thrombotic obstruction of some of the arterioles had 
 given rise to the formation of many microsco])ic anaemic necroses. Both 
 the small and the lartjcr arteries showed a ver\- marked thickening of 
 the intima. ]iartly with liypcrjilastic development of the elastic tissue, 
 partly without. Similarl\- the two [jrocesses were mi.xed in case 17. 
 In case 20 the arterial changes seem to be old, l>oth in arterioles and in 
 the larger arteries, and we find much elastic tissue in both places. In 
 case 22 some small arteries show "endarteritis," others "arteriosclerosis." 
 In this and many other specimens (see individual records) one finds all 
 transitional stages between these two conditions. 
 
 In a general way one may state that the arterioles in the kidney are 
 aiifected in all cases, but that even in the oldest and most severe cases, like 
 cases 31 and 32, the larger arteries in the kidneys and elsewhere may 
 show very little evidence of disease. 
 
 It appears therefore ill advised to indulge in too much speculation in 
 regard to the etiology of the process in the arteries from the histological 
 appearance of the lesions, and I believe that until further proof to the 
 contrar}' is forthcoming we are justified in assuming that the changes in 
 the arteries in these diseased kidneys are of an inflammatory nature, just 
 as the rest of the lesions. This interpretation would harmonize very well 
 with the observation that in the small arteries at least the proliferation of 
 the intima is frequently preceded by lateral thrombosis, bearing in mind 
 the fact that inflammation of the arterial wall necessarily would favor 
 thrombosis. 
 
 In conclusion I ma}- be permitted to add a few general statements. 
 It may seem as if this were hardly warranted on account of the small 
 number of cases studied: and there certainly would be justification for 
 criticism, if an attempt were made to elaborate a complete pathology and 
 symptomatology of chronic nephritis on such a slender basis. On this 
 account all preceding statements have been worded so as to refer to the 
 individual cases only. But, on the other hand, a few thoroughly studied 
 cases may give .some food for general reflection. 
 
 If these cases teach anything, they certainly bring out very clearly 
 the loose association which e.xists between the condition in the kidneys 
 and a number of other phenomena which have usually been rather loosely 
 described as "nephritic." Terms like "nephritic" oedema or "nephritic" 
 hvpertension cannot fail to give the impression that the oedema or the
 
 COXCl.L'SIONS Jj 
 
 liy]iertensioii i1c])cik1 directly dm the coiiditioii of tlie kidneys. Tn my 
 mind nothing could be further from the truth. These conditions are fre- 
 Cjuenliy associated with nephritis, but the kidneys themselves plav no 
 demonstrable role in their origin. 
 
 This will be perhaps more easily conceded in case of the oedema. All 
 attempts at explaining the oedema on the basis of the disease in the 
 kidneys have failed, and as a matter of fact a cursory study of these 
 thirty-two cases will show that there is no one element in the pathology 
 of the kidneys with which the oedema could be connected. Practically 
 the same lesions may be observed in the kidneys of patients which were 
 "water-logged" long and often, and in jjatients who had oedema rarely 
 or not at all. One may object that the anatomical picture of the kidney 
 does not give a true rejiresentation of its functional capacity, and that 
 functional tests show that certain functional derangements of the kidney 
 are apt to be associated with oedema. I very much hesitate to express 
 an opinion on this latter point on account of lack of ex])erience and 
 knowledge: but this much is certain, that in these functional studies it is 
 often difficult to determine what is cause and effect ; and there is cer- 
 tainly no unanimity of opinion among those most competent to judge in 
 questions of this character. But a])art from all such controversies, how 
 much easier of solution does the whole question become if we give up 
 this idea and state the relation somewhat in the following manner : 
 The agency which produces the nephritis (certain bacterial toxins), in 
 addition to injuring the capillaries in the kidneys also injures them else- 
 where, and this produces the oedema. 
 
 \\'e need only to think of the word "intlammation" to realize that 
 this is possible, because the most striking effect of bacterial toxins in 
 the tissues is injury to the capillaries. Of diffuse injury to the renal 
 capillaries (besides the characteristic lesions in the glomeruli), we have 
 ample evidence in the acute and subacute cases of the disease. The 
 oedematous swelling of the kidneys is often extreme, and the extent and 
 imjjortance of this oedema seems to have hardly sufficiently impressed 
 itself upon anatomists and clinicians. If this is the true relation of 
 things, we can understand much more easily why the relation of the 
 nejjhritis to the oedema should be so varying. In a certain case the 
 kidneys may be damaged very severely, but the capillaries in it or else- 
 where much less so; and vice versa. Given damaged capillaries, the 
 factors which damage them additionally or which in other ways favor 
 the development of oedema may naturally provoke to manifestation a 
 condition which may be more or less latent, or aggravate an oedema 
 that is already plainly in existence. The damage being general, the
 
 34 THE PATHOLUliV OF NEPIIKITIS 
 
 capillaries in the delicate structure of the eye-lids may show the damage 
 first ; whereas in other cases the oedema may first show in places where 
 the circidation is relatively poor, as in the region of the ankles. 
 
 It appears to me that an assumption like the one made above clears 
 away innumerable difficulties, and at the same time permits the utilization 
 of all the important data which have gradually accumulated as a result 
 of patient clinical investigation. I should suggest, therefore, that the 
 term "nephritic oedema" should be replaced by "'oedema in nephritis." 
 
 The same way with "nephritic" hypertension. Here also the loose- 
 ness of the interrelation of this phenomenon to the disease of the kidneys 
 is so evident that it does not need special emphasis ; in fact, this lack 
 of correlation has been the despair of all those who have attempted its 
 e.xplanation scientifically. It appears a little more hazardous to ascribe 
 these differences also to differences in the action of the causative agent 
 which provokes the nephritis. It is not known of bacterial toxins that 
 they affect the tonus of the arterioles, and yet, whatever causes the hy- 
 pertension must affect them. The condition of the large arteries is im- 
 material. An increased activity of the heart would be easily compensated 
 for by the vasomotor regulatory mechanism ; but when the tonus of the 
 arterioles is increased the vasomotor regulation breaks down, as we 
 know in the case of adrenalin and pituitrin hypertension, probably be- 
 cause the mechanism works by means of the arterioles and has little reflex 
 control over the heart action. If it could be shown that substances pro- 
 duced by bacteria directly or indirectly had a pressor action, then all 
 difficulties would disappear, as in the similar case of the oedema. Then 
 one would be able to understand why we should have sometimes early 
 and extreme hypertension, at other times none at all. If we make the 
 further assumption that these or similar substances soinctiincs do not only 
 stimulate the arterial wall to contraction, but also injure it, we would come 
 much nearer to the solution of the "arteriosclerosis" problem : in fact it 
 might lead us to an entirely new conception of the etiology of arterio- 
 sclerosis and its puzzling relation to hypertension and nephritis, because 
 after all is said and done arteriosclerosis and arteriosclerotic hyperten- 
 sion have some intimate relation to nephritis, but certainly not the one 
 usually thought of, namely, that the nephritis is the primary factor. .\n 
 assumption like the one mentioned above is naturally still altogether spec- 
 ulative, and it will take much work to get close enough to these important 
 problems to make positive statements ; but, whatever the relation is, 1 
 believe it may be positively asserted that nephritis and hypertension are 
 not related to one another as cause and effect. 
 
 Clinicians have alreadv recognized that certain forms of uraemia
 
 arc not iliie lo the injury to kidney tissue, luit to other factors. The 
 convulsive form of uraemia is, for instance, ahtiost certainly ihie to dis- 
 turbances in the cranial cavity, tiie exact nature of which is still far from 
 beint;- recognized: and similarly it may be with other forms of this 
 protean symi)tom-com|ilcx. The onlv condition in which we have good 
 reason to believe that it is directly the consequence of ilestruclion of 
 kidney tissue is what clinicians now usually speak of as "true" uraemia; 
 and in this condition the evidence that it is due to an inefficiency on the 
 part of the kidneys to excrete some as yet tuiknown substance or sub- 
 stances has been accumulating rapidly in the last years. 
 
 In regard to the changes in the cuiiif'osiliun of the urine and its 
 sediment I wish to emphasize once more, as has been done often enough 
 before, that the condition of the urine is a fairly accurate measure of 
 the severity of the disease in the kidneys at a given time, and no measure 
 at all of the extent of the damage to the renal tissue. Polyuria and 
 hyi)osthenuria more particularly point to serious involvement of much 
 kidney tissue, although of course other possible factors have to be taken 
 into account. The records also bring out clearly that frequent careful 
 urinanalyses arc of great importance in the clinical recogniticju ol the 
 disease. 
 
 It is impossil)le to condense the result of these observations into a 
 few phrases, but our main conclusions might be formulated as follows : 
 
 1. Diffuse glomerulo-nephrilis is a disease which may occur in acute, 
 subacute, or chronic form. 
 
 2. The etiology of the acute and subacute forms is evidently to be 
 found in bacterial infection, and this is quite probably true of the chronic 
 form. 
 
 3. The bacteria concerned are commonly, but not necessarily, mem- 
 bers of the streptococcus family. 
 
 4. It is probable that the continuance of the disease in the kidneys 
 is due to the continuance of the infection in some often more or less 
 hidden focus. 
 
 5. It is suggested that one should look upon the oedema, the hyi)er- 
 tension, the arteriosclerosis, and certain uraemic manifestations merely 
 as being frequently associated with nephritis, rather than as being directly 
 dependent upon it. 
 
 6. It is quite conceivable that these manifestations are the result of 
 the fortuitous action upon other tissues of the same cause which injures 
 the kidneys.
 
 36 THE l'ATHOLOi;V OF NKI'HRITIS 
 
 RECORD OF CASES 
 
 Case I. Old focal and acute diffuse glomerulo-nephritis in man of 52 
 
 years, with chronic diplostreptococcic endocarditis. 
 
 X\ II, 60. — J. K., strongh- built, emaciated American engineer, 52 years 
 old. 
 
 The patient had had occasional attacks of sore throat. His tirst 
 definite S3mptoms were observed eight years before death, when he de- 
 veloped palpitations with dyspnoea. A similar attack with chills and 
 fever was observed three years later. Eight months before death he had 
 oedema of the legs. His last attack began four months before his death 
 with abdominal cramps, diarrhoea, dyspnoea, and expectoration. During 
 this last attack he ran an irregular septic temperature. Clinically he 
 showed evidences of aortic regurgitation. There was marked oedema of 
 the legs and later of the trunk, and symptoms of hydrothorax. Towards 
 the end oedema and hydrothorax disappeared. He had a slight anaemia 
 (4,000,000 reds; Hb. 60%), no leucocytosis (3-10,000). He had a posi- 
 tive Wassermann reaction, although he denied lues and nothing sugges- 
 tive of syphilis was found at autopsy. Two blood cultures were nega- 
 tive. Diplostreptococci were found in the urine. The urine showed a 
 heavy cloud of albumin, many hxaline and granular casts. It was first 
 decreased in amount, later increased with the disappearance of the 
 oedema. The phenolsulphone-phthalein secretion was slowed ( iS7o ^'^^ 
 hour, 15% the 2d). 
 
 Necropsy revealed an old, aortic diplostreptococcic endocarditis 
 with regurgitation, and a large spleen with numerous large areas of 
 haemorrhagic softening which were full of streptococci. There was a 
 slight general arteriosclerosis. 
 
 The kidneys were slightly swollen (12 x 6 x 3 cm.) and smooth. 
 The cortex was fairly wide, opaque, and showed a moderate luimber of 
 haemorrhagic spots. There was a small anaemic infarction in the right 
 kidney. 
 
 Sections showed few fibrous glomeruli with areas of cellular in- 
 filtration and moderate thickening of the connective tissue about them ; 
 few neutrophilic and eosinophilic leucocytes in these areas of cellular 
 infiltration ; infiltration of most glomeruli with neutrophilic leucocytes ; 
 recent hvaline necrosis of loops in a fair number : no extra-capillary
 
 I'lK- I. 

 
 38 
 
 ■iin-: i'.\'iii(>i.n(,\- i)\- xicpHRiTis 
 
 proliferation: very marked liyperaemia : few haemorrhages ; few casts; 
 little epithelial degeneration ; beginning "arteriosclerosis" of some small 
 arteries. Many small vessels \yere fillerl with coccus-emboli. The tissue 
 ahmil some of these was necrotic and showed beginning suppuration. 
 No cocci were found in am of the diseased glomeruli. 
 
 Case 2. Old focal and acute diffuse glomerulo-nephritis in man of 54 
 
 years, following recrudescence of chronic diplostreptococcic 
 
 endocarditis. 
 
 X\ II, 31. — J. N., American kitchen-heliier, 54 years of agfc. 
 
 Patient had an attack of acute [lolyarticular rheumatism followed 
 b_\- sharp precordial pain radiating into arms twenty years before death. 
 Since th.en he had had three to four attacks a vear. He was alwavs 
 
 WW 
 
 short of breath, and had |>alpitations of the heart. He was nervous and 
 slept poorlw At times he had severe headaches, dizziness and night 
 sweats. Lately he complained of renewed ])ain over the heart, shortness 
 of breath, and oedema at the ankles which he observed for the first time. 
 Clinically he presented evidences of aortic stenosis and regurgitation.
 
 Rr.coKi) OK CASKS 39 
 
 Ili-s blood pressure was 170 on entrance, Imt later went down to 140-150. 
 lie had a sli.yht anaemia (4,000.000 reds; lib. 85%) and a slight Iciico- 
 cvtosis ( 10,000). He had a positive Wassermann reaction, although he 
 denied lues; nothing suggestive of syphilis was found at autoi)sy. His 
 temiierature was at times subnormal, and his jiulse rate varied between 
 80 and 100. His urine showed a light cloud of albumin and few granu- 
 lar casts. 
 
 Necrops)' revealed an old aortic diploslreptococcic endocarditis with 
 recent exacerbation, moderate general arteriosclerosis. 
 
 The kidneys were of about normal size and full of minute haemor- 
 rhages. 
 
 Sections showed few glomeruli with old glomcrulo-nepiuilis and 
 ^mall areas of cellular infiltration and connective tissue ])roliferation in 
 the vicinity ; infiltration with neutro])hilic leucocytes in majority of 
 glomeruli; necrotic loops in few of them; extra-ca))illary proliferation 
 about some of these tufts; many haemorrhages, few leucocytes, few 
 casts in tubules ; marked leucocytosis in capillaries and few neutrophilic 
 leucocytes in the interstitial tissue ; marked fatty degeneration and bc- 
 L^inning necrosis of the e])ithelium ; beginning "arteriosclerosis" in some 
 -mall arteries. Xo pathogenic bacteria were found in the sections. 
 
 Case 3. Old focal and acute diffuse glomerulo-nephritis in a man of 
 
 41 years, with old diplostreptococcic endocarditis. 
 W II. 188. — M. K., fairly strongly built, fairly well nourished Spanish 
 farmhand and teamster. 41 years of age. 
 
 History imperfect on account of condition of ])atient. who died one 
 day after entrance. He claimed to have been well until a sudden break- 
 down three weeks before, while at work in the fields. Since then he 
 became weaker, dyspnoeic and oedematous. .\t first he had frequent 
 urination of small amounts of urine; later he had to urinate less fre- 
 (|uently, and the oedematous swelling increased correspondingly. A few 
 days before death he began to have bloody expectoration. Clinical ex- 
 amination showed extreme dysjinoca. much cough with bloody expector- 
 ation, a heart of apiiarently normal size, a blowing systolic murmur, 
 much oedema. He had a high pulse rate (103) and a moderate tempera- 
 ture 101° F). His blood-pressure was 140. His urine had a specific 
 gravity of 1012, contained much albumin, many h\aline and granular 
 casts, and few leucocytes. 
 
 Necropsy revealed an old aortic dijilostreptoccic endocarditis witii 
 some stenosis, a heart about one and one-fourth times normal size, cyan-
 
 Fig. 4. 
 
 Fig. S.
 
 RKCORD OK CASKS 41 
 
 Otic atropliy of liver, much oedema, ascites and hycirollioiax. also an 
 acute glaucoma of the left eye. Tiie arteries were practically normal. 
 
 The kidneys were swollen (13 .x 7 x 4J/ cm.) and smooth. The 
 cortex was wide, yellow, opaque, and full of minute haemorrhages. 
 There was an old infarct in the left kidney. 
 
 Sections showed old glomerulo-nephritis in few glomeruli, which 
 were surrounded by small areas of cellular infiltration, and librous thick- 
 ening of the connective tissue. The majority of the glomeruli were in- 
 filtrated with neutrophilic leucocytes : hyaline necroses were found in 
 several, and beginning extra-capillary i)ro]iferation in some. Some 
 tubules were filled with blood : many also contained leucocytes. The 
 interstitial tissue was moderately infiltrated with neutrophiles. There 
 was little degeneration in the e])ithelium : beginning "arteriosclerosis" in 
 few small arteries. The sections were loo badly contaminated to permit 
 of bacterioloijical examination. 
 
 Case 4. Acute glomerulo-nephritis in woman of 33 years, with cir- 
 rhosis and large septic phagedenic ulcers of leg. 
 X\lll. 138. — Mrs. A. 1!., delicately built, fairly well nourished Italian 
 housewife, 33 years of age. 
 
 I'atient came to clinic two years before death. ci;niplaining of swell- 
 ing of abdomen and feet. Five years before death she had her first 
 attack of swelling of the abdomen with jaundice. About three months 
 before death ulcers developed on the right leg, which became |)rogress- 
 ively worse. One month before death the symjjtoms of cirrhosis became 
 more aggravated. Clinical examination showed the usual symptoms of 
 cirrhosis, large phagedenic idcers on right leg. Treatment with salvar- 
 san made the ulcers on the legs much worse. 1 ler temperature was high 
 and somewhat irregular: her pulse accelerated and irregular. Towards 
 the end she became irrational, and some oedema appeared on her face. 
 The W'assermann reaction, which had been negative before, became posi- 
 tive at this time. She was tjuite anaemic (lib. 637c)- The urine con- 
 tained much albumin, at times many granular and cellular casts, and very 
 many leucocytes. 
 
 Necropsy revealed extensive old cirrhosis and several large phage- 
 denic ulcers on right leg. Smears from the most acute one of these 
 ulcers showed many streptococci. Streptococci were also found in a 
 thrombus in the right auricle and in the spleen. The heart was slightly 
 dilated on the right side. The large blood-vessels were normal.
 
 42 
 
 THE PATHOLOC.V OF NEPHRITIS 
 
 The capsule of the kidneys stripped easily. The surface was very 
 slightly granular. They v\'ere extremely hyperaemic and oedematous, 
 and very distinctly swollen (12JX x 6 x 43^ cm.). On the cut surface 
 the cortex was wide, and showed a certain number of small opaque spots. 
 No haemorrhages were seen in the gross specimen. 
 
 Microscopic sections showed a diffuse intra-capillary. and in places 
 extra-capillary, giomerulo-nephritis. The glomeruli were heavily in- 
 
 filtrated with polymorphonuclear leucocytes. Many of them showed 
 hyaline necrosis of some of the loops. In few glomeruli the changes 
 were advanced to the subacute stage. Many tubules were filled with 
 blood and leucocytes. The eiiithelium showed some granular and a little 
 fatty degeneration. The interstitial tissue was hyperaemic, oedematous, 
 and slightly proliferated. There was a moderate infiltration, with gran- 
 ular leucocytes and lymphocytes. \o bacteria were found in sections. 
 The small arteries were normal, the larger ones were slightly "arterio- 
 sclerotic."
 
 RKCORP OF CASES 
 
 43 
 
 Case 5. Early subacute glomerulo-nephritis in a woman of 33 years 
 
 with subacute diplostreptococcic endocarditis. 
 XX'III, 166. — Mrs. K. 11., .stroiiLjly built, jioorly nourisla-d llalian liou.sc- 
 wife, 33 years of age. 
 Patient was admitted to hospital ten days before her ilealh, com- 
 plaining of vomiting, shortness of breath, and swelling of feet. Nine 
 months liefore, she had an attack of acute ])olyarticnlar rheumatism, 
 ushered in by tonsillitis. The ])ains in die joints continued intermit- 
 
 tently for about >ix months. Ten weeks before admission her stomach 
 trouble began, and she vomited fre(|uently. I ler d\ si)noea .started six 
 weeks later, and the oedema commenced one week before entrance. 
 Clinical examination showed marked dyspnoea, slight icterus, coateil 
 tongue, an enlargement of the heart lo the left, a systolic blowing murmur 
 at the apex, transmitted to axilla and back, also a i)resytolic murmur, 
 marked general cyanosis and oedema. ])etechial haemorrhages in skin 
 and mucous membranes. The patient vomited very much, was very 
 restless at times, at others drowsy, had some muscular twitchings in face, 
 and died of gradual circulatory failure. She was distinctly anaemic 
 (3,392,000 reds; 48^ lib.). There was some leucocytosis (12.740).
 
 Fig. 9.
 
 KIKOKII OK CASKS 45 
 
 Diploslrcptococci were olitaincd in blood culture. I Ur liluod pressure 
 was loo. The temperature was sulinorinal. witli ele\ations to 99^ !■'. 
 The pulse rate varied between So and 100. The urine contained much 
 albumin, many hyaline, "granular an<l cellular casts, manv leucoc\tcs and 
 much blond, also diplnstrei)tococci. 
 
 XecropsN revealed subacute diplostre|)tococcic endocarditis of mitral 
 .111(1 iricuspicl \alves. embolic septic foci in heart-muscle, infarcts in 
 s|»lcen and kidney, septic necroses in liver, cholelithiasis, and terminal 
 broncho-pneumonia. 'J"he heart was moderately enlartjed on the rig^ht 
 side on account of mitral disease. The blood-vessels were normal. 
 
 The kidneys were swollen f 1 1 ^ x 6^ .x 4 cm. : 1 2 .\ 7 .\ 5 respcct- 
 ivelxi. The capsules stripped easily. The surface was smooth, dark 
 greyish red. and studded with minute haemorrha,u;es. On the cut surface 
 the corte.x was wide, distinctly oedematous. and greyish red. 
 
 Microscopic sections showed diffuse acute and subacute glomcrulo- 
 n('|ihritis (intra- and e.xtra-capillary ) : much blood and m;mv leucocytes 
 in tubules, many ncutro])hilic leucocytes in glomeruli and in interstitial 
 tissue, few eosino])hiles and basoi)hiles, comj^aratively little epithelial de- 
 generation, and beginning proliferation of the connective tissue: arter- 
 ies normal. \'o bacteria were found in sections, in spile of careful 
 M-arch. 
 
 Case 6. Early subacute glomerulo-nephritis in an infant with con- 
 genital syphilis and suppurative colon-bacillus pyelitis. 
 .\\ 1, 50. — .\. C, anaemic female child, i ,' _> months of age. 
 
 The child was apparently normal at birth, was sick for about two 
 weeks with sanguino-purulent discharge from nose, and fever to 101' F. 
 .Several blisters developed on abdomen. .\t the hosi)ital occurred a more 
 general eru])tion of red blisters. The hands were oedematous on en- 
 trance, but the oedema disajipcarcd later. Moist rales were heard over 
 the lungs. The W'assermann reaction was positive. A heavy cloud of 
 albumin was found in the urine, a few doubtful hyaline casts, and many 
 leucocytes. Patient died in collapse witii symptoms of pulmonary oedema. 
 
 .\'ecro])sy revealed syphilitic rhagades at mouth, syphilitic pneinnonia 
 ,tnd subacute septic pneumonia, syphilitic cirrliosis and miliary syphil- 
 omata of the liver, subacute dcej) idcerative infection of renal jielvis 
 with colon-bacilli and beginning involvement of kidneys. The arteries 
 were normal. 
 
 The kidneys were large. The cortex was o|)ar|ue and swollen. 
 
 Sections showed hyaline necrosis of vascular loops in the majority 
 of the glomeruli, with subacute glomerulitis (extra-capillary). Many
 
 46 
 
 rin-; patiiolocv oi-" nepiikiti;- 
 
 tubules were filled with lilciod, others contained leucocytes. There was 
 a marked infiltration of the interstitial tissue with nculroiiliilic. eosino- 
 
 philic leucocytes and plasma cells, and cellular proliferation of the con- 
 nective tissue. The \essels were normal. Xo bacteria were found in 
 the sections, excejit at the evidently infected places. 
 
 Case 7. Subacute glomerulo-nephritis in a man of 40 years, following 
 
 subacute endocarditis. 
 XVII, 163. — E. G., dishwasher, 40 years of age. 
 
 Patient had a paralytic stroke associated with left-sided hemijilegia 
 and sensory aphasia seven months before death. He had a chancre two 
 years before, and at the time he came to the hospital had a |>ositive 
 Wassermann reaction. Clinically he showed a systolic murmur at the 
 apex, general oedema, some anaemia (4,800,000 reds, 85% Hb.). and 
 slight leucocytosis (11,200). He had an irregular temperature varying 
 between 96° and 102° F. His ])ulse rate varied between 70 and 100. His 
 urine contained a moderate amount of albumin and a few hyaline casts. 
 
 Necropsy revealed a subacute diplostreptococcic endocarditis of the 
 mitral valve, with regurgitation, an embolic softening in the region of
 
 iHl) Ol' CASKS 
 
 47 
 
 the right island of Keil. a hci^iiinin:; cyanotic alrojjhy of tin- li\ir. •jcii- 
 eral oedema, marked h\drothora.\ and normal arteries. 
 
 The kidneys were swollen: the corte.x was rather wide an<l i)|)a(|ue, 
 and full of jietechiai haemorrhages. 
 
 Secticjns showed hyaline necroses in many glomeruli, tvpical diliuse 
 subacute and more chronic glomerulo-nephritis ( intra- and e.\tra-cap- 
 illary i : moderate diffuse cellular thickening of the connective tissue, in 
 which there were (|uite a few neutro|)hilic and less numerous eosino])hilic 
 and basophilic leucocytes: marked hyperaemia : Mood antl leucocytes in 
 many tubules: much epithelial degeneration: normal blood-vessels. Xo 
 pathogenic b:icleria were found in llie sections. 
 
 Case 8. Marked subacute glomerulo-nephritis in a man of 45 years, 
 
 following streptococcic infection of compound fracture. 
 
 .\l\ . :!4. — I. \\'., slrongK built. luuscular .American carpenter. 45 years 
 
 old. 
 
 Patient had a compound fracture of the left leg ei.yht and o:ie-lialf 
 
 months before death. The bones became united, but the wound never 
 
 (|uite healed and later broke ojien. leaving a constantly discharging ulcer
 
 48 
 
 THE P.\TII()1.0(;^• OK NEPHRITIS 
 
 from which a small piece of necrotic bone came away at one time. Many 
 streptococci were found in the infected tissues. The temperature was 
 normal most of the time, but there were sharp rises off and on. His 
 
 urine was smoky, contained much albumin, many h\aline and waxy casts. 
 many red cells. 
 
 X'ecropsy revealed, in addition to the infected fracture, a marked 
 anaemia and broncho-pneumonia, possibly a slight hypertrophy of the left 
 ventricle, slight oedema of leg, slight general arteriosclerosis. 
 
 The kidneys were somewhat swollen ( 12 x 7 x 4 cm.). The surface 
 was smooth, mottled grey and red. The cortex was wide, hyperaemic 
 and oedematous, and full of minute haemorrhages. 
 
 Sections showed hyaline necrosis in vascular loops of many glom- 
 eruli; very characteristic acute and subacute glomerulo-nephritis (extra- 
 capillary) in i)ractically all; moderate diffuse infiltration of interstitial 
 tissue with neutrophiles,. eosinophiles, basophiles, and marked diffuse 
 fibrous thickening of the connective tissue. Many tubules were filled 
 w4th blood, others with leucocytes. The epithelium showed much fatty 
 degeneration. Slight "arteriosclerosis" in a few of the larger arteries. 
 A few doubtful diplococci were found in the diseased glomeruli and in 
 the leucocvtes in some of the tubules.
 
 RIXORD OF CASliS 
 
 49 
 
 Case g. Subacute glomerulo-nephritis in a man of 33 years, following 
 
 subacute diplostreptococcic endocarditis. 
 X\ . i_^5. — H. D., stronijly Wuilt. ciiiaciatcil, AnuTicaii iiospital (irdi'rJN-, 
 33 years of age. 
 Patient infected his finger eight months before his death. The in- 
 fection was followed by chills and fever, increasing weakness, and grad- 
 ual development of symptoms of septic endocarditis, with remittent fever 
 and progressive anaemia (eventually 3.800,000 reds; 56':; Mb., 5,000 
 leucocvtes, and occasional mvcloc\tes ). Three months before his death 
 
 patient noticed oedema at ankles, increased thirst, and increased urina- 
 tion. Since this time he compla.ined of headaches and dyspnoea. The 
 W'assermann reaction was negative. Blood cultures were negative on 
 two occasions. His urine was increased in quantity (specific gravity 
 1010-1016), showing a heavy cloud of albumin (about 0.5%), many 
 hyaline and granular casts, a moderate number of leucocytes, and at times 
 many red cells. Phenolsulphone-phihalein excretion two weeks before 
 death : 40% in two hours. 
 
 Necropsy revealed a subacute aortic di])lostreptococcic endocarditis 
 with moderate stenosis and some insufficiency, a purulent mcdiastinilis.
 
 50 THE PATHOI.OCV OF .NEI-HRITIS 
 
 and a fibrinous pleurisy, both due to the diplostreptococci, a large spleen 
 with a septic infarction, no oedema, normal arteries. 
 
 The kidneys were of about normal size ; the surface was smooth. 
 The cortex was wide, opaque, intensely hyperaemic, and full of haemor- 
 rhages. 
 
 Sections showed hyaline necrosis of loops in many glomeruli, very 
 typical subacute glomerulo-nephritis ( intra-capillaryj in practically all, 
 large areas of cellular infiltration (containing neutrophilic leucocytes), 
 and much fibrous thickening of the connective tissue, with beginning 
 atrophy of the tubules. Some tubules were full of blood, others con- 
 tained casts. Much granular and fatty degeneration was found in the 
 epithelium, also extensive necrosis. Normal blood-vessels. No patho- 
 genic bacteria were found in sections. 
 
 Case 10. Subacute glomerulo-nephritis with continued hypertension 
 
 and cardiac oedema in woman of 27 years, following abscess 
 
 of jaw. 
 
 X\TII, 106. — M. O. A., poorly nourished Spanish housewife, 2~ years 
 old. 
 
 Twenty-one months before death, patient had considerable trouble 
 with her teeth, lasting for eight months : finally alveolar abscess devel- 
 oped, and one tooth had to be removed. This abscess involved lower jaw, 
 and had to be drained from outside. She had been apparently well since 
 then, until four weeks before her death, when she developed a painless 
 oedema of the legs, without an}- other symptoms. The swelling con- 
 tinued, and the abdomen also became involved. Ten days before death, 
 symptoms of an acute infection developed in the right leg. She developed 
 an irregular fever to 102° F; her pulse rate varied l)etween lOO and 140. 
 There was also some leucocytosis ( 10-15,000). Clinically there were no 
 important findings except oedema and evidences of cellulitis. Her haemo- 
 globin was 8o7c, her blood pressure 160. gradually rising to 170. Her 
 urine was quite scanty, specific gravity loio: it contained much albumin, 
 many hyaline and granular casts, many red and white cells. She had no 
 symptoms of uraemia, and died of the acute strejjtococcic infection of 
 her leg. 
 
 Necropsy revealed streptococcic cellulitis of the right leg, broncho- 
 imeumonia, some ascites fa pint of fluid), and an acute cystitis. Her 
 left ventricle was slightly hypertrophied. There was no arteriosclerosis 
 except in the renal arteries, where it was of a moderate degree.
 
 THI-; PATHOLOGY OF NEPHRITIS 
 
 Her kidneys were of about normal size (12 x 5 x 4 cm. ) : the cap- 
 sule was slightly adherent ; the surface slightly roughened. The cortex 
 was rather wide, yellow, and opaque. 
 
 Microscopical sections showed subacute, peri-capillary glomerulo- 
 ne])hritis in many glomeruli, with development of fibrous connective tis- 
 sue between ca])illaries, hyaline degeneration of the wall of some of the 
 
 ca])illaries in the tufts, moderate diffuse thickening of the connective tis- 
 sue with beginning atrophy of some of the tubules, leucocytes in manv 
 tubules, many hyaline casts, no haemorrhages, and much epithelial de- 
 generation. The thickened interstitial tissue is almost altogether fibrous. 
 There are very few small areas of lymphocytic infiltration ; no granular 
 leucocytes were found in the tissues. Xo bacteria were found in the 
 sections, in spite of continued search. 
 
 Case II. Late subacute glomerulo-nephritis in a man of 51 years, fol- 
 lowing chronie diplostreptococcic endocarditis. 
 
 X\'II, 119. — M. A., well nourished Norwegian male cook, 51 years of 
 age. 
 Patient began to complain of heart trouble four years before his 
 death. He had had some oedema. He came to the hos])ital about six
 
 RirCORD OF CASKS 
 
 53 
 
 weeks bi'tore death, complaiiiim; of vomiting and dyspnoea. Clinically, 
 lie showed evidence of an enlargement of the heart, and a marked dias- 
 tolic murmur, also symptoms of aortic aneurysm. The hackgrounds of 
 his eyes were normal: there was no definite evidence of uraemia. His 
 temperature was subnormal and slightly irregular. His ])ulse rate varied 
 between 90 and r>). ilis blood showed a secondary anaemia (3,312,000 
 reds, 6o</( Hb. 1 and a lcuco])enia (6200). He had a syjihilitic history 
 and a jiositive W'assermann reaction. Ilis blood jiressure, gradually 
 
 rising, varied from i.So to 220. .'^incc over onc-balf year before death. 
 he had noticed polyuria u\> to one gallon a day. The ])olyuria continued 
 while he was at the hospital. Ilis urine contained much albumin, many 
 epithelial and granular casts, a few leucocytes, occasionally many red 
 cells. It had a low sjjecific gravity ( 1005-1010). There was jjractically 
 no elimination of i)henolsidphone-|)hthalein in three successive tests. 
 
 .\ecro])sy revealed sy])hilis of the aorta and an aneurysm of the arch : 
 a chronic diplostre])tococcic endocarditis on the ventricular side of the 
 large sail of the mitral valve and of the aortic valves with little ileformity 
 of the aortic cusps, and acute dijilostreptococcic jiericarditis, slight 
 ascites, and moderate hydrothora.x ; old cyanotic atrophy of liver: be-
 
 54 Till'. j'.\iiioi.()i;v oi- Ni:i'iiRiTi.s 
 
 ginnint; amvloid degeneration of t!ie spleen, no amyloid in the kidneys. 
 The heart was twice normal size, with a very marked hypertroi)hy of the 
 left ventricle. The renal and splenic arteries were markedly sclerotic. 
 
 The kidneys were slightly enlarged ( 13 x 7 x 4 cm.), the surface 
 was somewhat rough, dark red, and full of haemorrhages. On the cut 
 surface the cortex appeared slightly reduced and opaque. 
 
 Sections showed very marked diffuse, chronic, subacute and acute 
 glomerulo-nephritis (intra- and peri-capillary), with hyaline necrosis of 
 many vascular loops, fibrin in capsules of many glomeruli, much infiltra- 
 tion with granular leucocytes, especially with eosinophiles, and marked 
 diffuse thickening of the connective tissue with atrophy of many tubules : 
 blood, leucocytes, and casts in tubules: much granular degeneration and 
 necrosis of the epithelium : slight "arteriosclerosis" of a few of the small 
 arteries and several of the larger ones. No bacteria were found in sec- 
 tions. 
 
 Case 12. Late subacute glomerulo-nephritis in woman of 26 years 
 
 with repeated attacks of tonsillitis, a general diplostrepto- 
 
 coccic sepsis with infection of the urinary tract, 
 
 multiple thrombotic arterial obstruction. 
 
 Will, Oi. — E. AI., frail and extremely emaciated Irish-American house- 
 wife, 26 years of age. 
 Patient had numerous attacks of tonsillitis from infancy to four 
 years before death. She was treated six years before death for nephritis 
 following miscarriage. I"or the last five years she had much headache, 
 associated with vomiting. Occasionally she had slight oedema of feet 
 and ankles. I'our months before death she complained of marked weak- 
 ness, headaches associated with vomiting, pains in shoulders and arms, 
 loss of ])ower in left arm. She bled easily from her mucous membranes. 
 Left foot had been cyanotic in region of big toe during cold spells for 
 the past two years ; she also had attacks of syncope in her fingers. Her 
 eyesight began to fail at this time. When she entered the hospital a 
 month before death, the toes of the left foot were cold and blue and hor 
 left arm contracted and atrophied. Later she developed dry gangrene of 
 the left foot. Her tongue was dry and red. her breath uraemic. The heart 
 action was heaving. There was a slight systolic and diastolic murmur. 
 and considerable ascites. . She later developed some oedema of the legs. 
 Towards the end there was marked pufffness of the face. She had 
 been complaining of failing eyesight for some time, and ophthalmoscopic 
 examination revealed retinitis albuminurica. Shortlv before her death.
 
 Ki:C()RU OF C.\S12S 
 
 55 
 
 slie had protusf liainiorrliaj^cs from the rectum. Slic died in uraemic 
 coma. Iler temperature was irreguhir, sliovvins;' aUcniatiug periods of 
 slight rises to 1 00° I-", and of sulmormal temperature. Iler pulse rate 
 was very irregular, varying- between Xo and 130. She was very anaemic 
 (Hb. 50%, 3,000,000 red>i. Iler leucocytes were normal except for a 
 terminal leucocytosis. In a Mcod culture a pin-e growth of dipiostrepto- 
 cocci was obtained: similar organisms were found in her urine. She 
 denied all venereal infection, and had a negati\e W assermann reaction. 
 Iler lilood pressure was iC)5 cm entrance, went up to 1S5, and then grad- 
 
 # A 
 
 ^^■ 
 
 uall_\- dfiwn to 140. She had hafl nocturia ' for the last ten years. Iler 
 urine was of about normal amoinu, of low specific gravity (1004-iOoSi. 
 It contained nuuii albimnin, sometimes few, at other times many casts of 
 various kinds, some red blood corpuscles and leucocytes. Towards the 
 end there was much pus in the urine. The i)henolsulphone-phthalcin 
 secretion was much delayed (12% in two hours 1. 
 
 Necropsy revealed slight oedema of hands and legs, marked ascites. 
 The ai)pendix was surrounded by old adhesions. There was also some 
 
 " Urination at night.
 
 Fig. 19-
 
 RIXORD OF CASES 57 
 
 peritoneal thickening in the upper jiart of the ahdoniinal cavity. The 
 liver showed an old cyanotic atrophy. A large, deep, recent ulceration 
 evidently due to arterial obstruction was found in the sigmoid tlexurc. 
 The heart was of normal size: the left ventricle firm, full of small irreg- 
 ular necrotic spots, due to obstruction of small arteries. There were a 
 few small yellow sjjots in the aorta. The renal pelves were slightly 
 dilated. They contained a few drops of pus in which there were some 
 diplostreptococci. The bladder also was infected with diplostreptococci. 
 The left arm was contracted, and there was a dry gangrene of the left 
 foot. 
 
 The left kidney was of about normal size ( I0^4 x 43./> x 3 cm. ), the 
 right kidney smaller. The surface was mottled grey and red, and stud- 
 ded with petechial haemorrhages. The renal tissue was distinctly in- 
 durated, and the cortex narrowed to about 3 mm. Unfortunately an 
 examination of the brain and of the peripheral arteries, and a thorough 
 search for an old septic focus, was impossible. 
 
 Sections showed marked diffuse, subacute, and chronic glomerulo- 
 nephritis (intra-capillary form), moderate cellular infiltration, and marked 
 diffuse fibrous thickening of the connective tissue with atrophy of many 
 tubules: much epithelial degeneration and many casts; blood and pus 
 in the tubules, thrombotic hyaline deposits along inside of walls of many 
 arterioles, anaemic necroses in pyramids due to thrombosis of small arter- 
 ies. Other small arteries showed marked "endarteritis,"" and all the 
 larger ones moderate "arteriosclerosis." \o bacteria were found in sec- 
 tions. 
 
 Case 13. Subacute and chronic glomerulo-nephritis in a child of 8 
 
 years following infectious aneurysm of aorta. 
 W I. i()0. — \'. I'., female child, 8 years of age. 
 
 The ])atient had had measles, pertussis, mumps, and chickenpox. 
 There was no history of sore throat, rheumatism, or scarlet fever. She 
 was apparently perfectly well until about five months before death, when 
 she began to have severe continuous headaches in the frontal region with 
 much vomiting. .About three weeks later she had a "spasm" lasting an 
 hour and a half, with tongue bite and twitching of muscles of eyes and 
 face. This was repeated six days later, and again after a few weeks. 
 .\fter the spasms she was unable to see well. The vomiting continued, 
 and she developed increased thirst and polyuria. The |)atient lost much 
 weight.
 
 Fi-. 21. 
 
 Fig. 22
 
 mXORl) OF CASKS 
 
 59 
 
 Clinical fxaniinatioii llncc nioiillis luldit- dcalii bhuwcil iR-iirili;. in 
 left eye. enlargement of the liearl with Unu\ systolic murmur, |)aii)fiil 
 enlargement of liver, no oedema. Later a papular eru[)tion appeared on 
 the extensor surfaces of extremities and on body. .\ retinal detachment 
 developed in the left eye. At one time puffiness of the face was noticed. 
 She complained of nnuli pain in the \nt of the stomach: nausea and 
 vomiting continued intermittently. She suffered much from dvspnoea. 
 and occasionally had pain in the region of the heart, ."^igns developed 
 
 of the jiresence of tluid in the ])leural cavities. She had nuich cough, 
 with blood-tinged sputum. Two months before death, the arteries in 
 both eyes were found iinich contracted, and there was marked optic 
 neuritis and retinitis in both eyes, iter temperature was sliglitly ele- 
 vated and irregular. The W'assermann reaction was negative. There 
 was a marked anaemia (Mb. 60%) and some leucocytosis (28,000 grad- 
 ually decreasing to 10-12,000). The blood pressure was about 140. Siie 
 had a very marked polyuria all the time: the urine was of low specific 
 gravity (1002-1005). It contained little albumin and few hyaline casts, 
 some leucocytes.
 
 60 TIIIC I'ATIllll.Oll'i- OF N'EPIIUITIS 
 
 Necropsy revealed an infectious ( diplostreptococcic ) aneurysm of 
 the upper abdominal aorta, involving the orifice of the left renal artery, 
 which was entirely occluded; infarcts in lungs and spleen; and an old 
 tuberculous focus in the left peribronchial lymph-glands. The heart 
 showed normal valves. It was considerably enlarged, about twice nor- 
 mal size, with marked hypertrophy of the left and dilatation of the right 
 ventricle. The left forearm and hand were oedematous on account of 
 thrombosis of the subclavian vein. There was much chyloid fluid in 
 both pleurae. The arterioles in the spleen were greatly thickened and 
 hyaline. The other arteries were normal. 
 
 The left kidney was quite small (8 x 4 x 3"/^ cm. ) with flat purple 
 scars at upper pole and along the convexity. The right kidney was con- 
 siderably swollen ( 12 X 5 X 4J/3 cm. ) ; the cortex was wide, yellow, and 
 opaque 
 
 Sections of the left kidney showed old focal glomerulo-nephritis 
 with numer(3us scars, no recent processes. Sections of the right kidney 
 showed old glomerulo-nephritis in few glomeruli with scar formation 
 near them ; hyaline necrosis and subacute glomerulo-nephritis ( intra- 
 capillary) in many glomeruli ; slight infiltration of interstitial tissue 
 with neutrophilic, eosinophilic, and basophilic leucocytes; considerable 
 proliferation of the connective tissue ; much granular degeneration of 
 the epithelium ; many casts, and leucocytes in some tubules. The blood- 
 vessels were normal. No pathogenic bacteria were found in sections. 
 
 Case 14. Chronic glomerulo-nephritis in a child of 10 years with a 
 
 history of repeated attacks of tonsillitis. 
 XVIII, 17. — A. B., poorly developed female child, 10 years of age. 
 
 The child had smallpox at an early age and had frequent attacks of 
 tonsillitis. For the last two years she had had attacks of precordial 
 pain, shortness of breath, and vomiting. She had been gradually run- 
 ning down with periods of exacerbation and remissions. She had had 
 transient joint pains at times. Severe disturbance of compensation 
 commenced about two weeks before death with oedema involving the 
 face. Clinical examination one week before death showed a poorly devel- 
 oped, poorly nourished child with very marked dyspnoea, some oedema 
 of the face but none elsewhere, heavily coated tongue, marked enlarge- 
 ment of heart; rapid, regular pulse (gallop rhythm), no murmurs, en- 
 largement and tenderness of liver. A petechial rash appeared on the skin 
 about one week before death. Towards the end she was semi-comatose, 
 verv restless (uraemia). There was some anaemia (3,696,000 reds,
 
 I'iji. -M-
 
 (>2 rin-: i'a-i-iioi.oi;'!- ok mkimiritis 
 
 111). (So'/( I anil u sli,L;lit k-iicocytosib (11.400). The temperature was 
 suljiiormal (about (/r b' ) with rises to 99° and 100° !•". The W asser- 
 mann reaction was negative. The urine (quantity could not he determ- 
 inedj showed a specific gra\ity of about loio, a heavy cloud ot albumin. 
 several hyaline casts, and a tew red cells. The blood pressure was lOo 
 on entrance, but later fell to about 145. 
 
 Xecro])s\' revealed a recent jjurulent diplostrei)tococcic vulvitis, a 
 congenital fold at the hiwer end of the left ureter with slight hydrone- 
 l)hrosis, ascites, hydrothora.x, and slight oedema of the legs. The heart 
 was at least twice normal size, with marked hypertrophy of the left 
 ventricle. Except for a few small yellow spots in the abdominal aori.a, 
 the arteries were normal. 
 
 The kidnexs had tirmh adherent capsules. They were small ( lelt 
 X 3 X 2 cm., right 11x4x3 cm. ), finely granular, and the cortex w.as 
 distinctly narrowed. 
 
 Sections showed ver\- extensive inxohement of glomeruli ; some 
 showed recent hyaline necrf)sis of loo])s, others typical suhamite and 
 chronic giomerulo-nephritis ( intra-capillary I . There was a marked 
 diffuse thickening of the interstitial tissue, with heavy infiltration with 
 neutrophilic, eosinophilic, and basophilic leucocxtes : large areas oi 
 cicatrization ; blood and leucocytes in few tubules : many casts, much 
 e])ithelial degeneration : marked "endarteritis" in the small, and mod- 
 erate "arteriosclerosis" in the large arteries. Xo pathogenic liacteria 
 were found in sections. 
 
 Case 15. Chronic giomerulo-nephritis in boy of 6 years following 
 
 streptococcic infection of urinary tract in nephrolithiasis. 
 X\', 120. — E. R., emaciated anaemic boy, 6 years of age. 
 
 Two \ears before the patient's death, a large stone was removed 
 from the bladder. The urine at that time contained pus. The heart 
 was clinically normal, hive months later evidences of cardiac hyper- 
 trophy developed. Later he had a right facial palsy. He had to urinate 
 verv frequently. The boy gradually went down-hill, and eventually died 
 in uraemic coma. The history is incomidete, and there is no record of 
 urinary analysis. 
 
 Necropsy revealed a small stone ( 1 ' .. cm. in diameter) in right 
 renal pelvis, with streptococcic infection of the urinary tract. The heart 
 was somewhat enlarged, wdth definite hypertrophy of the left ventricle. 
 Except for a few vellow spots in the aorta and in the coronaries, his 
 arteries were normal.
 
 64 
 
 Till-: I'ATIKll.llliV or XKI'llKITIS 
 
 The left kidney sliowed many superficial purple scars, with narrow- 
 ing- of cortex. In other places the cortex was wide and ojjaque. The 
 right kidney showed much more extensive cicatrization, with small nod- 
 ules of fairly normal kidney tissue. 
 
 Sections showed very e.xtensixc chronic glomerulo-nupliriti.'-, with 
 complete fibrosis of the [glomeruli : large areas of cellular iufiltraticjn, and 
 
 fibrosis, with atro])hy of tubules; many hyaline casts in the atr()|)hic 
 tubules. In the comparatively normal parts much recent and subacute 
 glomerulo-nephritis ( intra-capillary i : and a few granular leucocytes in 
 the tissues. Blood and leucocytes were found in some tubules. Much 
 granular degeneration and necrosis of the epithelium. Hyaline throm- 
 bosis along wall in some small arteries. \'ery marked "endarteritis" in 
 small and larger arteries, especially in the fibrous areas. The sections 
 were too badlv contaminated in i)ermit of a bacteriological examination.
 
 RKCORl) t .1- I .\.->l„- 65 
 
 Case i6. Chronic glomerulo-nephritis in man of 53 years with diplo- 
 
 streptococcic sepsis (infected atheromatous ulcers in aorta). 
 Will. 70. — M. K.. strongly huilt, fairly wi-ll nmnishcd Japanese laiin- 
 dryman, 5^^ years of ai^e. 
 
 (The history is imperfect, because the patient did not speak Knt^rjish. 
 and was observed for a few days onl\ . 1 
 
 Patient had beri-beri at the ai.;o nf ji,:;. I k- was a heavy smoker. an<l 
 he used much alcohol. For about the last three years his face and feet 
 would become swollen at intervals, especially when he drank heavily, and 
 at these times he complained of distress and of difficulty in breathins^. 
 His present attack started seventeen days before his death, with oedema. 
 Later he developed a white membrane in the throat, which first appeared 
 on his tonsils, spreading over the uvula and inside of the cheek. He de- 
 veloped a high fever, and had a very foul breath. Clinical examination 
 showed i)uffiness of face, slight oeilenia of legs, angina and stomatitis, 
 an apparently normal heart. The pul>e was small, regular, rhytlimical, 
 and of low tension. The patient died with the signs of jjulmonary 
 oedema. His urine a few days before his death was of a very low 
 specific gravity (1002), contained much albumin, occasional granular 
 casts, and many white and red blood corpuscles. 
 
 Necropsy revealed slight oedema of conjunctivae and of cheeks, 
 septic angina and stomatitis (dii)lostreptococcus infection). In the lower 
 thoracic and in the abdominal aorta there were large atheromatous 
 plaques, many of them ulcerated. In smears from these ulcers many 
 diplostre])tococci were found. There was an old thrombosis of the left 
 iliac artery. The other arteries were somewhat dilated, otherwise nor- 
 mal. The spleen was of normal size, and contained many diplostrepto- 
 cocci. The arterioles in the sjileen were distinctly thickened. Tiie liver 
 showed an incipient cyanotic atro]ihy. There were 51X) cc. of lluid in 
 the ali<l(iinen. The i)alii-iit died of broiicho-pneimionia and beginning 
 jileuris} . 
 
 The lieart was enlarged (one and one-half times normal size I. The 
 wall of the left ventricle was greatly thickened (16 mm. in diameter)."* 
 The heart muscle showed a marked fatty degeneration. 
 
 The kidneys were of about normal size (11 .v 6 x 5 cm.), with 
 granular surface. The tissue was greyish, with red blotches. Small 
 petechial liaemorrhages could be made out on the surface. On the cut 
 surface the cortex was found distinctly narrow and opaque. Tiie mucous 
 
 ■• .Measured from base of Irabcculac cariicac to outer siirlacc.
 
 Fis. 29. 
 
 Fig. 30.
 
 RKCORP Ol' I ASIC: 
 
 67 
 
 membrane of the renal pelvis and of the lilaiider was li\ i>ei aiTnie. l-'ew 
 diploeocci were found in smears from the renal iielvis. 1h\v dijilococci 
 were found in smears from tlie kidney tissue. 
 
 Microsco|)icaI sections showed a suliacute and chronic ditfu^e inlra- 
 and extra-cajnilary _t;lomerulo-nei)hritis. marked cellular infiltration and 
 fibrous tliickenint; of the interstitial tissue, with atrophy of many tubides : 
 many neiitro|>hilic lcucoc\tes. much eiiithclial deijcneratiiin. and many 
 
 Fig. ^'■ 
 
 ca.st>. l)i]>lostreplococci were found in many capillarie.-- ami in tlie in- 
 flamed connective tissue near them : none were seen in the t,^lomeruIi or 
 elsewhere. Many arterioles were either filled or lined on tiic inside with 
 hyaline thrombus: sometimes these hyaline masses were found above, 
 sometimes underneath the endothelial lining;. In other arterioles there 
 was a marked endarteritis, jirobably as a result of oru;anization of these 
 hyaline masses : others a.L^^ain showed a marked "arteriosclerosis." The 
 lars/e arteries showed a marked "arteriosclerosis."
 
 68 
 
 THK PATIlfH.Oi 
 
 IK XKI'HRITIS 
 
 Case 17. Chronic glomerulo-nephritis in man of 48 years with a his- 
 tory of scarlet fever and rheumatism. 
 
 X\ J. 2^j. — J. A]cL., fairly well nourished Scotch butcher, 48 years old. 
 Patient had scarlet fever as a child, rheumatism at about the age 
 of 20. Eight years before death he had pleurisy. For the last two and 
 one-half years he had often had chills in the evening and night sweats; 
 since that time he had also noticed shortness of breath and oedema. One 
 year before death he observed pufifiness of the face. .\t times he had 
 
 slight pains around the heart, radiating toward the arms, lie com- 
 plained of failing eyesi.ght and frontal bilateral headaches. For these 
 complaints he had been at the hospital ofT and on, where a peripheral 
 arteriosclerosis, a cardiac enlargement with systolic and diastolic mur- 
 murs, was made out, and a severe anaemia (3,000,000 reds, 507c lib.!. 
 He had a negative W'assermann reaction. Eight months before death 
 his blood pressure was 200. .\t his last entrance it was 210, gradually 
 falling to 165. Eight months before his death, examination of the 
 fundus of the eyes showed an old disseminated syphilitic choroiditis, well 
 defined arteriosclerosis, and evidence of former optic neuritis. The last
 
 KllKiKI) (IK c ASICS f)9 
 
 mtiiitli Ik- was more ur less iinc()iiscit)iis. at times liclirions and noisy, and 
 towards tlic end had several uraemic convulsions. While al the liospital 
 his temperature and pulse were normal. lie had had nycturia (six to 
 seven times a night ) for several years. Mis urine was greatly increased in 
 (|uantity, to two liters and more, showed a fixed low specific ijravity, 
 contained much albumin and usually many hyaline and yrannlar casts, 
 and many leucocytes. 
 
 .Necropsy revealed a large heart, twice the size of the fist ; general 
 nedema and hydrothorax : a marked general arteriosclerosis, and almost 
 complete closure of the right coronary artery. The kidneys were of 
 ahout normal size, granular. 
 
 Sections showed very marked, difi'use chronic and subacute intra- 
 capillary glomerulo-nei)hritis. with unusually extensive hyaline necroses 
 of the vascular loops: many large areas of ccllnl.ir infiltration, and 
 marked diffuse cicatrization with atrojihy of many tubules: few granu- 
 lar leucocytes: casts in many uibnles : leucocytes in some. 'There was 
 some fatty degeneration anii necrosis of the epithelium : and hyaline 
 masses in many small arteries causing sometimes complete obstruction. 
 -Marked "endarteritis" and marked ■"arteriosclerosis" were found both in 
 the small and in the large arteries. The sections were liadh contamin- 
 ated with colon bacilli. 
 
 Case i8. Chronic glomerulo-nephritis with recent exacerbation, in 
 
 man of 45, of unknown etiology. 
 .\\ 1. JiJ. — .\. L.. well ncjurished Danish male cook, 45 years of age. 
 
 rile history is imperfect, because the patient entered the hospital in 
 a dazed condition and could not give a clear accoimt of himself. lie 
 claimed to have been sufl^'ering for about two years from headache, dizzi- 
 ness, loss of memory, failing eyesight, shortness of breath, jirogressive 
 weakness, and fretjuent urination. He never had oedema. 
 
 Clinical examination showed s}mptoms suggestive of partial sensory 
 aphasia, a marked jjerijiheral arteriosclerosis, enlargement of heart w^ith 
 accentuation of second aortic tone, lessened reflexes on the left side of 
 the body, and horizontal nystagmus to the left. His blood w-as normal 
 excejn for a slight leucocylosis (11.000 whites, 82'/, nentro|>liiIes ). The 
 W'assermann reaction was negative on repeated tests, both in blood and 
 s])inal fluid. His blood-pressure was constantly very high, varying from 
 235 to 280. He had a retinitis albuminurica : towards the end he had 
 convulsions. Shortly before death a petechial rash develoi)ed in the skin 
 on hands, chest, and back. Towards the last there was some oedema of
 
 70 
 
 TIIR PATMOLOCS nV XKI' 1 1 K ITIS 
 
 the eyelids, lie died in uraemic coma. Mis urine was increased in ciuan- 
 tity, pale, clear, of low specific i;ra\ity, and contained much albumin, 
 many hyaline and granular casts. 
 
 Necropsy revealed a heart which was somewhat enlar<;'ed (about 
 one and one-fonrth normal size), with small scars in the wall of the 
 
 left ventricle. There was a rather well marked Ljeneral arteriosclerosis 
 involving' aorta, cerebral and coronary arteries, the small arteries in 
 spleen and pancreas, and manv others. 
 
 The kidneys were small ( ii x 5 x 3 cm.) and full of small haemor- 
 rhages. The cortex was quite narrow. hy];eraemic, and ojiaque. 
 
 Sections showed marked diffuse chronic and subacute glomerulo- 
 nephritis (intra-capillary ), with hyaline necroses in vascular loops; large 
 areas of cellular infiltration, and fibrous thickening of the connective 
 tissue with atrophy of tubules : blood and leucocytes in many tubules : 
 much epithelial degeneration, few casts : marked thickening of intima 
 both in small and in large-arteries, partly with hyperplastic development 
 of elastic tissue, partly without. The sections also showed numerous 
 small old necrotic foci, — situated near badly affected glomeruli with 
 thrombotic obstruction of vasa aflferentia, — in which the capillaries w^ere
 
 RKCORI) OK CASRS 71 
 
 liy]K'raemic, ami slinwcd imicli lilniii in ami near tlicm. wiiitli licranic 
 hyaline eventually. .Many s^ranular lencncytcs were fmmd in and about 
 sneli foci. Some of them showed hei^inning' orf>;anization. No bacteria 
 were tkteoted in .sections, in spile of esiiecially careful search. 
 
 Case ig. Chronic glomerulo-nephriiis in man of 37 years. No old 
 
 septic focus found, but a diploslreptococcic infection of the 
 rectum of unknown duration, and a terminal(?) 
 diplostreptococcic sepsis. 
 -W 1. 10. — J. .M.. well nourished Mexican sailor. 37 years of age. 
 
 I'atient claims to liave always been healthy and well, denies any dis- 
 eases of childhood. He suffered from "asthma." for the first time four 
 years before entrance. Two months before death he had achinu: pains in 
 neck. back, and extremities, which were worse at nit^iit. He had a syphil- 
 itic history and a ])ositive W'assermann reaction. Clinical examination 
 showed an enlart^cment of the heart and a soft systolic murmur, ascites, 
 proctitis, tjeneral oedema. Towards the end he develoi)ed a marked 
 dyspnoea. There were no definite uraemic symptonfis. His temperature 
 showed slijjht occasional rises, and his pulse varied from 80 to too. His 
 blood ])ressure was 182. He had a marked anaemia (2.350.000 reds: 
 ^o'/c Hb.), and on entrance to the hospital (two months before death) a 
 Icucocytosis (18,000), which disappeared later. I lis urine contained a 
 moderate amount of albumin, few hyaline and t^ranular casts, and later 
 many red cells. 
 
 Xecrojjsy revealed a muco-purulent proctitis due to (li])lostrepto- 
 coccic infection. l"e\v diplostreptococci were found in li\er. spleen, 
 kidneys, and lungs. There was also a terminal jiarotitis. The heart was 
 one and one-half times normal size, with a very marked concentric hyper- 
 trophy of the left ventricle ( 14 mm. 1. The arteries, including the cere- 
 bral arteries, were normal, except tiie renals, which showed a marked 
 arteriosclerosis. There was also prestnt a general oedema, ascites. h\- 
 drotliorax. and a cyanotic atrophy of the liver. 
 
 The kidneys were small ( 10 x 3 x 3'.. cm.), the surface was finely 
 granular, mottled purple and grey. .\'o haemorrhages were seen. The 
 cortex was moderately narrowed and opa(|ue : the markings were poor. 
 
 Sections showed mostly chronic glomerulo-nei>hritis ; recent hyaline 
 necroses in few glomeruli : large areas of cellular infiltration and cicatri- 
 zation with atrophy of tubules: few granular leucocytes; some tubules 
 filled with casts, blood and leucocytes. The epithelium was tilled with
 
 Fig. 35
 
 KKlOKU Ol' I ASliS 
 
 in^meiu in jilacfs and >lin\\i(i nnuli fatty and granular dcijiTKTaliun. 
 Ilvalini- df|>(isits in llic walls nf many >niall arlirii's, apparently iindt-r- 
 
 ncatli i'ndi]t];(.-liuni. I'.i-^iiniini; "endarU-ritis" in tht- small arteries con 
 nected with diseased t^lomeriili, moderate "arteriosclerosis" in the 
 arteries. Xo hacteria were found in sections. 
 
 er 
 
 Case 20. Chronic glomerulo-nephritis in Japanese of 35 years with 
 
 old diplostreptococcic infection of tonsils. 
 .Will. 1O7.— M.. stroni^ly l.nilt. well nourished iajianese farmer. 35 
 years of aj.^e. 
 Patient was admitted to hosiiilal live days hcfore his death, com- 
 plainintj of pains all over body, and of drowsiness. Tiie first symjjtoms 
 of renal disease were observed four years before, when lie had y;eneral 
 oedema and ascites, and was told that he iiad kidney disease. Two 
 months before death swelling; returned sliijhtly, but disa|>iK'ared a.L;ain ; 
 since then he noticed shortness of breath and pains all over the body. 
 l""or some days before admission he had headache, and voniite<l several 
 times. Clinical examination showed semi-stupor, considerable puffiness 
 around the eyes, heavily coated tontjuc and foul breath, normal heart-
 
 <i:iliKn (IF I'ASKS 
 
 7^ 
 
 ilulliH'ss, systolic muniuir at liase. accentuated sccoiui aortic tone, marktMi 
 treneral hvperaesthesia. especiallx of muscles, and scaly skin. The 
 temperature was normal. I lis |)ulse rate was rather slow, averaj^in"; 
 about 64. His lilood-])ressure, durintj the last days of his life, was 115. 
 1 le had a severe anaemia ( 2.804.000 reds : 41,'/, Hb. ) with poikilocy- 
 
 tosis and anisocytosis and some leucocytosis ( 18,000). The Wassermann 
 reaction was negative both in blood and spinal Huid. Towards the end 
 the patient had occasicnal attacks of severe dysjHioea, in one of which he 
 died (uraemia). His urine was of low specific gravity ( loioi, contained 
 much albumin, and in one specimen many granular casts and leucocytes. 
 
 Necropsy revealed chronic tonsillitis with old pus-pockets in crypts 
 (diplostrei)tococcic infection). The heart was about one and one-half 
 times normal size (left ventricle not dilated, averaged 12 mm.). The 
 aorta was markedly atheromatous: the other arteries, including renals. 
 were normal. 
 
 The kidneys were small I 9>4 x 4>4 x 3K' cm.). The capsules were 
 thickened and adherent. The surface was somewhat rough and (|uite 
 ])ale. ( )n the cut surface the cortex was distinctly narrowed ( to 2-,^ 
 mm. 1 and opaijue.
 
 76 Till'. I'A'lliol.ur.v (IF XEI'HRITIS 
 
 Microscopic sections showed diffuse, chronic, intra-capillary glom- 
 erulo-nephritis, more subacute lesions in few glomeruh, marked diffuse 
 fibrosis with large areas of cellular infiltration, some of which contain 
 man)' neutrophilic and basophilic leucocytes, marked atrophy of many 
 tubules, compensatory enlargement of others, little epithelial degenera- 
 tion, blood and leucocytes in many tubules, also many hyaline casts, 
 slight "arteriosclerosis" of arterioles in most fibrous areas, moderate 
 "arteriosclerosis" of larger ones. No bacteria were found in the sec- 
 tions, in spite of careful search. 
 
 Case 21. Chronic glomerulo-nephritis in woman of 36 with old scar 
 
 in base of aorta, old pericarditis, septic thrombosis of left 
 
 auricle, and old septic infarct in spleen containing 
 
 influenza bacilli. 
 
 X\l, 260. — Mrs. K., emaciated English housewife, 36 years of age. 
 
 Patient's health was goofl until she was 22, when she had a severe 
 infection ("touch of typhoid"). Since she was 23 years old, she had 
 spells of intense headache, vomiting, nausea, and occasional nose-bleeds. 
 She had oedema at times. Eight years before death, premature delivery 
 in eighth month of pregnancy became necessary on account of albumin- 
 uria. Before the birth of her second child, two years later, there was 
 much oedema. She suffered much from severe dyspnoea, pains over 
 heart and kidneys, and sleeplessness. In the last months she had much 
 stomatitis and tonsillitis. Towards the end she was very weak, rest- 
 less, and delirious (uraemia). The pleurae had to be tapped several 
 times for hydrothorax. She had a marked anaemia (3,500,000 reds; 
 65% Hb. ) and a normal leucocyte count. Her temperature was normal, 
 her pulse rate quite varying, sometimes increased to 120 or over. Her 
 respiration was about 30. Her blood-pressure varied between 160 and 
 190. She urinated once at night. Her urine on frequent examination 
 had a low si)ecific gravity and contained a heavy cloud of albumin (0.5% 
 or over ) , many granular and hyaline casts ; blood was found on one oc- 
 casion. Phenolsulphone-phthalein was slowly excreted (20 resp. 11% 
 first hour, 15 resp. 21% second hour). 
 
 Necropsy revealed an old scar in one of the sinus \'alsalvae, a healed 
 pericarditis, septic thrombi in left ventricle and left auricle, an old septic 
 infarct in spleen (many influenza bacilli in thrombi and in infarct), 
 marked oedema and slight hydrothorax. The heart was one and one- 
 half times normal size. The left ventricle measured 13 mm., and was
 
 78 
 
 Till-; l^\Tllnl.()<■.^■ fii" neimiritis 
 
 firm. The renal arteries were moderately sclerosed, the others jjractically 
 normal. 
 
 The kidneys were small (10x5x3 and 8>^ x 4>4 x 2>4 cm. resp. ) : 
 the capsule was adherent: the surface distinctly granular; the cortex 
 much reduced (to 3 mm. in places). The tissue was soft, oedematous, 
 
 Fig. 42. 
 
 and full of opaque spots. There were few haemorrhages in the cortex 
 of the right kidney. 
 
 Sections show mostly chronic, but also some recent, glomerulo- 
 nephritis (intra-capillary ) ; large areas of cellular infiltration and fibrous 
 thickening of the connective tissue with atrophy of tubules : few granu- 
 lar leucocytes ; little blood in tubules : granular and fatty degeneration 
 of the epithelium, moderate number of casts: much hyaline underneath 
 endothelium in several small arteries : marked "endarteritis" of the small 
 arteries and moderate "arteriosclerosis'" of the larger ones. Xo jjatho- 
 genic bacteria were seen in sections.
 
 KIX'IIKI) (IF ( ASIiS 
 
 79 
 
 Case 22. Chronic glomeriilo-nephriiis in man of 42 years with old 
 tuberculosis and continued suppuration of the lymph-glands 
 of the neck. 
 X\'ll. 184. — K. .M., poorly nourished Scotcii clerk, 42 years of age. 
 
 Patient had had chronic tuberculosis of lym])h-glands of neck since 
 childhood, which necessitated twelve operations. I'^or the last three 
 years before entrance he had had occasional nycturia: for the past three 
 weeks he liad lu-en casiK' fatigued, and siirfrred fnini indii/csliun : ;ind 
 
 I'iH. 4X 
 
 for the ])ast ten days he noticed shortness of breath, ccdema ol legs, and 
 oliguria. On clinical examination he showed a very marked dyspnoea 
 and cyanosis, very pcjor teeth, slight enlargement of heart, a soft systolic 
 murmur at apex, petechiae on right arm and left thigh, marked oedema 
 of lower extremities. The ])erii)heral arteries appeared sclerotic. Later 
 he develo])ed pericardial friction and signs of ])leurisy. Towards the end 
 the patient was very dyspnoeic and drowsy, sometimes delirious, and 
 showed muscular twitching. Me died in uraemic coma. Me was anaemic 
 (3,ir)0,ooo reds: (12'/, llti. »: he had a leucocytosis (14-25,000 leiico- 
 cvtes. go'; neutroiihiles 1 . Mis li!oo(l-|iressiu-e varied from 2(X) to 235.
 
 I'-iR- 45.
 
 RIXOKl) OK CASKS 81 
 
 ilis temperature was subnormal (97 I'"), witli rises to 99^ I". His urine 
 while at hospital was scanty, of low sjiecific Ljravity, and contained much 
 allntmin. many hyaline. e]>ithclial. and i^ranular casts: no hlood was 
 found. 
 
 Necropsy revealed numerous old scars on necU and slii^ht remnants 
 of old tubercular infection, recent haemorrhaiijic dii)lostreptococcic peri- 
 carditis and pleurisy, broncho-pneumonia. The heart was one and one- 
 half times normal size (left ventricle averaged 14 mm. 1. The renal 
 arteries were moderately sclerosed, the others [iractically normal. 
 
 The kidneys were small ( 10 .\ 4 x _^ cm.), the capsule firmly ;iilher- 
 ent. surface granular, small haemorrhages in cortex, which was much 
 reduced (4 mm.). The markings were indefinite. 
 
 Sections showed chronic glomerulo-nephritis in the majority of the 
 glomeruli : more recent changes in a few : diffuse cicatrization with 
 small areas of cellular infiltration; few granular leucocytes; many casts 
 in collapsed tubules; leucocytes in some of the tubules; little cjjithelial 
 degeneration ; hyaline in few small arteries ; marked "endarteritis" in 
 many small arteries; marked "arteriosclerosis" in few small and all 
 larger arteries. Xo pathogenic bacteria were found in sections. 
 
 Case 23. Chronic glomerulo-nephritis in man of 55 with chronic en- 
 docarditis. 
 X\ 11. iiO. — J. 11.. well nourished Canadian sailor. 55 years of age. 
 
 Patient had repeated attacks of tonsillitis, was in hospital three years 
 before death for rheum.atism ; reentered shortly before death w-ilh acute 
 rheumatism of hands. There was no history of syphilis. The Wasser- 
 mann reaction was negative. Patient had "epileptic" attacks at various 
 times, last one three months before death, lie comi)lained of shortness 
 ot breath, increasing dimness of vision, cram])s in legs, and deep pains 
 ill bones. I le never had any oedema. 
 
 Clinical examination showed marked nervousness, hacking cough, 
 contr.uture in left leg. arteriosclerosis of radial artery, heart within 
 normal limits, a soft systolic murmur, no oedema. The backgrounds of 
 his eyes showed small, slightly tortuous arteries, otherwise they were 
 normal. Towards the end he had bleeding from nose and mouth, vom- 
 ited daily, .md developed uraemic coma. His blood-pressure varied from 
 190 to 2io. lie had a severe anaemia (2.150.000 reds; 30% lib. aniso- 
 cytosis ). no leucocytosis. 1 lis temperature was subnormal. His ])idse rate 
 varied between 70 and 95. His lu'ine was scanty, of low specific gravity,
 
 82 
 
 TFIK I'ATIIIII.OCN- (IF X i;i' 1 1 U ITl.'; 
 
 C(intaiiR'(l mucli alluimin. many i^rannlar casts, few leucocytes, few red 
 cells. 
 
 Necropsy revealed an old endocarditis of the mitral \al\'e. Tlie 
 heart was somewhat enlarged. There was a terminal hroncho-imeii- 
 
 monia. The radial artery showed a marked arteriosclerosis : the cjthers 
 were much less involved. 
 
 The kidneys were small and pale : the capside adherent, surface 
 granular, cortex narrow, full of cysts. 
 
 Sections show chronic glomerulo-nephritis in many glomeruli ( intra- 
 capillary), more recent lesions in few; very extensive cicatrization of 
 cortex with much cellular infiltration : few granular leucocytes ; much 
 epithelial degeneration and many casts ; leucocytes in few tubules ; mucli 
 subendothelial hyaline in many small arteries ; marked "endarteritis'" in 
 most small arteries, more "arteriosclerotic" lesions in others ; very 
 marked "arteriosclerosis" of larger arteries. No pathogenic bacteria 
 were found in sections.
 
 KI-UOKl) UK BASICS 
 
 83 
 
 Case 24. Chronic practically healed glomerulo-nephrilis in man of 61 
 
 with old history of rheumatism. 
 X\ II, \(>4.- I), (i., emaciated I'rciicli male cnoU. ()i years of atje. 
 
 Patient had rheumatism w lun he was yoimg. lie denied all venereal 
 disease. His present illness liei^an two years as;o with loss of weijjfht 1 ,^5 
 lbs.), shortness of hreaih, and iiicreasinj; weakne^s. lie had to void his 
 urine at night two to ihree times. 
 
 Clinical examination showed a marked puffiness of skin about eyes, 
 much dyspnoea, coated tonnne. and fmil breath, enlarged heart, a rough 
 
 .-^^S^liv^^i 
 
 systolic and faint diastolic murmur o\er the heart. 'I'lie rhythm of the 
 heart was absolulel\ irregular. Mi-- li\ei- was enlarged. His blood- 
 pressure on entrance was 170. later u;ra<luall\ went down to 137. I'atient 
 had no marked oedema at any time, lie had a severe anaemia (3.500,- 
 000 reds and 4S' ; lib. 1. also a slight leueoeytosis ( I4,C)(X)). The VV'as- 
 sermann reaction was negative. The urine was scanty at first, later 
 about normal in (|uautity. The specilie gravity was about loio. It 
 contained e(jnsiderable .albiunin. ami at times many granular casts and 
 red cells. The patient at no time showed detinite symptoms of uraemia. 
 lie died with the clinical symptom> of an acute i)ulmonary infection.
 
 84 
 
 THK l'ATll()|.(li;V OF NKI'Il RITIS 
 
 Necropsy revealed marked general arteriosclerosis, a very marked 
 enlargement of the heart (about three times normal size), small scars 
 in heart muscle, gouty deposits in kidneys and toe joints, a terminal 
 broncho-pneumonia, beginning cyanotic atrojihy of liver. 
 
 The kidneys were small ( lo'/j .\ 4 x 4 cm. ) : the capsule stripped 
 easily. The surface was coarsely granular. The cortex was much re- 
 duced, and the markings were very indistinct. 
 
 Sections show chronic glomerulo-nephritis in many glomeruli with 
 large areas of cicatrization in cortex, comparatively little cellular infiltra- 
 tion, few granular leucocytes : subacute glomerulo-nephritis ( intra-cap- 
 illary ) in few glomeruli ; leucocytes in few tubules ; little epithelial de- 
 generation ; very marked "arteriosclerosis" of large and small arteries. 
 Xo bacteria were found in sections. 
 
 Case 25. Chronic glomerulo-nephritis, in man of 60 years, of unknown 
 
 etiology. 
 XVni, 108. — T. H. D., poorly nourished man, 60 years of age. 
 
 No history could be obtained on account of the condition of the 
 
 patient. Patient entered the hospital in a delirious condition. He showed 
 a coarse tremor of the extremities, a jerking of the head, and consider-
 
 Uli liKli 111- I ASKS 85 
 
 alilt,- ri^itlity of tlic m-ck. Tlu- rt-lloxes were exaggeratetl. Tliere was an 
 infected wduiul (i\er the iicri|nit. I lis tem])eratiire ranj^ed between 9//)° 
 and yy.5 i'. J lis pulse was Jiiiili and irregular. He had no oedema, lie 
 died three days later in coma. 
 
 Necropsy revealed a hejjinninj^ ])rostatic hypertrophy and terminal 
 hroncho-pneumonia. His heart was of normal size. There was a slight 
 concentric hypertrophy of the left \entricle. .\11 arteries, the aorta and 
 cerebral vessels included, showed a marked arteriosclerosis. 
 
 The kidneys were small t').~ .\ 4 \ J.^i. The capsule stripped with 
 dil'licnJiy. The surface was granular. Tlie cortex was narrow and 
 opa<|ue. There were no \isilile JiaemorrhaLjes. 
 
 .Microscopical sections sjiowcd very extensive (jld i^lonierulo-nephritis 
 of many glomeruli, much cellular infiltration and fibrous ihickeninjj; of 
 tlie connective tissue with atro])hy of L^roujis of tubules, much epithelial 
 detjeneration. many casts and leucoc\tes in tubules, considerable \n<^- 
 mentation of the epitliehinii. 'i'lie arterioles and llic lari.;er arteries 
 sliowed a \er\- marked "arteridsclerdsis." 
 
 Case 26. Chronic glomerulo-nephritis, in man of 54 years, of unknown 
 
 etiology. 
 Will, ly. — S. G., emaciated Irish teamster, 54 years of age. 
 
 I'atient did not recall any diseases except measles in infancy. He 
 was a heavy beer drinker. He had gonorrhoea at 35, denied lues. Five 
 years before death he became dropsical for the first time ; he had another 
 attack one year ago, associated witli "rheumatism." He comjilained of 
 dropsy, shortness of breath, |ial|iitaIions. and jirecordial pain, heailache, 
 and [jains in legs. 
 
 t'jinical examination showed marked drowsiness, marked oedema of 
 face, coated tongue, poor conditiim of few lemaining teeth, enlargement 
 of heart, distant heart scninds but no definite murmurs, ascites, general 
 oedema. Towards the end he became delirious, and died in uraemic 
 coma, llis blood-pressiu'e \aried between icjo and 210. He had some 
 anaemia 178'; Mb. 1. no leucocytosis. llis temperature was normal and 
 at times subnormal, llis pulse rate varied between 80 and 130. His 
 urinary output \aried between 1400 and 2500 ccm. daily. The s])ecific 
 gravity was low. Tlie urine contained a heavy cloud of albumin, occas- 
 ional hyaline casts, few leuc<)C\tes. no blood. There was practically no 
 excretion of i)henolsul])hone-i)hthalein. 
 
 Xecrojisv revealed a slightly enlarged heart ( left \entricle avera.ged 
 I J mm. I. marked arteriosclerosis of coronaries and of all abdominal 
 .arteries, c\anotic atrojibv of the liver, much oedema, ascites and hydro-
 
 86 
 
 THK I'ATIIOl.OCY ()!•• N'EI'IIRITIS 
 
 thorax, recent haemorrha,t,MC iiericarditis without bacterial finding-.s. He 
 also had f^outy joints. 
 
 The kidneys were small ( 8>2 x 3,!-.. x 3 cm. 1 : the capsule was thick 
 and adherent : the surface granular. The corte.x was much reduced (to 
 about 3 mm. 1 and full of c}sts ; the markings were poor. 
 
 Sections showed chronic glomerulo-nephritis in man}- anrl subacute 
 lesions in few glcmeruli ; large areas of cellular infiltration and fibrous 
 
 thickening of the connective tissue with atro])hy of the tubules ; moderate 
 infiltration with neutrojihilic leucocytes, few eosinophiles and basophiles ; 
 slight epithelial degeneration, many casts in atrophic tubules : subendothe- 
 lial hyaline in few small arteries : marked "arteriosclerosis" and "en- 
 darteritis" in small arteries, marked "arteriosclerosis" in large arteries. 
 No bacteria were found in sections. 
 
 Case 27. Chronic glomerulo-nephritis in man with old "malaria" and 
 
 terminal septic lesions. 
 X\'II, 82. — C. S.. well nourished .\merican male nurse, 31 years of age. 
 The history is imperfect. "He had "malaria" two and one-half years 
 ago which was recurrent." He had syphilis at the age of 26, and sev- 
 eral attacks of gonorrhoea.
 
 OS Till-: IV\TII(i|.n(i\- III" NKI'IIRITIS 
 
 Necrop.sy rc-\calcd an ulctralivu diplcjstreptococcic stomatitis, an 
 acute suppurative pericarditis without bacterial findings, and an acute 
 endocarditis of the mitral valve. 'J'he heart was one and one-fourth 
 times normal size, and the left ventricle averaged 15 mm. There was a 
 marked arteriosclerosis of the aorta, coronaries, splenic, renal, and cere- 
 
 bral arteries. The liver showed cyanotic atrophy with compensatory 
 hypertrophy of the peripheral parts of the lobules. 
 
 The kidneys were small (8^4 x 4 x 3 cm.) and granular, showing 
 grey spots on a red background. There were many haemorrhages in 
 the cortex. The latter was nuich reduced. Some gouty deposits were 
 found in the pyramids. 
 
 Sections showed chronic glomerulo-nephritis of most glomeruli and 
 more subacute lesions (intra-capillary ) in a few; almost total destruc- 
 tion of the cortex by fibrosis, much cellular infiltration ; few granular 
 leucocytes ; blood and leucocytes in many tubules, much epithelial degen- 
 eration, many casts : "endarteritis" in few small arteries, very marked 
 "arteriosclerosis" in the rest. No bacteria were found in sections.
 
 Ki;C()Kl> OK CASKS 
 
 89 
 
 Case 28. Chronic glomerulo-nephritis in man of 24 years with chronic 
 
 endocarditis. 
 W'll. 149. — L. A., well noiirislied Italian hoxniakc-r, 24 years i)f a^e. 
 
 The patient's general health had heen good until one year he fore his 
 death, when he had rheumatism in feet and hands. His present illness 
 started four months ago with ejiistaxis. shortness of hreatii and jiain in 
 the epigastrium. 
 
 Clinical examination showed continued iiieeding from nasal mucous 
 membrane, a heavily coated tongue. \ery marked dyspnoea in si)ite of 
 comparatively little circulatory disturhance ( m'aeniic air hunger 1. mod- 
 
 erate dilatation of the heart towards the right, a i)resystolic murmur, nor- 
 mal rate and rhythm of heart beat. Patient had no oedema at any time. 
 He had a severe anaemia (3,100.000 reds: 48'^ lib. > : towards the end 
 much leucocytosis (39,600; c;3^r neutrophiles ). llNind culture was nega- 
 tive. His temperature was subnormal. I'^or the last one and one-half 
 months he voided urine four to five times at night. It was <if low 
 s]>ecific gravity (loii) and contained much albumin: no casts. ( (Jne 
 examination, as patient was in hosj)ital one day only. I No coma.
 
 tig. 54- 
 
 I'lg^ 55.
 
 RKlOKI) OK lASKS 91 
 
 Xfcro]isy revcali'<i an did cnilncarclitis of tlif mitral \al\i- with iinid- 
 t-rate stenosis (no bacteria loundi. recent ai)|)arently emliolic imstiilcs on 
 chin and left liand. a heart of normal size on tlie left, slight dilatation 
 on the rii,dit side; an old primary tnbercidosis of the intestines and of 
 tile mesenteric lymi)h-_t;:lan(ls. The arteries were normal. 
 
 'VUe kidneys were small (9J/2 x 4>4 x 3 and 7 x 4 x 2'/^ cm., res])ec- 
 tivel\ I. I'he ca]isiile was adherent: snrface coarsely ijranular, cortex 
 very narrow, o[)a(|ue, very liijht in color, almcjst yellow. 
 
 Sections show chronic £;lomeriilo-ne])hritis in many glomeruli, more 
 recent changes ( intra-ca|)illary ) in few; large areas of fibrosis with 
 atrophy of tubules: few areas of cellular inl'iltration : considerable num- 
 ber of eosinophiles. fewer ueutrophiles and basophiles; many casts, few 
 leucocytes in some liiimles: little ei)ithelial degeneration: marked "en- 
 darteritis" of small arteries, slight "arteriosclerosis" of the larger ones. 
 Xo bacteria were found in sections. 
 
 Case 29. Chronic glomerulo-nephritis in man of 59 years with pos- 
 sibly old septic focus in urinary tract. 
 .\\ 1. iH'). — S. (i.. emaciated Chinese male cook. 59 years of age. 
 
 The history is incomplete, because patient did not speak English, 
 lie had noticefi puffiness of the face, shortness of iireath. paljiitation and 
 pain over heart, and swollen legs for the last four to live months. He 
 vomited occasionally, liut had no headaches. Clinical examination 
 showed poor teeth, a normal heart, and oedema of the lower extremities, 
 lie had a \ery marked anaemia (2,iC)o,cxx) reds: 35'/? 111).), no leuco- 
 cytosis. I lis temi)eratnre was subnormal. His pidse rate varied between 
 60 and 80. The urine (one examination) contained a moderate amount 
 of albumin, no casts, many epithelial cells, and few leucocytes. 
 
 .Xecropsy revealed a small heart, normal arteries excejjt some ather- 
 f)ma of the aorta and moderate arteriosclerosis of the renal arteries, 
 beginning cyanotic atrophy of liver, general oedema, marked ascites and 
 Indrothorax : gouty deposits in ears, basal joints of great toes, and kid- 
 neys : i)urulent cystitis and prostatitis. 
 
 The kidneys were very small (S x 3>4 x 2]/: and 7 x 3'-< x 2'/; cm., 
 respectively) : the capsule was adherent, the surface granular, the cortex 
 very narrow {2-^ mm.). 
 
 Sections showed chronic glomerulo-nephritis of most glomeruli, 
 more sub-acute lesions ( intra-capillary ) in others, considerable hyaline 
 necrosis in affected glomeruli : very extensive cicatrization of cortex
 
 i<"ig- 57.
 
 Ki:a)KI> OK I ASK: 
 
 93 
 
 with some ureas of cellular infiltration; very few tjranular leucocytes; 
 inticli epithelial defeneration; very many casts, hinod in some tuhules; 
 
 very marked ''arteriosclerosis" of the small arteries, less in the lartje ones. 
 Xo pathos;;enic bacteria were found in sections. 
 
 Case 30. Chronic glomerulo-nephritis in man 38 years of age with 
 a history of repeated attacks of tonsillitis. 
 .\\ . ,^,V — I. C'.. stronsjly liuilt l)oilermaker and bartender. 38 years old. 
 
 Patient had been subject to strain and bad weather for twenty-five 
 years, lie had frequent attacks of sore throat and many colds. lie li.id 
 used alcohol to c.xcess. lie had ijonorrhoea and chancroid at 24. When 
 he was 30 he had an attack of "rheumatism" in the risjlit great toe; 
 about one year before his death he had "rhciunatism" in .several joints 
 and facial palsy following i)ain at base of skull. Clinical examinatinn 
 showed marked anaemia, coated tongue, bad teeth, heart within normal 
 limits, no murmurs. No oedema. At the hospital he had a fit of "epi- 
 lepsy." lie had a suspicious Wassermann reaction. His blood-|)ressurc 
 was iTio. He had a severe anaemia (2.700,000 reds; .^3% HI), no leucn-
 
 94 
 
 •IHI-; l'.\Tll()l,()l;^ (ii-- .\i:i'i iritis 
 
 cytosis). His temperature was .slij;htly sulmormal. Ills pulse rate 
 varied from 84 to too. The last three days he had coiUiiiued epistaxis. 
 He had to void urine fre(|uently and to get up several times at nii^ht. 
 L'rinanalysis (one examination) showed specific gravity of 1023, no 
 albumin, few granular casts, leucocytes and erythrocytes. 
 
 Necropsy revealed purulent bronchitis and broncho-pneumonia. 
 haem(jrrhagic pleurisy and pericarditis. The heart was slightly enlarged 
 
 I'iy. .SQ. 
 
 I left ventricle averaged 12 mm.). The blood-vessels were practically 
 normal. There were gouty deposits in toe joints and kidneys. 
 
 The kidneys were small (9/^ x 4 x 2J/2 cm.) and granular. The 
 cortex was much reduced, and the markings were indefinite. 
 
 Sections show chronic glomerulo-nephritis in the majority of the 
 glomeruli, more subacute lesions (intra-capillary ) in the few remaining 
 ones, very marked dififuse cicatrization of cortex — with little cellular in- 
 filtration : few small, fairly intact areas of kidney tissue ; much epithelial 
 degeneration, many small epithelial cysts; blood and leucocytes in few- 
 tubules ; hyaline masses in few small arteries ; marked "arteriosclerosis" 
 of many arterioles ; moderate "arteriosclerosis" in larger arteries.
 
 RKl(lKl) OF (.ASKS 
 
 95 
 
 Case 31. Chronic glomerulo-nephritis in woman of 28 years with old 
 ulcer of tonsil and chronic diplostreptococcic infection 
 of urinary tract. 
 X\ 11. ()8. — Mrs. Li. li., emaciated .\mcricaii domestic, J8 year.s of age. 
 I'atient had always been in poor health: had "La (jrippe" as a girl; 
 iiad liad chronic catarrh for many years. Nine years before death ap- 
 pendectomy was performed for acute ai)])endicitis. She had kidney 
 
 I'it;. (n 
 
 trouble while carrying her first child, live years before death, again when 
 carrying the second. About one year before death she noticed pro- 
 gressive debility with anorexia and vomiting. A little later she had some 
 attacks of violent delirium with comi)lete unconsciousness. She voided 
 much ])ale urine. For the last seven months she had headache, vomiting, 
 jerking and cramjjs in legs, palpitations of the heart, progressive weak- 
 ness and loss of weight. i>n)gressive amaurosis, and at times oedema of 
 the feet ; towards the end jjatient was very noisy, restless, and delirious.
 
 FiK. 6i. 
 
 Mg. 6.
 
 Kit 111(11 (II- CASKS 97 
 
 llcr ton,mic was heavily coated and lur luealli uiainiic. I icr tfm|KT- 
 atiire was normal, her pulse varied i^reatly (l)etweeii So and uoi. 
 Ophthalmoscopic examination showed an albiiniinnric retinitis. Her 
 hiood-])ressiire was 185. She died in uraemic coma. She had a marked 
 anaemia {2,700.000 reds; 40';} Hb.), some lencocvtosis (14.000), 867^, 
 nentrophiles. The W'assermann reaction was netjalive. The phenolsnl- 
 phone-phthalein excretion was diminished (i. hour 5'/; ; 2. hour 25% I. 
 The urine was increased in (|nantity. nf Inw si)ecific gravity ( loio or 
 less), contained much alliuniiii (tn _>' , 1, occasional showers of casts, 
 few red cells, and few leucocytes. 
 
 Necropsy revealed a heart aliout one and une-hall tinu> normal size 
 I left ventricle averatjed about 11 mm.), normal blood-vessels, an old 
 ulcer of the tonsil, chronic diplostreptococcic cystitis and i>yelitis ( diplo- 
 streptococci also found in risjht kidney 1. liaeniorrhaLjic tlnid in both 
 pleurae and terminal broncho-pneumonia. 
 
 The kidneys w'ere very small, cspeciall\' in aniercj-posterior diameter 
 (9x4x3 cm.), coarsely granular, full of lar<;e retracted scars: the 
 cortex was very narrow and full of opaque spots. 
 
 Sections showed mostly chronic ^[^lomerulo-neijliiitis. more recent 
 lesions in few t^lomeruli (intra-capillary ) ; large areas of cicatrization 
 with much cellular infiltration : few granular leucocytes ; moderate epi- 
 thelial degeneration : many casts, blood and leucocytes in some tubules : 
 marked "arteriosclerosis" of small, less so of large arteries. No Ijacteria 
 were found in >cctions. 
 
 Case 32. Chronic glomerulo-nephritis in man of 24 years with in- 
 definite septic history. 
 X\'. <>/. — (i. .\., emaciated Canadian jockey, 24 years of age. 
 
 History imperfect. Patient when a boy had "malaria" several times, 
 a definite attack of rheumatism one year before death. When n; he had 
 a chancre without secondaries, lie had been losing weight, had fre(|uent 
 nose-bleed, and was markedly anaemic. His tem])erature was subnormal. 
 
 Necropsy revealed a rather small heart, normal blood-vessels, slight 
 ascites, more marked hydrothorax, no subcutaneous oedema, and terminal 
 lironcho-pneumonia. 
 
 The kidneys were very small ( 8J4 x 3>< x 2 and 7J/2 x 3>^ x 3 cm., 
 respectively) : the cajisule was firmly adherent; the corte.s was thin and 
 opaque, and full of yellow sjxits.
 
 Fig. 6,v 
 
 Fig. 64.
 
 UKlOKIi (IF lASi;s 'W 
 
 Sections sliowcci clironii- i;l()iiu-nilc)-iu-|iliTiiis of piairtically all glom- 
 eruli, — much hyaline in the affccled s^iunieruii ; almost complete destruc- 
 tion of cortex by cicatrization, many lari;e areas of cellular inliltration ; 
 much epithelial degeneration, moderate numher of casts, blood, ancl 
 leucocytes in some tubules ; moderate "endarteritis" and "arteriosclerosis" 
 in small \essels, slight "arteriosclerosis" in large ones. The sections 
 were too badly contaminated to ])ermii of bacteriological examination.
 
 SUMMARY OF CASE 
 
 Sex and 
 Age 
 
 Etiology 
 
 Condition of Kidney 
 
 I. xvii, 60 M,5J 
 
 2. XVII, 31 
 
 3. xvii. 188 
 
 4. xviii, 158 
 
 Mo4 
 M.4I 
 F, 33 
 
 Diplostreptococcic 
 
 endocarditis. 
 Diplostreptococcic 
 
 endocarditis. 
 Diplostreptococcic 
 
 endocarditis. 
 Streptococcic 
 
 ulcers of legs. 
 
 Swollen, opaque, few haemorrhage! 
 
 6x3) 
 Xormal size, many haemorrhages 
 
 Much swollen, opaque, few haemo 
 
 (13x7x4;/;) 
 Distinctly swollen, hv|ieracmic, oede 
 
 (12^^x6x4/2) 
 
 11. SUBy^ 
 
 5- 
 
 xviii, 
 
 166 
 
 F, 
 
 33 
 
 Diplostreptococcic 
 endocarditis. 
 
 Swollen, many Iiaemorrhages (I2x 
 
 6. 
 
 xvi. 
 
 56 
 
 F,2 
 
 nio. 
 
 Colon bacillus 
 pyelitis. 
 
 Swollen, opaque 
 
 7. 
 
 xvii. 
 
 163 
 
 M 
 
 40 
 
 Diplostreptococcic 
 endocarditis. 
 
 Swollen; cortex wide, opaque, m.mj 
 orrhages 
 
 8. 
 
 xiv. 
 
 34 
 
 M 
 
 4.T 
 
 Streptococcic 
 infection. 
 
 Swollen, opaque, mottled, many 1 
 rhages (12x7x4) 
 
 9- 
 
 XV, 
 
 135 
 
 M 
 
 33 
 
 Diplostreptococcic 
 endocarditis. 
 
 Xormal size, cortex wide, opaque 
 haemorrhages 
 
 10. 
 
 xviii. 
 
 106 
 
 F. 
 
 -7 
 
 Abscess of jaw. 
 
 Xormal size, cortex wide, yellow, 
 
 1 1 
 
 xvii. 
 
 119 
 
 M 
 
 51 
 
 Diplostreptococcic 
 endocarditis. 
 
 Swollen, many haemorrhages, cortex 
 
 ij. 
 
 x\iii. 
 
 61 
 
 F. 
 
 26 
 
 Tonsillitis 
 
 Slightly reduced in size, many 1 
 rhages ( io"4 x 4'S x 3) 
 
 III. SUBACUTE AND CHR 
 
 i^. xvi, 190 
 
 F, 8 
 
 Infectious aneu- 
 
 Rt. kidnev swollen, pale, opaque ; U 
 
 
 
 rysm, diplostrep- 
 
 traded (8 x 4 x 3'<) 
 
 
 
 tococcic. 
 
 
 14. xvii, 17 
 
 F, ID 
 
 Tonsillitis. 
 
 Small, granular (6x3x2; 9 x 4 x 3 
 tex narrow 
 
 15. XV, 120 
 
 M, 6 
 
 Streptococcic cys- 
 titis :ind pyelitis. 
 
 Small, with large deep scars
 
 ,ERULO-NEPHRITIS 
 
 ;rl'lo \i;i'iiKiTis 
 
 idilion of Urine 
 
 Hypertension and 
 Cardiac Hypertrophy 
 
 Arterioscle- 
 rosis, Local 
 and General 
 
 Oedema Uraemia 
 
 Retinitis 
 albu- 
 min- 
 uricB 
 
 Anae- 
 mia 
 
 r,M, Erylhro- Leuco- 
 '''^'^ [ cytes 1 cytes 
 
 .^. 
 
 - - 
 
 _ 
 
 I0C.+ 
 gen.+ 
 
 card. 
 
 - 
 
 - 
 
 + 
 
 _ _ 
 
 — 
 
 1 I0C.+ 
 
 card. 
 
 _ 
 
 _ 
 
 ■H 
 
 
 
 
 ■ gen.+ 
 
 
 
 
 
 
 — — 
 
 — 
 
 I0C.+ 
 gen- 
 
 4+ 
 
 — 
 
 — 
 
 > 
 
 ■HH- 1 — 4-H 
 
 — 
 
 I0C.+ 
 gen.- 
 
 + 
 
 — 
 
 — 
 
 « 
 
 ■Il'LO XICPllRITl 
 
 s 
 
 
 
 
 +++ 
 
 +++ +++ 
 
 - 
 
 loc- 
 gen.- 
 
 + 
 
 + 
 
 - 
 
 ++ 
 
 
 — — 
 
 — 
 
 loc- 
 gen.- 
 
 + 
 
 — 
 
 — 
 
 — 
 
 
 ~ — 
 
 — 
 
 loc- 
 gen.- 
 
 + 
 
 — 
 
 — 
 
 + 
 
 
 
 SI. livi)ort. of left 
 
 I0C.+ 
 
 + 
 
 — 
 
 — 
 
 ■H- 
 
 
 
 ventricle? 
 
 geii.+ 
 
 
 
 
 
 
 ■\-^ ++ 
 
 " 
 
 loc- 
 gen.- 
 
 4- 
 
 — 
 
 — 
 
 ++ 
 
 -H+ 
 
 ++ ++ 
 
 I?. I'. 170; 11. si. h. 
 
 I0C.+ 
 gen.- 
 
 ++ 
 
 — 
 
 
 
 +++ 
 
 ++ , -H- 
 
 H. F. -'00 ; H. 2x 
 
 I0C.+ 
 gcn.+ 
 
 + 
 
 — 
 
 — 
 
 -H- 
 
 +++ 
 
 4+ ++ 
 
 H. I'. 180: 11. n. 
 
 loC.-H- 
 
 gcn.-H 
 
 +-+ 
 
 ^ 
 
 ( 
 
 4-(- 
 
 ^ULO-NI£PHRITI 
 
 S IN" CHILDREN'. 
 
 
 
 
 + 
 
 — 
 
 P. I' 140: H. 2x 
 
 loc- 
 gen.- 
 
 
 - 
 
 
 + 
 
 + 
 
 + — 
 
 H. 1' 150: H. 2x 
 11 hyp Irft 
 
 I0C.+4 
 gcn.- 
 
 
 
 1 

 
 IV, cm 
 
 Case No. 
 
 Sex and 
 Age 
 
 Eliolooy 
 
 Condition of Kidney 
 
 l6. xviii, 170 
 
 M.S3 
 
 Diplostreptococ- 
 
 Normal size, slightly granular, r 
 
 
 
 cus sepsis. 
 
 some haemorrhages 
 
 17. xvi,257 
 
 M.48 
 
 Rheumatism. 
 
 Normal size, granular 
 
 18. xvi. 212 
 
 M.45 
 
 ( ?) History imperf. 
 
 Small (11x5.x 3). many haenior 
 cortex narrow 
 
 19. xvi, 10 
 
 M,37 
 
 Diplostreptococ- 
 
 Small (lOxSy-S'A), mottled; cort 
 
 
 
 cus sepsis ( ?). 
 
 row, opaque 
 
 20, xviii, 167 
 
 M,3S 
 
 Tonsillitis. 
 
 Small (9>^x4!/i x3!^), pale; cort 
 row, opaque 
 
 21. xvi, 260 
 
 F, 36 
 
 Old infection with 
 
 Small (9x5x3), granular, cortex 
 
 
 
 influenza-bacilli 
 
 opaque, few haemorrhages 
 
 22. xvii, 184 
 
 M,42 
 
 Chronic tuberculo- 
 
 Small {10x4x3), granular; cortt 
 
 
 
 sis and suppura- 
 
 row, few haemorrhages 
 
 
 
 tion of glands 
 
 
 23. xvii. 1 16 
 
 M,5S 
 
 Old endocarditis 
 
 Small, pale, granular; cortex narrow 
 
 24. xvii. 164 
 
 M,6i 
 
 RlicuTuatism 
 
 Small ( io.'/l> X 4 X 4) , granular ; cort 
 narrow- 
 
 25. xviii, 108 
 
 M,6o 
 
 ( ?) \o history 
 
 Small ( 10 X 4 X 2'/,), granular ; cort 
 row, opaque 
 
 26. xviii. 19 
 
 M,54 
 
 (?) 
 
 Small (8i4x3!^x3), granul.ir; 
 narrow, cystic 
 
 27. xvii, 82 
 
 M,3i 
 
 ( ? ) History imperf. 
 
 Small (8'<ix4x3), granular; many 
 orrhages 
 
 28. xvii, 149 
 
 M,24 
 
 Old endocarditis 
 
 Small (8x4x3), granular; cortex 
 pale 
 
 29. xvi, 189 
 
 M,59 
 
 ( ?) History imperf. 
 
 Small (8x3x25^), granular; cort 
 narrow 
 
 30. XV, 33 
 
 M,38 
 
 Tonsillitis 
 
 Small (9^/2x4x2;/^), granular; 
 very narrow 
 
 31. xvii, 68 
 
 F, 28 
 
 Tonsillitis 
 
 Small (9x4x3), granular; corte 
 narrow 
 
 32. XV, 97 
 
 M,24 
 
 Old sepsis suspected 
 
 Small (S'/zx 3'A x2). granular; 
 very narrow 
 
 Key to abbicviations : M, male ; I*", female ; P, polyuria ; B. P., blood-p 
 +-H-, marked ; — , negative ; ?, unknown or questionable. All measui
 
 •.RLU)-.\l-:i'llKI I IS 
 
 edition of Urine 
 
 c«ts ^'!^'°- 
 
 I cytes 
 
 Hypertension and 
 Leuco- Cardiac Hypertrophy 
 cytes 
 
 Arleriosclc- 
 
 rosis, Local lOedema Uraemia 
 
 and General 
 
 Retinitis 
 albu- Anae- 
 min- I mia 
 urica 
 
 + ! ++ -H- 
 
 1 1 
 
 (?) 11. iKx 
 
 loc.-H- 1 ' 
 
 gcn.-f 
 
 
 - 
 
 
 B.P. joo: H. 2x 
 
 loc.H- 
 sen.-H- 
 
 
 ? 
 
 — — 
 
 B.P. .'50 : H. i''4X 
 
 loc.-t^+ 
 ;. en.-H- 
 
 
 •f 
 
 — 
 
 R.P. i8.': H. iVSx 
 
 loc.-r-i- 
 gen.- 
 
 
 — 
 
 
 li.r 115; H. i'Ak 
 
 loC.-r 
 
 gen.- 
 
 
 — 
 
 
 W.V. 180; M. i''2X 
 
 loc.-H- 
 
 gCMl.- 
 
 
 — 
 
 
 l!.P. 230; n. I'/'X 
 
 loc.-H H 
 gcn.- 
 
 ■f 
 
 — 
 
 
 R.P. 200: H. I'ix 
 
 loc.(-f! — 
 
 iicn.i 
 
 + 
 
 — 
 
 
 R.P, 170: H. .?x 
 
 lor.-i4- -I 
 gen .+-H- 
 
 — 
 
 — 
 
 
 R.P. (?): H. n. 
 
 loc.-t-H- — 
 gcn.-H-+ 
 
 + 
 
 — 
 
 
 R.P. 200: II. i'/4X 
 
 loc.-H-f + 
 gen.-H-l- 
 
 + 
 
 — 
 
 
 B.P. ( ?) ; H. i'4x 
 
 loc.-H-H ? 
 geii.-H- 
 
 5 
 
 — 
 
 
 B.P. (?); H. n. 
 
 Ioc.4-f — 
 gen.- 
 
 — 
 
 — 
 
 
 I'..P. ( ?) : H. sm. 
 
 loc.-H-i- -H 
 gcn.-h 
 
 + ? 
 
 — 
 
 
 R.P. 160; 11. i^x 
 
 10C.-H4 i — 
 gcn.- 
 
 ^- 
 
 — 
 
 
 R.P. 1S5: H. iV^x 
 
 loc.H -1 
 gcn.- 
 
 •H- 
 
 ■h 
 
 
 R.P. ( ?) : 11. sm. 
 
 I0C.+ ' + 
 Bcn.- 
 
 > 
 
 — 
 
 ^'cncral ; c.-irfl. cardiac. i. slight; 4-f. inodcrato ;
 
 The Birds of the Latin Poets. Ernest Whitney Martin, Associate 
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 Accei.er.\tion in the Development of the Fossil Cephalopoda. 
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 1914. Price, 75c. 
 
 A Morphological Study of Some Members of the Genus Pallavi- 
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 Anglo-Saxon America. Manuel de Oliveira Lima, Minister of 
 Brazil to Belgium. 160 pp. 1914. Price, $1.00. 
 
 The Hemolymph Nodes of the Sheep. Arthur William Meyer, Pro- 
 fessor of Anatomy. 74 pp., i plate, 4 colored plates. 1914. 
 Price, $1.00. 
 
 An Introduction to the Study of the Endocrine Glands and Inter- 
 nal Secretions. (Lane Medical Lectures.) Sir Edward Schafer, 
 Regius Professor of Physiology in the University of Edinburgh. 
 94 pp. 1914. Price, 75c. 
 
 The Pronoun of Address in English Literature of the Thirteenth 
 Century. Arthfir Garfield Kennedy, Instructor in English Phi- 
 lology. 91 pp. 1915. Price, $1.00. 
 
 The Anoplura and Mallophaga of North American Mammals. 
 Vernon Lyman Kellogg, Professor of Entomology, and Gordon 
 Floyd Ferris. 74 pp., 18 text figures, 8 plates. 191 5. Price, 75c. 
 
 The Flugel Memorial Volume. Papers by Ewald Fliigel, late Pro- 
 fessor of English Philology, his Colleagues and Students. 232 
 pp. 1916. Price, $1.50. 
 
 The Sesamoid Articular: A bone in the mandible of fishes. Edwin 
 Chapin Starks, Assistant Professor of Zoology. 40 pp., 15 text 
 figures. 1916. Price, 50c. 
 
 A Study of German Verbs co.mpounded with aus, ein, etc. as con- 
 trasted with those compounded with heraus, hinaus, herein, 
 hinein, etc. Charles Reining. 142 pp. 1916. Price, $1.00. 
 
 The Pathology of Nephritis. William Ophiils, Professor of Path- 
 oIog>'. 103 pp., 64 text figures and plates. 1916. Price, $1.00. 
 
 Done and Joint Studies, I. Leonard W. Elj', Associate Professor of 
 Surgery, and John Francis Cowan, Assistant Prof^-'ssor of Sur- 
 gery. T39 pp., 41 text figures and plates. 191''). Price, $1.00.
 
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