RENAL BIOPSY AND GLOMERULONEPHRITIS · 604 RENAL BIOPSY AND GLOMERULONEPHRITIS By J. H. Ross, M.D., M.R.C.P. Senior MedicalRegistrar, The ConnaughtHospital, andAssistant, The Mledical

604

RENAL BIOPSY AND GLOMERULONEPHRITISBy J. H. Ross, M.D., M.R.C.P.

Senior Medical Registrar, The Connaught Hospital, and Assistant, The Mledical Unit,The London Hospital

IntroductionSafe methods of percutaneous renal biopsy were

first described by Perez Ara (1950) and Iversenand Brun (I95I) who used aspiration techniques.Many different methods have since been described;the simplest is that of Kark and Muehrcke (1954)who use the Franklin modification of the Vim-Silverman needle.Brun and Raaschou (1958) have recently re-

viewed the majority of publications concernedwith renal biopsy and have concluded that the riskto the patients is slight. They mentioned threefatalities which have been reported but consideredthat, in each case, death was probably due to thedisease process rather than the investigation.Retroperitoneal haematomata have been recordedin patients with hypertension or uraemia but areunusual. Gross haematuria is uncommon (it oc-curred in 7.9 per cent. of 51o biopsy attempts byBrun and Raaschou, 1958, and 7 per cent. of ioobiopsy attempts by Muehrcke, Kark and Pirani,1955). Pain in the loin following the procedure isalso unusual. Although the procedure is simple,it should not be undertaken without carefulinstruction.The contraindications observed by those ex-

perienced in renal biopsy have varied considerably.A haemorrhagic diathesis is, of course, an absolutecontraindication. Patients with hydronephrosis,pyonephrosis, renal tuberculosis or neoplasm,very small kidneys, only one kidney or who areunable to cooperate, should not be submitted tothe procedure. Most authors have considereduraemia a contraindication because of the asso-ciated haemorrhagic tendency, but Brun andRaaschou (I958) have not found any significantincrease in the frequency of haematuria afterbiopsy in II9 uraemic patients and, in fact; con-sider acute uraemia of unknown aetiology to be anindication for the investigation.

Tissue, adequate for histological examination,can be obtained in about 75 per cent. of cases. Thespecimen may be regarded as representative of thekidney except in focal diseases such as pyelo-nephritis. Very small fragments of tissue may be

sufficient to establish a diagnosis in a few condi-tions such as amyloid disease and diabeticglomerulosclerosis, but cortex with at least ioglomeruli is necessary for an accurate assessmentof the renal structure; occasionally, up to 40glomeruli may be present in a single specimen.The revelation of gross structural changes in

the kidneys of patients who can be recognizedclinically as having chronic glomerulonephritis isof little value and does not contribute to manage-ment or prognosis. In contrast, biopsy specimensfrom patients in the early stages of glomerulo-nephritis, particularly those who have developedthe nephrotic syndrome insidiously withouthaematuria or renal failure or who showy noevidence of disease other than proteinuria, mayprovide useful information. The value of histo-logical study in such cases is, however, limited bythe interpretation of the significance of minornon-specific lesions. Insufficient time has passedsince the introduction of renal biopsy to allowmany conclusions to be drawn as to the correlationbetween such histological features and the sub-sequent progress of the patients.The application of renal biopsy to the study of

glomerulonephritis will be discussed in this article;many references to its use in other renal diseasesmay be found in the review by Bnm andRaaschou (1958).The Nephrotic Syndrome (Type U Nephritis)

Variations in terminology and diagnostic criteria,as with so much of the literature of renal disease,have made it difficult to compare the results ofdifferent workers, especially when full case reportshave not been presented.The term ' nephrotic syndrome' was first in-

troduced by Leiter in I931 to differentiate theassociation of massive proteinuria, oedema, hypo-proteinaemia and hypercholesterolaemia withrenal disease such as glomerulonephritis from' lipoid nephrosis ' which was considered to havethe same four features without hypertension,nitrogen retention, an excess of red blood cells inthe urine or histological glomerular lesions.

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November 1959 ROSS: Renal Biopsy and Glomerulonephritis 605

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FIG. i -Glomerulus with diffuse basement membranethickening. This feature was present in all of I5glomeruli in the specimen from a man aged 52 yearswith the nephrotic syndrome of seven monthsduration. Renal failure and hypertension havedeveloped. Heidenhain's Azan stain, x 310.

'Nephrotic syndrome' is not a diagnosis in itselfand should always be qualified by the associateddisease process or aetiological agent if these can berecognized clinically or histologically (Kark et al.,1958, listed 31 possible causes of the syndrome).The condition, when no cause has been identified,has been variously termed 'type II nephritis,''lipoid nephrosis,' the 'uncomplicated' or 'idio'-pathic' nephrotic syndrome or has been given ahistological label according to the school of thoughtof the observer. In this article, type II nephritiswill be the name used whether the fully developedlesions described by Ellis in 1942 (the mem-branous or lobular glomerulonephritis of Allen,I95I and 1955) are shown to be present or not.Amyloid disease may occasionally be revealed

unexpectedly by biopsy in patients consideredclinically to have early type II nephritis (Bjornoboeet al., I952; Ross and Ross, 1957). This findingsuggests a worse prognosis and may preventvalueless treatment with steroids.

Patients with early type Ir nephritis, whoseclinical features are similar, may be found to havestrikingly different histological lesions. Glomeru-

lar lesions at present give the best indication of thesubsequent progress which may be expected, butfurther study may reveal the significance of minortubular and interstitial features. The finding ofgeneralized basement membrane thickening (Fig.i) or intercapillary hyalinization in the glomeruliprobably indicates that recovery is impossible andthat progress to renal failure with hypertension,even though it may be delayed for many years, isinevitable; the use of steroids for the treatment ofpatients with these lesions is usually disappointing.The recognition of small increases in basementmembrane thickening is, however, difficult and, inaddition, Rich (957) has shown, in necropsyspecimens, that the lesions may be more pro-nounced in the juxtamedullary zone than in theouter cortex; such considerations may cast doubton the interpretation of some small specimens.The interpretation of minor focal lesions in the

kidneys of these patients is even more difficult.Increase in tuft cells, basement membranethickening, intercapillary hyalinization and capsu-lar adhesions are found diffusely or locally inoccasional glomeruli but are not generalized(Bjornoboe et al., 1952; Kark et al., I955; Rossand Ross, 1957; Joekes et al., 1958). Recoveryfrom the disease is still possible and the severityof the lesions may give some indication of thesubsequent progress of the patient; conclusionsbeyond these are not yet possible. There has beenonly one report of serial biopsies demonstratingthat such minor lesions precede generalized base-ment membrane thickening (Joekes et al., 1958)but circumstantial evidence suggests that this maybe a frequent structural sequence. It seems un-likely that any small structural differences in thesecases will be recognized by conventional micro-scopy which will allow the histologist to foretellrecovery, a long benign course or progress torenal failure.Some biopsy specimens from these patients

show no glomerular lesions at all; again, recoverymay occur but cannot be foretold with certainty.Prolonged follow-up of a large number of patientsis necessary before more definite conclusions canbe reached. Electron microscope studies (Far-quhar et al., I957 a, b and c; Folli et al., 1958;Brun and Raaschou, I958) have shown that anabnormality of the glomerular epithelial cells maybe found in biopsy specimens from patients withearly type II nephritis (the authors used differentnomenclature) even when conventional micro-scopy has revealed no abnormalities. The charac-teristic 'foot processes' of normal epithelial cells(podocytes) disappear and the epithelial cytoplasmbecomes closely applied to the basement mem-branes of the capillary loops. This change has notbeen noted in acute nephritis but it is still not clear



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FIG. 2.-Case i. One of the most severely affectedglomeruli in the specimen, showing intercapillaryhyalinization and capsular adhesion. Periodic-acid-Schiff stain, X 330.

if its recognition can be used to differentiate a'particular variety of nephritis or if it has anyspecial functional significance. Folli et al. (1958)reported reversal of this lesion with recovery of apatient from the nephrotic syndrome; they usedthe diagnosis 'lipoid nephrosis' for patients withelectronmicroscopic podocyte lesions but withoutmembranous glomerulonephritis.The following case notes illustrate some of the

points which have been discussed.

Case iA woman of 5I years developed the nephrotic

syndrome without hypertension or nitrogen re-tention. A biopsy specimen, obtained two monthsafter the onset of oedema, contained i8 glomeruli;one was completely hyalinized but the majorityshowed only slight hypercellularity with occasionalincrease in intercapillary material and a few cap-sular adhesions (Fig. 2). The tubules were normaland there was no increase in interstitial tissue. She-was treated with mercurial diuretics withoutresponse but had a large diuresis whilst receivingan ion-exchange resin. Four months after thebiopsy she was free from oedema, proteinuria dis-

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FIG. 3.-Case 2. Glomerulus with small areas of base-ment membrane thickening and intercapillaryhyalinization adherent to Bowman's capsule.Periodic-acid-Schiff stain, x 330.

appeared after another four months and she hasremained well for a further i i months.

Case 2A woman of 65 years, known to have had benign

essential hypertension without proteinuria pre-viously, developed the nephrotic syndrome with-out impairment of renal function tests. A biopsyspecimen, obtained I7 months later, contained 28glomeruli; the majority showed minor lesions, asin Fig. 3. There was slight tubular atrophy anddiffuse collagenous increase of the interstitialtissue. Oedema persisted for many months buthad disappeared and there was only very slightproteinuria I9 months after biopsy, when she un-fortunately died from causes unrelated to her renaldisease.

Case 3A Pakistani seaman, aged 4I years, developed

gross proteinuria and oedema with hypertensionbut without haematuria. Six months after theonset his renal function was normal (blood urea31 mg./ioo ml., maximum urine urea concentra-tion 25.2 g./l., creatinine clearance 98 ml./min.).



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When a biopsy specimen was obtained twomonths later there was moderate renal failure(blood urea 6o mg./ioo ml., maximum urine ureaconcentration 13.2 g./l., creatinine clearance34 ml./min.). I4 enlarged hypercellular glomerulihad many small areas in the tufts which were ad-herent to Bowman's capsule and contained in-creased intercapillary material and thickenedcapillary basement membranes. There was diffusecollagenous increase of the interstitial tissue andmany convoluted tubules were dilated and linedby ragged vacuolated cells. The lesions of thetubules may have been related to potassium de-pletion present at the time of the biopsy.The glomerular lesions in this case were similar

to those in cases i and 2 but were more intense andcould be correlated with the more severe clinicalfeatures of the disease. When the patient was lastseen, io months after the biopsy, renal failure wasfar advanced.

Case 4A renal biopsy specimen was obtained from a

boy aged nine years who had had the nephroticsyndrome for three and a half years with slightoccasional hypertension but without haematuria orimpairment of renal function. Immediately priorto the biopsy, a massive diuresis, accompanied bydiminution in proteinuria, followed a course ofACTH. Treatment with prednisone was con-tinued until seven months after the biopsy, whenhe lost proteinuria and was well in every respect.The specimen contained 14 glomeruli, four of

which were completely hyalinized. The re-mainder were normal apart from occasional cap-sular adhesions and a few small areas containingincreased cells and intercapillary material or slightbasement membrane thickening. The tubules werenormal but there was slight diffuse interstitialfibrosis.These findings were of particular interest,

demonstrating that recovery can occur in spite offocal glomerular hyalinization. It is possible thatthe higher recovery rate in children with type IInephritis is due to the disease remaining focal.Prolonged observation is necessary before re-covery can be considered complete, as relapseshavre been reported many months or years afterloss of proteinuria (Rennie, 1947; Roscoe, I956).

Case 5A woman, aged 49 years, developed the neph-

rotic syndrome which persisted, with intermittentgross oedema, for four years and then resolvedcompletely. She has remained well, withoutproteinuria, for a further five years. Raised bloodpressure, present during and since the disease, has

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FIG. 4.-Case 5. Glomerulus which is normal apartfrom capsular adhesion and very slight adjacenthyalinization. Heidenhain's Azan stain. X 370.

been considered to be due to benign essentialhypertension.A renal biopsy specimen was obtained three

years after proteinuria had ceased. There were noabnormalities in the eight glomeruli examinedapart from a few capsular adhesions associated withslight focal increase in intercapillary material(Fig. 4). There were no tubular abnormalities butthere was very slight focal interstitial fibrosis.The abnormalities in the glomeruli of this small

specimen were considered to be the healed remainsof focal glomerular lesions. It is much more likelythat diffuse basement membrane thickening hadnever developed, even after four years of thedisease, rather than that it had been pre3ent andhad resolved.

Case 6A man of 34 years was found to have heavy

proteinuria when he attended hospital with a com-plaint of backache. He had never had oedema, hisblood pressure was normal and renal function testswere unimpaired. A biopsy specimen showed IOof I7 glomeruli to be completely hyalinized; theremainder had diffuse basement membranethickening and patchy intercapillary hyalinization



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FIG. 5.-Case 6. Glomeruli with basement membranethickening and intercapillary hyalinization. Focaltubular atrophy and dilatation. Interstitial fibrosis.Periodic-acid-Schiff stain, X IOO.

(Fig. 5). There was focal tubular atrophy anddilatation as well as interstitial fibrosis.This illustrates the value of renal biopsy in

patients with proteinuria of obscure origin, for thelesions were those of fully developed type IInephritis and indicated a poor prognosis witheventual renal failure.

Acute (Type I) GlomerulonephritisHutt et al. (1958) have studied renal biopsy

specimens from I5 patients diagnosed clinically ashaving acute glomerulonephritis (three had noproteinuria or haematuria). They found areasonable correlation between the severity of theclinical and of the histological features. Theglomerular tuft lesions were those which havebeen described previously in post-mortem materialbut the three atypical cases mentioned above onlyhad minor changes in the cells of Bowman'scapsule. Impairment of renal ability to concen-trate was correlated with the severity of thetubular lesions.Brun et al. (1958) obtained biopsy specimens

from 9 to 49 days after the onset of symptoms in I3patients with acute glomerulonephritis. Again,there was a good correlation between the clinical

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FIG. 6.-Glomerulus with intercapillary fibrillar ma-terial. The specimen, from a man of 47 years, wastaken during recovery from acute nephritis whilstproteinuria and impairment of renal function testswere still present. Four months later he was wellin every respect. The glomeruli were also hyper-cellular with a slight excess of polymorphonuclearleucocytes in the tufts and there was focal perivas-cular fibrosis. Periodic-acid-Schiff stain, X 230.

and histological features. The finding of generalized' irreversible' changes in the glomeruli was con-sidered to indicate a hopeless prognosis in sixcases. The authors were surprised to observe' chronic' collagenous glomerular lesions in somespecimens; these may have been due to previousrenal disease or it is possible that such lesionsdevelop more rapidly than was previously thoughtpossible.The demonstration of intense inflammatory and

necrotic lesions in the kidneys of patients withsevere acute nephritis is not unexpected. It willbe of more value if structural changes can berecognized which will allow differentiation betweenmild cases who will recover and mild cases who willprogress slowly to renal failure. Hutt et al. (1958)obtained one specimen six weeks after the onset ofoedema and haematuria and about four weeksafter recovery had commenced; only slight pro-liferative changes and a patchy increase of periodic-acid-Schiff staining fibrils were present in theglomeruli. The author has observed similarlesions in specimens from two patients recovering



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FIG. 7.-Part of specimen from a boy aged I5 years whohad had at least six attacks of haematuria during thei8 months preceding biopsy. There is increase ofinterstitial tissue with focal chronic inflammatorvcell infiltration and two glomeruli show ischaemicchanges with shrunken tufts and thickened cap-sules. Haematoxylin and eosin, x IOO.

from the acute stage of the disease (Fig. 6); oneof them has made a complete recoverv, the otherstill has slight proteinuria one year after biopsy.Perhaps the finding of collagenous glomeruli ordiffuse interstitial fibrosis will be correlated withfailure to recover and a slowly progressive course,when more patients have been studied.

Farquhar et al. (I957 b and c) have describedthe electronmicroscopic glomerular lesions inacute glomerulonephritis. In the early stages thehypercellularity was found to be mainly due to anincrease in the number of the endothelial cells.The cytoplasm of both epithelial and endothelialcells was swollen but the foot processes werenormal except in severely affected areas. Materialresembling basement membrane substance andbelieved to originate from endothelial cells ac-cumulated within the tufts; this is probably thematerial forming the P.A.S. fibrils seen on conven-tional microscopy and which may accumulatesufficiently to form 'hyaline' glomeruli.Focal Glomerulonephritis

Bates et al. (I957) described renal biopsy

e.

FIG. 8.-Another part of the specimen shown in Fig. 7.Glomerulus with capsular adhesion. Red bloodcells in capsular space and in adjacent convolutedtubules. Increase of interstitial tissue. Haema-toxylin and eosin, x 410.

specimens from nine patients with very mildnephritis associated with acute pharyngitis. Clini-cal and immunological studies excluded recentgroup A haemolytic streptococcal infection andhaematuria alone was the predominant feature ofthe disease. The glomerular le3ions were mild anafocal and were contrasted with the more severeproliferative lesions observed in specimens frompatients with typical acute nephritis followinggroup A haemolytic streptococcal infections. Themild disease was presumably acute 'focal neph-ritis' occurring at the height of an unidentifiedinfection.

Ross (1959) has studied five specimens fromnine patients with recurrent focal nephritis. Thisunusual disease, which occurs in young patients, ischaracterized by repeated attacks of haematuriawithout oedema, hypertension or nitrogen reten-tion. Following a number of attacks, which can beinitiated by a variety of infections, proteinuria maypersist. Renal function remains normal even aftermany years. The glomerular lesions are focal andconsist of small areas in the tufts containing in-creased cells and intercapillary material with asso-ciated adhesions to Bowman's capsule. Intersti-



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610 POSTGRADUATE MEDICAL JOURNAL November 1959

tial inflammation also occurs and after repeatedattacks the structural damage may be quite severe(Figs. 7 and 8). Long-term treatment with peni-cillin and short courses of steroids have not beenfound to prevent or shorten the attacks ofhaematuria.

ConclusionsRenal biopsy may occasionally be a considerable

aid to diagnosis and prognosis in individualpatients with glomerulonephritis. Frequently,however, the lesions revealed are either those thatmight be expected from a study of the clinicalfeatures or are insufficiently specific to give in-formation of immediate value to the clinician.Further detailed studies with prolonged observa-tion of the patients and the new techniques ofelectronmicroscopy, histochemistry and antigen-antibody reaction localization (Mellors and Ortega,1956) should lead to knowledge which will in-crease the value of the procedure.

AcknowledgmentsI am grateful to Professor Clifford Wilson and

Professor Dorothy Russell for permission to quotecases studied at the London Hospital and to re-produce microphotographs prepared in the Bern-hard Baron Institute of Pathology.

BIBLIOGRAPHYALLEN, A. C. (gs19), 'The Kidney: Medical and Surgical

Diseases,' Grune and Stratton, New York, Ist ed.ALLEN, A. C. (i955), Amer. J. Med., 18, 277.BATES, R. C., JENNINGS, R. B., and EARLE, D. P. (1957),

Ibid., 23, 50o.BJORNEBOE, M., BRUN, C., GORMSEN, H., IVERSEN, P.,

and RAASCHOU, F. (1952), Acta. med. scand., I42, 233.BRUN, C., GORMSEN, H., HILDEN, T., IVERSEN, P., and

RAASCHOU, F. (1958), Ibid., x60, Is5.BRUN, C., and RAASCHOU, F. (1958), Amer. J. Med., 24, 676.ELLIS, A. (1942), Lancet, i, I, 34, 72.FARQUHAR, M. G., VERNIER, R. L., and GOOD, R. A. (I957a),

Amer. J. Path., 33, 791.FARQUHAR, M. G., VERNIER, R. L., and GOOD, R. A. (I957b),

Sckweiz. med. Wschr., 17, 50.FARQUHAR, M. G., VERNIER, R. L., and GOOD, R. A.

(I957c), J. exp. Med., Io6, 649.FOLLI, G., POLLAK, V. E., REID, R. T. W., PIRANI, C. L.,

and KARK, R. M. (1958), Ann. intern. Med., 49, 775.HUTT, M. S. R., PINNIGER, J. L., and DE WARDENER, H. E.

(I958), Quart. J. Med., 27, 265.IVERSEN, P., and BRUN, C. (i951), Amer. J. Med., II, 324.JOEKES, A. M., HEPTINSTALL, R. H., and PORTER, K. A.

(i958), Quart. J. Med., 27, 495.KARK, R. M., and MUEHRCKE, R. C. (1954), Lancet, i, Io47.KARK, R. M., MUEHRCKE, R. C., PIRANI, C. L., and

POLLAK, V. E. (1955), J. clin. Invest., 34, 944.KARK, R. M., PIRANI, C. L., POLLAK, V. E., MUEHRCKE,

R. C., and BLAINEY, J. D. (1958), Ann. intern. Med., 49, 751.LEITER, L. (I931), Medicine (Baltimore), o0, 135.MELLORS, R. C., and ORTEGA, L. G. (r956), Amer. J. Path.,

32, 455.MUEHRCKE, R. C., KARK, R. M., and PIRANI, C. L. (I955),.. Urol., 74, 267.PEREZ ARA, A. (1950), Bol. Liga Cdncer (Habana), 25, 121.RENNIE, J. B. (I947), Quart J. Med., I6, 21.RICH, A. R. (1957), Bull. Johns Hopk. hosp., 100, 173.ROSCOE, M. H. (I956), Quart..7. Med., 25, 253.ROSS, J. H., and ROSS, I. P. (1957), Lancet, ii, 559.ROSS, J. H. (1959), publication in preparation.

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Bibliography continuedfrom page 603-A. A. G. Lewis, B.Sc., M.D., M.R.C.P.SMITH, HOMER W. (x956), 'Principles of Renal Physiology,'

New York, O.U.P.SMITH, HOMER W. (1958), Bull. N.Y. Acad. Med., 35, 293.REUBI, F. (1958), Helvet. med. Acta, 25, 5I6.RHODIN, J. (1958), Amer. Y. Med., 24, 66i.

TRUETA, J., BARCLAY, A. E., DANIEL, P. M., FRANKLIN,K. J., and PRICHARD, M. M. L. (I947), 'Studies of theRenal Circulation,' Oxford, Blackwell.

ULLRICH, K. J., and JARAUSCH, K. H. (1956), Pflug Archiv.ges. Physiol., 262, 537.

VANDER, A. J., MALVIN, R. L., WILDE, W. S., andSULLIVAN, L. P. (1958), Amer. J. Med., 25, 497.

WALKER, A. M., BOTT, P. A., OLIVER, J., and MAC-DOWELL, M. (I941), Amer. J. Physiol., 134, 580.DE WARDENER, H. E., and HERXHEIMER, A. W. (1957),.7. Physiol., 139, 42.WINTON, F. R. (1956), in ' Moder Views on the Secretion of the

Urine,' London, Churchill.WIRZ, H. (x954), in the Ciba Foundation Symposium on theKidney, London, Churchill.WIRZ, H. (I956), in 'The Neurohypophysis,' London, Butter-

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Documents

RENAL BIOPSY AND GLOMERULONEPHRITIS · 604 RENAL BIOPSY AND GLOMERULONEPHRITIS By J. H. Ross, M.D., M.R.C.P. Senior MedicalRegistrar, The ConnaughtHospital, andAssistant, The Mledical