CLINICOPATHOLOGICAL STUDY OF RENAL BIOPSIES IN

GLOMERULAR DISEASES – 1 YEAR RETROSPECTIVE AND 2

YEARS PROSPECTIVE STUDY

BY

Dr. ABDUL HAKEEM ATTAR

DISSERTATION SUBMITTED TO THE

RAJIV GANDHI UNIVERSITY OF HEALTH SCIENCES,

BANGALORE , KARNATAKA.

IN PARTIAL FULFILLMENT

OF THE REQUIREMENTS FOR THE DEGREE OF

DOCTOR OF MEDICINE

IN

PATHOLOGY

UNDER THE GUIDANCE OF

GUIDE CO-GUIDE
DR.MEENA.N.JADHAV DR.R.M.MADRAKI
MD (PATHOLOGY) MD, DM. (NEPHROLOGY)
PROFESSOR, ASSO PROFFESOR
DEPT. OF PATHOLOGY DEPT OF MEDICINE

DEPARTMENT OF PATHOLOGY

B. L. D. E. Association’s
SHRI B. M. PATIL MEDICAL COLLEGE HOSPITAL
AND RESEARCH CENTRE BIJAPUR – 586103.

2008

I
 RAJIV GANDHIO UNIVERSITY PF HEALTH SCIENCES,
BANGALORE, KARNATAKA.

DECLARATION BY THE CANDIDATE

The dissertation work entitled “CLNICOPATHOLOGICAL STUDY

OF RENAL BIOPSIES IN GLOMERULAR DISEASES – 1 YEAR

RETROSPECTIVE AND TWO YEARS PROSPECTIVE STUDY” has

been carried out by DR. ABDUL HAKEEM ATTAR under the guidance of

DR. MEENA. N. JADHAV professor, department of pathology, for the award of

M. D. Degree (pathology) examination conducted by the Rajiv Gandhi University of

Health Sciences, Bangalore, Karnataka. This work is original and has not been submitted

for any other degree or diploma of this or any other University.

Place: Bijapur Dr. ABDUL HAKEEM ATTAR

Date:
 CERTIFICATE BY THE GUIDE

CERTIFICATE

This is to certify that dissertation entitled “CLINICOPATHOLOGICAL

STUDY OF RENAL BIOPSIES IN GLOMERULAR DISEASES – 1

YEAR RETROSPECTVE AND TWO YEARS PROSPECTIVE

STUDY” is bonafide research work done by Dr. ABDUL HAKEEM ATTAR.

under my overall supervision and guidance, in partial fulfillment of the requirement for

the degree of M.D. (pathology) examination to be held in April 2009.

DR.MEENA. N. JADHAV
MD (PATHOLOGY)
PROFESSOR,

DEPARTMENT OF PATHOLOGY

B. L. D. A ‘S SHRI B. M.PATIL

MEDICAL COLLEGE HOSPITAL

Place: Bijapur
Date: AND RESEARCH CENTRE

BIJAPUR .

III
 CERTIFICATE BY THE CO- GUIDE

CERTIFICATE

This is to certify that dissertation entitled “CLINICOPATHOLOGICAL

STUDY OF RENAL BIOPSIES IN GLOMERULAR DISEASES – 1

YEAR RETROSPECTVE AND TWO YEARS PROSPECTIVE

STUDY” is bonafide research work done by Dr.ABDUL HAKEEM ATTAR.

under my overall supervision and guidance, in partial fulfillment of the requirement for

the degree of M.D. (pathology) examination to be held in April 2009.

Dr. R. M. MADRAKI
MD, DM. (NEPHROLOGY)
ASSOCIATE PROFESSOR

DEPARTMENT OF MEDICINE

B. L. D. A ‘S SHRI B. M.PATIL

MEDICAL COLLEGE HOSPITAL

AND RESEARCH CENTRE

Place : Bijapur BIJAPUR

Date :
 ENDORSEMENT BY THE HOD AND PRINCIPAL

This is to certify that dissertation entitled “CLINICOPATHOLOGICAL

STUDY OF RENAL BIOPSIES IN GLOMERULAR DISEASES – 1

YEAR RETROSPECTVE AND TWO YEARS PROSPECTIVE

STUDY” is bonafide research work done by Dr. ABDUL HAKEEM ATTAR

under the guidance of DR. MEENA N. JADHAV, M.D. Professor, Department of

pathology, BLDEA’S Shri B. M. Patil Medical College, Bijapur.

Dr. B. R. YELIKAR Dr. R. C. BIDRI

M.D.(PATHOLOGY) M.D.(GEN.MED)

PROF & H.O.D. PRINCIPAL

DEPT. OF PATHOLOGY B. L. D. A ‘S SHRI B. M.PATIL

MEDICAL COLLEGE HOSPITAL

AND RESEARCH CENTRE

Place : Bijapur BIJAPUR

Date
 COPYRIGHT

DECLARATION BY THE CANDIDATE

I do hereby declare that the Rajiv Gandhi University of Health Sciences, Karnataka shall

have the rights to preserve, use and disseminate this dissertation / thesis in print or

electronic format for academic / research purposes.

Place : Bijapur Signature of Candidate

Date : Dr. ABDUL HAKEEM ATTAR

Rajiv Gandhi University of Health Sciences, Karnataka

 ACKNOWLEDGEMENT

I would like to acknowledge my deep sense of gratitude and indebt ness to my

teacher and guide Dr. Meena N. Jadhav, MD, Professor, Department of Pathology. I am

grateful for his able guidance, useful suggestions, constant inspiration and encouragement

for working out the minute details and giving proper direction, through out the study

period.

I am equally grateful to my co-guide Dr. R.M. Madraki, MD, DM, (Nephrology)

Associate Professor Department of Medicine, for his able guidance, valuable suggestions

and kind co-operation in bringing out this work.

I express my gratitude to my teacher Dr. B.R. Yelikar, MD, Professor and Head ,

Department of pathology, for his valuable guidance, conatant encouragement and thought

provoking ideas. His personal involvement and interest gave the necessary impetus for

the completion of this dissertation.

I express my sincere gratitude to Dr. S. U. Arakeri, MD, Dr. R. M. Potekar,

MD, Dr. S. B. Hippargi, MD, Professors of Pathology, Dr. Mahesh. H. Karigoudar,

MD. DNB, FAGE, Associate Professor of Pathology, Dr. Sanjeev Reddy, MD, Dr.

Ashwin PK,MD, Dr. Asif Baig, MD, Dr. Girish Kamat, MD, Dr. Savita shetter, MD,

Assistant Professors of Pathology, Dr. Keshav kulkarni, DCP, Jr Lecturer of pathology,

for their kind help and advise in preparing this dissertation.

 I am sincerely thankful to Dr. Mahesh Karigoudar and Dr. Karnik for sparing

his valuable time for helping in preparing excellent photographs amidst their busy

schedule.

My sincere thanks to Dr. R. C. Bidri, Principal Shri B. M. Patil Medical College,

Bijapur, and Dr. S. S. Jigajinni, Vice Chancellor B.L.D.E. University, Bijapur, for their

kind help and encouragement in completing this work.

My thanks to all technical and non-technical staff in the department of pathology

for having helped in the collection of material for the study.

My special thanks to Mr. Azhar Pasha, (MCA), for computerizing my

dissertation work in a right format and nicely binding of my dissertation in time.

I also wish to acknowledge my thanks to my colleagues for their help and co-

operation in preparing this dissertation.

Above all I remain forever grateful to all my patients for their willing co-

operation without whom this study would not have been possible.

Place : Bijapur

Dr. ABDUL HAKEEM ATTAR

Date :
 ABBREVATIONS

AMY - Amyloidosis

CN - Cortical necrosis

FSGS - Focal segmental glomerulosclerosis

H&E - Haematoxylin & Eosin

IF - Immunofluorescence

LN - Lupus Nephritis

MCD - Minimal change disease

MesPGN - Mesangioproliferative glomerulonephritis

MN - Membranous Nephropathy

MPGN - Membranoproliferative glomerulonephritis

MT - Masson’s Trichome

NS - Nephrotic syndrome

PAS - Periodic acid Schiff stain

RPGN - Rapidly progressive glomerulonephritis

SLE - Systemic lupus erythematosus

 ABSTRACT

BACKGROUND AND OBJECTIVES:

The technique of percutaneous renal biopsies is the cornerstone for our

understanding of diseases of the kidney. Studies done on percutaneous gun biopsies

performed under real-time ultrasound guidance have given higher diagnostic yield with

fewer complications.

The present study aims the spectrum of glomerular diseases which require renal

biopsy and to correlate the pathological findings of glomerular diseases with clinical and

laboratory parameters.

MATERIALS AND METHODS :

A total of 75 cases were studied over a period between 01-10-2005 and 31-07-

2008 which includes 1 year retrospective and 2 years prospective study. The renal biopsy

was performed by 18 gauze Bard’s ‘bioptic gun’ under real time ultra sound guidance and

a renal tissue ranging from 2-3cm was obtained. Sections were studied with H&E,

Special stains like PAS, Silver and Congo-red. Immunofluorescence was done where

ever necessary.
RESULTS:

The study showed that among 75 cases the majority of biopsies were of primary

glomerular diseases in which focal segmental glomerulosclerosis was most common

accounting for (25.42%) of cases followed by mesangioproliferative glomerulonephritis

(22.03%) of cases. Among the secondary glomerular diseases renal amyloidosis was

found to be more common in patients who presented with nephrotic syndrome and

maximum cases were of secondary amyloidosis in which tuberculosis and chronic

respiratory infections like bronchiectasis were common. Among 75 cases 2 cases (2.66%)

were inadequate and 2 cases (2.66%) were of other diseases like tubulointerstitial

nephritis and chronic pyelonephritis.

CONCLUSION:

Renal biopsy is the corner stone for diagnosing the glomerular diseases with

fewer complications. The clinical examination,laboratory findings including biochemical

tests and immunofluorescence findings were very much helpful in arriving at the

diagnosis. Focal segmental glomerulosclerosis, mesangioproliferatve glomerulonephritis

and amyloidosis of kidney were found to be common in the present study.

KEY WORDS

Renal biopsy, ultrasound, bioptic gun, focal segmental glomerulosclerosis,

amyloidosis, immunofluorescence.
 CONTENTS

S No Particulars Page No.

1 INTRODUCTION 1

2 OBJECTIVES 3

3 REVIEW OF LITERATURE 4

4 MATERIALS & METHODS 22

5 RESULTS 26

6 DISCUSSION 45

7 CONCLUSION 50

8 SUMMARY 52

9 BIBLIOGRAPHY 54

10 ANNEXURES

1) Proforma 63

2) Master Chart 65
 LIST OF TABLES

S NO TABLES PAGE NO.

1 Table -1 26

2 Table -2 26

3 Table -3 27

4 Table -4 28

5 Table -5 30

6 Table -6 31

7 Table -7 31

8 Table -8 32

9 Table -9 33
 LIST OF GRAPHS

S NO GRAPHS PAGE NO.

1 Graph -1 27

2 Graph -2 28

3 Graph-3 29

4 Graph -4 29

5 Graph -5 32

6 Graph -6 33
 LIST OF FIGURES

S NO FIGURES PAGE NO

1 Figure -1 36

2 Figure -2 36

3 Figure -3 37

4 Figure -4 37

5 Figure -5 38

6 Figure -6 38

7 Figure -7 39

8 Figure -8 39

9 Figure -9 40

10 Figure -10 40

11 Figure -11 41

12 Figure -12 41

13 Figure -13 42

14 Figure -14 42

15 Figure -15 43

16 Figure -16 43

17 Figure -17 44

18 Figure -18 44
 INTRODUCTION

The present knowledge of the pathology of renal diseases has been derived to a

large extent from the introduction of percutaneous needle biopsy of the kidney and the

systematic study of these small samples of renal tissue by light microscopy, electron

microscopy and immunofluorescence microscopy. The technique of percutaneous renal

biopsy was introduced in to clinical usage in the early 1950s and till today it is one of the

most common and widely accepted invasive procedures for the diagnosis of renal

diseases1.

It provides the cornerstone for our understanding of the diseases of kidney.

Recent advances in the biopsy techniques such as the use of real-time ultrasonography

and the “Bioptic gun” have made this procedure easier and have increased the yield of

diagnostically adequate tissue.

The renal biopsy provides critical information on evolution, precise diagnosis for

many kidney diseases and also serves as a guide to prognosis and treatment. There are

many advanced techniques on renal biopsies like molecular, cellular-biologic techniques 2

and glomerular morphometry3. These techniques are not easily available, nor economical

enough to be used in routine practice.

1
 The review of literature reveals that minimal change disease,

membranoproliferative glomerulonephritis, membranous nephropathy, focal segmental

glomerulosclerosis and crescentic glomerulonephritis can still be diagnosed by light

microscopy with more reoproducibility2.

Although the role of diagnostic tools like immunofluorescence and electron

microscopy in the study of renal pathology cannot be overemphasized, light microscopy

also has its own advantages. It is a simple procedure and it provide the first insight about

the renal pathology and in majority of cases it is also possible to come to a final

conclusive diagnosis. A three year study was done on renal biopsies performed in our

hospital .The biopsies selected were those which were performed by percutaneous route

for suspected glomerular diseases.

The purpose of the study was to interpret and classify the renal biopsies according

to the disease process. In this study, most of the biopsies were studied by light

microscopy and a few were subjected to immunofluorescence microscopy.

 OBJECTIVES

1) To study the spectrum of glomerular diseases which require renal biopsy.

2) To correlate the pathological findings of glomerular diseases with clinical and

laboratory parameters.
 REVIEW OF LITERATURE

The technique of percutaneous renal biopsy was introduced in to clinical

usage in the early 1950s as a relatively safe, routine procedure by Iverson and

Brun. It should be pointed out that Alwall performed a total of 13 percutaneous

renal biopsies as early as 1944. However after the death of one patient, Alwall

abandoned its use because he believed the technique was too risky4.

Pirani in 1980 noted that the history of percutaneous renal biopsy could

be divided in to three major periods, 1952-1961: during which time very few

nephrologists employed this technique, 1961-1975: by this time most of

nephrologists considered renal biopsy a valuable and safe diagnostic procedure.

Also during this period, electron microscopy and immunofluorescence

microscopy added greatly to the diagnostic potential of the procedure. The third

period 1975 until the present is one of the most common and widely accepted

invasive procedure for the diagnosis of renal diseases. The renal biopsy provides

one of the few objective measurements of the type, nature, site, extent and the

state of evolution of renal diseases.

During the CIBA Foundation Symposium on kidney biopsy, which was

held in London in 1961, investigators from Europe and the United States shared

their experiences based on more than 5000 renal biopsies. Kark, Muchrcke and
Pirani did an analysis of 500 percutaneous renal biopsies in 1958 and stressed the

importance of renal biopsy in diagnosis and management of renal diseases5

Nyman and Cappelen have compared ultrasound guided biopsy and

manual techniques in total 448 renal biopsies which comprised of 124 manual and

131 gun biopsies. A significant higher diagnostic yield and fewer complications in

the gun biopsy group were noted. The authors were of opinion that gun biopsy has

got more diagnostic accuracy together with low risk of complications as

compared to manual technique 1.

Rayat CS et al have studied glomerular basement membrane thickness

(GBMT) in 25 normal adults aging between 18-58 years. The study revealed a

mean GBM thickness of 321 nm with a standard deviation (SD) of 28 nm. Mean-

2 SD (321-56) that is 256 nm was fixed as a cut off value for GBM thickness for

the diagnosis of thin basement membrane disease (TBMD). Another systematic

split study of control subjects revealed thicker GBM in higher age group (35-58)

years as compared to GBM in lower age groups (18-30) years. Males in higher

age group revealed thicker GBM than females. Ten patients with hematuria of

non urologic origin and having GBMT <265 nm were diagnosed as cases of

TBMD. Patients with TBMD revealed significantly attenuated GBM as compared

to age and sex matched controls. Hence they revealed morphometry is the

ultimate and appropriate method for diagnosing thin basement membrane disease

(TBMD) 3.
 Lange and Tresser in their commentary on the ethics of renal biopsy in

1974, did a study on the impact of renal biopsy on patient care and management

and its rightfulness and ethical value6.

Burstein et al have reviewed 200 renal biopsies performed as a primary

indication to evaluate proteinuria and renal manifestations of systemic lupus

erythematosus . Material for light microscopy, immunofluorescence and electron

microscopy was obtained. Adequate tissue for histological diagnosis was obtained

in 97.5% of patients. They concluded that real-time ultrasound is a safe, accurate

method in localizing the kidney for percutaneous renal biopsy7.

Gadgil et al have studied 27 ANA and dsDNA positive cases from surgical

files from year 1986 to 1987. Clinical, biochemical, morphological and

immunofluorescence findings were correlated. Routine haematoxylin and eosin,

periodic-acid-Schiff and methenamine-silver stains were used for all cases. Direct

immunofluorescence was done whenever possible. Morphologically cases were

grouped as per WHO criteria. In this study age groups between 20 – 30 years ,

males , high BUN , creatinine levels , high activity and chronicity indices were

associated with poor prognosis8 .

Hass have reviewed reports from all non-transplant adult renal biopsies

from year 1974 to 1993 which comprised of 7,420 cases. The authors were of the

opinion that among all biopsies there was increase in the incidence of focal
segmental glomerulosclerosis over the 20 years between 1974 to 1993, which

comprised 10% to 15% of idiopathic nephrotic syndrome cases in adults9.

Today , in all major clinical nephrology centers around the world ,

percutaneous renal biopsy is commonly used to establish an accurate diagnosis ,

to obtain data of prognostic value , and there by to select the most appropriate

therapeutic intervention for the patients affected by renal disease .

Sahney and Chandramohan in 1994 evaluated the safety and efficacy of

renal biopsies in 43 children10. Although extensively used in children, renal

biopsy is a technically difficult procedure in children.

Because the procedure is not without morbidity and occasional mortality,

the risk to benefit ratio must be evaluated carefully for each patient in whom a

biopsy is being considered .In a survey done by Hlatky in 1982 on the

complications of renal biopsy, which included the need for blood transfusion,

nephrectomy or puncture of other organs, the complication rate was

2.1%11.However Gault et al in 1980 reported that in the hands of experienced

operator, the percutaneous renal biopsy is a safe and reliable technique 12.

Originally, the procedure involved aspiration of tissue sample with patients

in sitting position. The Iversen Rohim cannula and syringe used by Brun and

Raaschou yielded a cylinder of tissue of about 1.5mm in diameter4. However,

Kark and Muchrcke placed patients in prone position and elected to use the

Franklin modification of the Vim Silverman cutting needle in place of the

aspiration technique.

In early 1950’s, a suction needle attached to a syringe was used. Later the

Vim Silverman needle and the True cut needle have been used extensively. These

are both hand driven needles.

Mal, Meyrier, Callard, and Altman tried a new approach in 1992. They

performed transjugular renal biopsy. Under radiographic control, a guide wire was

inserted in to the right internal jugular vein and into the inferior venacava and

renal biopsy was taken .They performed 200 biopsies. On an average, the biopsy

specimen contained 10 glomeruli. They preferred this route to the percutaneous

route in patients with bleeding disorders and in cases which needed both hepatic

and renal biopsies13.

In 1993, Leal tried the transurethral approach for renal biopsy. He

concluded that the transurethral approach was less painful, less invasive and more

easily accomplished. It could be readily used as an extension of cystoscopic

evaluation. Anatomical considerations suggested that there would be less bleeding

than the percutaneous approach and it was especially useful for studying the

medulla14.
 Richards et al did a prospective study of 276 biopsies to assess the effect

of the knowledge of renal histology on patient management. Data that was

available by renal biopsy suggested that it was essential to have knowledge of

renal histology in patients of renal disease before management15.

Various automated and semi automated biopsy devices have been in use

recently. Recently “bioptic gun” has been introduced. This is a small diameter

spring driven needle. Recent studies 16 compared the results of percutaneous renal

biopsy by hand driven needles and smaller diameter spring driven needles (biopty

gun) they found that both gave similar results with a slight decrease in

complications using the bioptic gun.

Percutaneous renal biopsy was usually performed under ultrasound

guidance and if ultrasound failed to visualize kidney, biopsy was done under

computerized tomographic guidance17

Many nephrology and transplant centers have turned to the use of 18

gauze spring driven needles especially for pediatric and transplant recipient

patients18.

According to Pirani because of its small size, the kidney biopsy specimen

required a systematic, detailed, and analytic approach for an accurate evaluation

of the histopathologic findings4.

 Corwin , Schwartz and Lewis in 1988 studied that the adequacy of a

needle biopsy specimen of the kidney was determined not by its size ( length ) ,

but by the presence of renal cortex and by the type of renal disease represented in

the material . A minimum of 5-10 glomeruli were considered necessary to obtain

a reasonably accurate diagnosis and to consider a biopsy specimen adequate19.

Renal Biopsy is used to:

1) Establish a specific diagnosis in patients with renal dysfunction

2) Determine prognosis in patients with renal disease

3) Evaluate the extent of renal injury

4) Determine appropriate therapy

Indications for Renal Biopsy:

Because of the likelihood of obtaining helpful information from any test

varies with the pretest probability of disease, a discussion of the indications for

renal biopsy was best considered in the context of various clinical manifestations20

Acute Renal Failure:

On many occasions, the etiology of acute renal failure secondary to

intrinsic renal disease was not evident. After non renal causes were excluded, the

most common etiologic factor of acute renal failure was acute tubular necrosis20.
A renal biopsy may be performed to establish a specific diagnosis for case in

which an accurate diagnosis cannot be made clinically.

Chronic Renal Failure:

In most patients with end stage renal disease, a renal biopsy provides little

useful information. A renal biopsy may be performed for patients who are to

undergo renal transplantation20.

Nephrotic Syndrome:

A study by Carome and Moore reinforced the theory that high grade

proteinuria was likely to be associated with glomerular pathology 21

Biopsy was reserved in children with nephritic syndrome. They were

treated initially with high dose corticosteroids, since most will have minimal

change disease on biopsy.

Levey and associates questioned the value of renal biopsy in the

management of Idiopathic nephrotic syndrome22

Non nephrotic Proteinuria :

In otherwise asymptomatic patients, isolated non nephrotic proteinuria of

less than 3.5 gm / 24 hrs was non specific and relatively common clinical

problem. In 1989 Stone stated that these patients progressed to renal failure or that
they were candidates for some form of specific medical therapy. Therefore renal

biopsy was generally reserved for those patients who had progressive disease 23.

Asymptomatic Hematuria:

In a study on isolated hematuria in 1984, Trachtman et al found that

asymptomatic hematuria was a frequent problem in children and young adults.

Trachtman and coworkers suggested that renal biopsy should be performed when

hematuria had been present for 6 months or longer or one or more episodes of

gross hematuria had occurred or both 24.

Systemic Diseases:

Renal lesions associated mainly with diabetes mellitus and SLE are severe

enough to require renal biopsy. It was well documented that 40% of patients with

diabetes would eventually develop end stage renal failure 2

Mclaughlin et al stated that controversy still surrounded the role of renal

biopsy in managing patients with systemic lupus erythematosus . Biopsies should

be performed on all patients with clinical evidence of active lupus nephritis unless

a medical contraindication existed26.

The Role of Immunopathology and Immunofluorescence studies:

According to Pirani in most renal pathology laboratories,

immunofluorescence microscopy was preferred to immunoperoxidase methods

for the routine study of renal biopsy specimens. Fluorescein labelled antibodies

yield an apple green fluorescence that should be differentiated from

autofluorescence that was evident in the elastic lamina in the arteries4.

Interpretation of immunofluorescence findings was based on recognition

of positive staining for immunoglobulin, complement fractions and other proteins

and their predominant pattern of localization20

Immunofluorescence studies determined the type and distribution of

immune complex deposition in glomerular disease. Fresh specimens were placed

in isopentane and snap frozen in liquid nitrogen. Cryostat sections 4 micrometer

thick were prepared and samples were reacted with fluoresceinated antisera

specific for IgG, IgA, IgM, C1a, C3 ,C4, fibrinogen, albumin K light chain and

lambda light chain . Renal immunofluorescence material was evaluated related to

staining intensity (absent, trace, 1+, 2+, 3+) 20.

Morphometric studies:

Kenji et al in 1995 did a morphometric study of the glomerulus . These

measured the glomerular size by computerized digitometry27. In a study

performed by Kenji , Richard and Raafat glomerular morphometry was done in

childhood reflux nephropathy, emphasizing the capillary changes . As a

consequence of nephron loss, reflux nephropathy caused considerable glomerular

hypertrophy. Using the computerized digitometry , the mean glomerular tuft area
(GTA) was measured in all complete undistorted non sclerotic glomeruli in

periodic acid Schiff stains.

Electron microscopy:

Ultrastructural study of kidney biopsy specimens was needed to establish

correct diagnosis and gain a better understanding of renal disease process. Sidhu

et al did an ultrastructural study of AIDS and stated that some glomerular diseases

such as Alport syndrome, thin basement membrane disease, acquired

immunodeficiency syndrome nephropathy could be diagnosed by electron

microscopy only28.

Only by electron microscopy, gaps in glomerular basement membrane or

electron dense deposits of SLE could be recognized. This role of electron

microscopy was emphasized by Pirani and Olesnicky in the classification of lupus

nephritis29

In the lumen of tubules, detection of fibrils of Tamm Horsfall protein and

of small crystals in plasma cell dyscrasias required ultra structural study. This was

observed by Pirani et al who did an ultra structural study of renal lesions in

plasma cell dyscrasias30.

The renal lesions seen in renal biopsy specimens have been traditionally

compartmentalized in to 4 major components of the renal parenchyma (glomeruli,

tubules, interstitium and blood vessels). A review of literature of the diseases

affecting these compartments is mentioned briefly in the following discussion.

Glomeruli :

The glomerulus was first described by Marcello, Malphigi, the famous

Italian anatomist, in1687. More than 150 years later, Bowman provided a more

detailed description of glomerular tuft and the surrounding capsule. Jorgensen in

1966 in an excellent review provided one of the earliest as well as the finest

original ultra structural description of the normal human glomerulus .

According to Benjamin and Boltine , proliferative glomerulonephritis was

a common term used to describe an increase in the number of endogenous

glomerular cells , an expansion in extracytoplasmic matrix or an infiltration of the

glomerulus with exogenous cells .

In 1827, Bright laid the foundation of glomerulonephritis . Longscope in

1927 and Ellis in1942 distinguished 2 types of glomerulonephritis , Type 1 and

Type 2 .Type 3 glomerulonephritis was described by Burkholden4 .

In the CIBA foundation symposium in 1961 the term rapidly progressive

glomerulonephritis was first described by De Wardener . In 1968, however,

Bacani and colleagues first identified rapidly progressive glomerulonephritis as a

distinct clinicopathologic entity. Oleh et al classified proliferative

glomerulonephritis in to post infectious, non infectious and crescentic forms4.

The term membranous glomerulonephritis had been used by Schreiner to

describe multiple glomerular abnormalities like minimal change disease, focal and

diffuse thickening of glomerular basement membrane.

The concept of nephrosis was developed by Muller in 1905. Munk in

1913 described the term lipoid nephrosis4. In recent years the term minimal

change nephrotic syndrome was used because of the minimal glomerular changes

that were noted 31.

In the international study of kidney disease in children (nephritic

syndrome), it was found that 67% of the affected children were boys. Cameron

and coworkers in 1986 noted that in adults with nephritic syndrome, the male and

female ratio was 1:1 32.

Rao et al described the nephropathy related to acquire immunodeficiency

syndrome. They found an increased incidence of focal sclerosis in such patients.

The abbreviation HIVAN (HIV associated nephropathy) was used 33.

Nossent in 1990 described the contribution of renal biopsy data in predicting the

outcome of lupus nephritis 34.

 The year book of pathology and clinical pathology 1994 mentioned

peripolar cells in renal biopsies. These were granulated glomerular epithelial cells

that formed a cuff around the vascular pole within Bowmans capsule. These cells

were present in mesangioproliferative glomerulonephritis, IgA neohropathy,

diffuse and membranous lupus nephropathy, focal segmental glomerulosclerosis

and membranous glomerulonephritis 35.

The role of immunopathologic mechanisms in glomerular injury was

extensively being studied. Abrahamson described the ultrastructure of the

basement membranes36. Butkowski et al described the characterization of type IV

collagen in human renal basement membranes 37.Kenneth, Earle and Gian

described the effect of diabetes on glomerular structure, function and its

importance as a major cause of renal failure in the symposium on the

glomerulus38.

Renal tubules and Interstitium:

According to Robert and Leslie, a major group of renal diseases had

interstitial inflammation as a defining and dominant characteristic 4. Often the

term tubulointerstitial nephritis was used as there was accompanying

inflammation of the tubules.

Extensive accounts of the early history of ischemic tubular necrosis have

been given by Brun in 1954 and reviewed by Schubert in 1963. During world war
I German Surgeons noted that soldiers with crush injury developed renal failure

and called it Trench Nephritis.

Neilson in 1989 described the pathogenesis of interstitial nephritis. The

inflammatory process is complex, and normally involves an immune system

focused on the kidney leading to the release of paracrine cytokines39

Blood Vessels:

In 1986, Bright suggested that a relationship between chronic renal disease

and hypertrophy of left ventricle may exist. The first diagnosis of renal infarction

is attributed to Traubes who reported a case in the German literature in 1856.

Some decades later, Gull and Sutten observed the microscopic feature of arterial,

arteriolar, capillary and interstitial lesions in kidneys of hypertensive patients.

In 1936, Kimmelsteil and Wilson described the pathological alterations of

kidney in diabetes mellitus. The glomeruli and blood vessels displayed the most

striking alterations in diabetic patients.

The importance of renal failure as a cause of death in diabetic patients was

emphasized by Entmacher and associates in 1964. As discussed by Heptinstall 40

the arteries and arterioles manifest some of the most striking alterations. The

presence of marked hyaline sclerosis should alert to the possibility that diabetes
mellitus is the underlying cause. In 1994, Hostetter studied the mechanisms of

diabetic nephropathy and the involvement of blood vessels41.

Rudberg et al described in their 8 year prospective study on increased

glomerular filtration rate as a predictor of diabetic nephropathy42

Kobert and Schwartz studied HIV and Nephrotic syndrome. They found

HIV associated nephropathy was associated with a rapid deterioration in renal

function resulting in end stage renal disease within a few months. The common

renal lesions associated with HIV was focal segmental glomerulosclerosis , but

mesangial hyperplasia and minimal change disease had also been noted . Viral

antigens had been demonstrated in visceral and parietal epithelial cells from

glomeruli of HIV associated nephropathy43.

Classification of Renal Diseases: (Based on Renal biopsy specimens) 44

Primary Glomerulopathies :

1. Acute diffuse proliferative glomerulonephritis :

i. Post streptococcal

ii. Non post streptococcal

2. Rapidly progressive ( crescentic ) glomerulonephritis

3. Membranous glomerulopathy

4. Lipoid nephrosis ( minimal change disease )

5. Membranoproliferative glomerulonephtitis
 6. IgA nephropathy

7. Mesangioproliferative glomerulonephritis

8. Chronic glomerulonephritis

Systemic Diseases :

1. Systemic lupus erythematosus

2. Diabetes mellitus

3. Amyloidosis

4. Goodpasteur’s syndrome

5. Polyarteritis nodosa

6. Wegener’s granulomatosis

7. Henoch Schonlein purpura

8. Bacterial endocarditis

Hereditary Disorders:

1. Alports syndrome

2. Fabrys disease

Tubulo Interstitial Disease :

1. Interstitial nephritis

2. Acute tubular necrosis

i. Ischemic ATN

ii. Toxic ATN

 3. Renal infarction

4. Cortical necrosis

5. Atheroembolic disease

6. Pyelonephritis

7. Reflux nephropathy

Vascular Diseases:

1. Nephrosclerosis

i. Benign

ii. Malignant

2. Renal artery stenosis

3. Thrombotic microangiopathies.
 MATERIAL AND METHODS

Renal biopsy specimens for the present study were obtained from the department of

Medicine (Nephrology Unit), B. L. D. E. A’s Shri. B. M. Patil Medical College, Hospital

and Research Centre, Bijapur. All the renal biopsies over a period from 1 st August 2005

to 31st July 2008 were recorded which included 1 year retrospective and 2 years

prospective study. A total of 75 renal biopsies were obtained during the 3 years.

A detailed clinical history, examination findings, laboratory findings of the patient

were recorded from the patients of prospective group undergoing percutaneous renal

biopsies for suspected glomerular diseases. Non glomerular and neoplastic diseases were

excluded.

Indications for percutaneous renal biopsy in suspected glomerular diseases.

1. In children with nephrotic syndrome who are steroid resistant, present

with frequent relapses, steroid dependent children who require cytotoxic

therapy.

2. In adults all the patients who presents with nephrotic syndrome

3. Acute renal failure – unexplained renal failure, ATN not responding by

4-6 weeks

4. Persistent hematuria of suspected glomerular etiology

5. Acute glomerulonephritis with worsening renal failure

6. Patients with all suspected glomerular diseases

 The biopsies were done by using 18 gauze Bard’s bioptic gun under real-time

ultrasound guidance and a renal tissues ranging from 1-2 cm was obtained. The

specimens obtained were immediately fixed in 10% formalin for histopathological

examination and in isopentane, snap frozen in liquid nitrogen and sent for

immunofluorescence study where there was difficulty in diagnosis by light microscopy.

Thin sections of 3 to 4 microns thickness were taken and stained with

haematoxylin and eosin, PAS and methenamine-silver. In selected cases of amyloidosis

and interstitial fibrosis, Congo red and Massons Trichome were done respectively.

The haematoxylin and eosin sections were examined by light microscopy and the

findings were noted using the following proforma:

A) Glomeruli

1) Number of glomeruli

2) Pattern of involvement - focal / diffuse

global / segmental

3) Size - swollen / contracted / normal

4) Cellularity - increased / decreased / normal

Increased cellularity

Endocapillary / Neutrophilic / Mesangial

Extracapillary partial crescents

Circumferential crescents
 Capsular reaction

5) Basement membrane

Diffuse thickening

Focal thickening (Wire loop)

Double contour

Spikes

6) Mesangial matrix – normal / increased

7) Capillary lumina - patent / narrow / obliterated

8) Sclerosis and hyalinization – segmental / global

B) Tubules

1) Focal tubular atrophy

2) Compensatory hypertrophy

3) Degenerative changes

4) Dilatation

5) Casts

6) Others

C) Interstitium :

1) Oedema

2) Congestion

3) Fibrosis

4) Inflammatory cells
 Lymphocytes

Plasma cells

Foam cells

D) Blood vessels :

Lumen - narrow / normal

Arteriosclerosis

Arteriolosclerosis

Hyaline

Hyperplastic

Fibrinoid necrosis.
 RESULTS

During the three years study from August 2005 to July 2008 which included a 1

year retrospective and 2 years prospective study, a total of 75 renal biopsies were

reviewed for suspected glomerular diseases and classified as glomerular diseases, other

diseases and inadequate tissue sample.

Table no 1: Classification of renal biopsies of suspected glomerular diseases.

Diseases No of cases Percentage

Glomerular diseases 71 94.66%
Other diseases 2 2.66%
Inadequate tissue sample 2 2.66%
Total 75 100.00%

The glomerular diseases accounted up to 94.66% of the all renal biopsies. Other

diseases like tubulointerstitial nephritis and inadequate biopsies accounted up to 2.66%

each.

Table no 2: Classification of glomerular diseases.

Diseases No of cases Percentage

Primary glomerular diseases 59 78.66%
Secondaryglomerular 12 16.00%
diseases

Among all the glomerular diseases, maximum were due to primary causes, which

accounts for about 78.66% of the total biopsies.

 Table no 3: Classification of primary glomerular diseases

Glomerular diseases No of cases Percentage

FSGS 15 25.00%
MESPGN 13 22.03%
MPGN 9 15.00%
MN 9 15.00%
MCD 4 6.66%
DPGN 3 5.00%
CGN 2 3.33%
Cortical necrosis 2 3.33%
Chr.GN 2 3.33%
Total 59 100.00%

Out of 59 cases of primary glomerular diseases, the maximum cases were of

focal segmental glomerulosclerosis (25.005%), while mesangioproliferative GN

accounted for second category of about 22.03%.

Graph - 1

Bar chart showing the distribution of various types of primary GN

16 15
14 13
12
10
No of cases

8 9 9
6
4
2
0 4
3
2 2 2

Types of primary GN
 Graph - 2

Increasing trends in primary glomerular diseases

30
25
25 22
20
Percentage

20
15 15 15
15
10
10 8
5
0
FSGS MESPGN MPGN MN
Diseases

PRESENT PREVIOUS

FSGS and MesPGN have got increasing trends as compared with the previous studies.

Table no 4: Classification of secondary glomerular diseases.

Secondaryglomerular No of cases Percentage

diseases
Amyloidosis of kidney 7 55.00%
Lupus nephritis 5 45.00%
Total 12 100.00%

Among the twelve cases of glomerular diseases which occurred secondary to

some systemic causes the highest were due to amyloidosis followed by systemic lupus

erythematosus .
 Graph – 3

Bar chart showing the distribution of

secondary GN
8
7
7
6
5 5
No of cases

4
3
2
1
0

AMYLN
Secondary GN

Graph-4

Increasing trends in secondary glomerular

diseases

70
58
60

50 45
Percentage

40
PRESENT
PREVIOUS
30

20 16
10
10

0
Amy LN
Diseases
 Amyloidosis of kidney & LN have got increasing tends in secondary

glomerular diseases as compared to previous studies.

Table no 5: Clinical features of various glomerular diseases.

Glom. diseases Facial puffiness Pedal edema Hematuria Hypertension

FSGS 13 7 - -

MesPGN 10 4 - -

MPGN 7 3 - -

MN 6 3 - -

MCD 4 - - -

CGN - - 2 -

Chr.GN - - 1 1

DPGN 2 - - 1

Amy 7 7 - 2

LN 4 1 - 1

Out of 59 primary glomerular diseases 42 cases presented with facial puffiness,

17 cases with pedal edema, 3 cases with hematuria and 2 cases with hypertension. Out

of 12 secondary glomerular diseases 11 cases presented with facial puffiness, 8 cases

with pedal edema and 3 cases with hypertension. Rashes and joint pains were seen in 5

cases of lupus nephritis.

 Table no 6: Laboratory findings in various glomerular diseases.

Glom. Proteinuria Raised serum Raised Raised C3 ANA

diseases Creatinine blood Urea positivity
FSGS 15 8 5 6 -
MesPGN 6 2 - - -
MPGN 9 7 3 - -
MN 9 6 4 - -
MCD 4 - - - -
DPGN 3 1 2 - -
CGN 2 1 - - -
Chr.GN 1 2 1 - -
Amy 7 7 7 - -
LN 3 4 3 - 3

Out of 59 primary glomerular diseases 39 cases presented with proteinuria, 23

cases with raised serum creatinine levels, 15 cases with raised blood urea levels and 6

cases with raised C3 levels. Out of 12 secondary glomerular diseases 10 cases presented

with proteinuria, 11 cases with raised serum creatinine levels and 10 cases with raised

blood urea levels. ANA/AntidsDNA positivity was seen in 3 cases of lupus nephritis.

Table no 7: Sex distribution of various glomerular diseases.

Glomerular diseases Mal Femal

FSGS 9 6
Mesangioproliferative GN 7 6
Membranoproliferative GN 8 1
Membranous Nephropathy 7 2
Amyloidosis 6 1
Lupus Nephritis 1 4
Cortical Necrosis 0 2
 Male predominance was seen in FSGS, MPGN, MN and Amyloidosis of

kidney. Lupus nephritis and cortical necrosis showed female predominance.

Graph - 5

SEX DISTRIBUTION OF BPRD

10 9
9
8
8
7 7 7
6 6 6 6
RATIO

5 male
4 4 female
3
2 2 2
1
1 1 1
0
0

DISEASES

Table no 8: WHO classification of Lupus Nephritis.

Lupus Nephritis No of cases Percentage

Class IV 4 80%
Class V 1 20%
Total 5 100%

A total of five cases of lupus nephritis were seen, maximum were of class IV

(80%).
 Graph - 6

Pie chart showing cases belonging to various classes of Lupus Nephritis

20%

80%

Class IVClass V

Table no 9: Immunofluorescence studies of glomerular diseases.

S.no Biopsy No Diseases IgG IgA IgM C3

1 1196/05 FSGS + -ve -ve ++

2 381/08 FSGS -ve -ve ++ -ve

3 109/06 FSGS -ve -ve + +

4 767/06 FSGS -ve ++ -ve ++

5 1278/06 FSGS -ve -ve + -ve

6 1568/06 MesPGN --ve -ve -ve -ve

7 143/06 MesPGN -ve -ve -ve -ve

8 52/07 MesPGN -ve -ve -ve -ve

9 145/07 MesPGN -ve -ve + -ve

10 481/07 Mes PGN -ve -ve +++ -ve

11 748/07 MesPGN -ve -ve +++ -ve

12 786/07 MesPGN -ve -ve +++ -ve

13 1414/07 MesPGN -ve -ve -ve -ve

14 1541/07 MesPGN -ve -ve -ve -ve

15 1388/06 MPGN + -ve -ve ++

16 618/07 MPGN -ve -ve -ve ++

17 1071/07 MPGN +++ -ve -ve +

18 408/06 MPGN -ve -ve -ve +++

19 512/08 MPGN -ve -ve -ve +++

20 749/07 MN +++ -ve -ve +++

21 1363/07 MN +++ -ve -ve -ve

22 284/08 MN +++ -ve -ve -ve

23 227/08 MN ++ -ve -ve -ve

24 22/08 MCD -ve -ve ++ -ve

25 92/08 MCD -ve -ve + -ve

26 133/08 LN(IV) + ++ ++ +

27 33/08 LN(IV) +++ +++ ++ +

28 392/08 LN(IV) ++ ++ ++ ++

29 240/08 AMY -ve -ve + -ve

30 262/08 Chr.GN -ve -ve + -ve

31 574/06 Chr.GN + -ve + +

32 404/07 Cres.GN +++ -ve -ve -ve

33 1266/06 Cres.GN -ve -ve -ve +++

34 1136/05 Diff.PGN ++ -ve -ve -ve

35 1357/07 Diff.PGN ++ +++ -ve -ve

 Immunofluorescence studies were done for 35 cases where there was difficulty in

diagnosis by light microscopy. IgG, IgA, IgM and C3 were used and the pattern of

deposition was studied. Systemic lupus erythematosus class IV showed full house

positivity that is all the four IgG, IgA, IgM and C3 deposits were positive.
 DISCUSSION

In the seventy five cases reviewed in three years which included one year

retrospective and two years prospective study, two cases (2.66%) had inadequate

tissue sample. According to Bolton and Vaughan adequate samples of tissue were

obtained in 90% - 95% cases by an experienced operator by percutaneous

biopsy45. In the present study the adequate tissue was obtained in 97.5% of cases.

Among seventy five cases 25% cases were of FSGS in the age group of

10 – 35 years, followed by Mesangioproliferative glomerulonephritis which

contributed to 22.03%. These cases were predominantly seen in males and they

presented with nephrotic range proteinuria and some patients with elevated Urea

and Creatinine levels .

Incidence of FSGS in various studies.

S.NO Studies FSGS %

1 Winn PM & Daskalakis46 35%
2 Haas et al9 35%
3 Abrantes MM et al53 32%
4 Rana K et al 49 20%
5 Rennke & Klein et al 50 20%

6 Chandrika KB51 18.84%

7 Presnent study 25%

 In the present study Nephrotic syndrome was the commonest presentation

in primary glomerular diseases with FSGS accounting for 25% of cases.

Winn and Nikki revealed FSGS is the most common cause of nephrotic

syndrome in adults accounting for 35% of cases. The clinical hallmark of these

cases had nephrotic range proteinuria46.

Schwartz et al revealed that the prevalence of nephrotic syndrome in

primary glomerular diseases ranges from 44% to 74% 47.

Pointer and Patel showed that Focal segmental glomerulosclerosis is the

most common cause of nephrotic syndrome in adults occurring in 36% to 86% of

cases 48.

Rana K et al revealed FSGS is the most common cause of nephrotic

syndrome in adults49.

50 51
Rennke et al and Chandrika KB revealed FSGS was the commonest

occurrence in their studies.

Overall incidence of FSGS is increasing over the past two decades and the

commonest cause of nephrotic syndrome in adults is Focal segmental

glomerulosclerosis .
 Minimal change disease is more common in boys than in girls. It is most

common in young children less than six years. However MCD can occur at any

age and is the commonest cause of nephrotic syndrome in adults. The incidence of

minimal change disease is 2 to 16 / 100,000 per year in children younger than 16

years52.

In the present study Minimal change disease seen commonly below 10

years of age with male predominance.

In the present study out of 59 primary glomerular diseases, 52 cases

showed clinical and laboratory finding correlation in arriving histopathological

diagnosis.

Abrantes MM et al53 studied 110 patients with biopsy proven FSGS and

compared with clinical and laboratory data. The clinical data included nephrotic

syndrome symptoms, height, weight, response to steroid therapy and laboratory

data included urea, creatinine , 24- hour protein excretion and hematuria .

In the present study out of 12 secondary glomerular diseases 7 cases

(58.33%) were of renal amyloidosis and clinically these cases were in the age

group of 40 – 60 years. There was male predominance with high creatinine and

urea levels with nephrotic range proteinuria > 3.5gm/kg and clinical features of

nephrotic syndrome. All the cases were associated with chronic inflammatory
states in which tuberculosis, bronchiectasis and rheumatoid arthritis were

common.

There were totally five cases of Lupus nephritis which showed class IV

and class V changes. Four showed diffuse proliferative glomerulonephritis (class

IV) and one case showed membranous nephropathy (class V). All the cases were

seen in adult females with features of nephrotic syndrome. Laboratory data of

these patients showed ANA, AntidsDNA positivity .

Incidence of Amyloidosis and Lupus nephritis in various studies.

S.NO Studies Amyloidosis % Lupus nephritis %

57
1 Agarwal et al 16.4% ----
2 Agarwal et al57 ------ 8.3%
3 Austein et al 58 ------- 10%
4 Present study 55.00% 45.00%

Agarwal revealed that among the secondary glomerular diseases diabetic

nephropathy was the commonest cause of nephrotic syndrome (53%) followed by

57
amyloidosis (16.4%) and Lupus nephritis (8.3%) .Tuberculosis was the

commonest cause of renal amyloidosis seen in 50% of cases54

Dikman and Thomas compared the clinical and morphological course of

amyloid renal disease. They showed that the renal amyloidosis was common in

adults and these patients presented with nephrotic syndrome symptoms with

nephrotic range massive proteinuria with elevated blood urea nitrogen and
creatinine levels. Progression to azotemia and renal failure was common in all

forms of renal amyloidosis55.

Primary amyloidosis is common in developed countries and secondary

amyloidosis common in developing countries. AA amyloidosis affects patients of

various ages with median age of 50 years. However in younger patients affected

by AA amyloid a hereditary component must be considered. The conditions

associated with secondary amyloidosis are Inflammatory arthritis, Chronic

inflammatory states, Chronic infections and malignancies56. The overall incidence

of renal amyloidosis is 3% and nephrotic syndrome was the commonest

presentation 57.

According to Austin et al who performed sixty four biopsies in patients

with lupus nephritis fifty six were diffuse proliferative glomerulonephritis and

five cases were focal segmental glomerulonephritis and three were mixed

membranous and focal proliferative glomerulonephritis58.

Balakrishnan revealed among the biopsy proven renal diseases Systemic

lupus erythematosus and cortical necrosis has got female predominance59.

 CONCLUSION

1. A one year retrospective and two years prospective study was done on

percutaneous renal biopsies which was performed under real time ultrasound

guidance from 1st August 2005 to 31st July 2008 and a total of 75 biopsies were

reviewed in 3 years.

2. Among the 75 cases, 2 cases (2.66%) were inadequate for opinion and 2 cases

(2.66%) were of other diseases like tubulointerstitial nephritis and chronic

pyelonephritis.

3. A protocol was prepared for standardizing the interpretation of renal biopsies and

all the biopsies were studied according to that proforma .

4. Special stains were used and they were helpful in confirming the histopathologic

findings seen in Haematoxylin- Eosin stained sections.

5. Among 75 cases the majority of the biopsies were of primary glomerular diseases.

6. Among all the primary glomerular diseases, FSGS was the most common

accounting for (25.42%) of cases followed by MESPGN (22.03%).

7. Among the secondary glomerular diseases, renal amyloidosis was found to be

more common in the patients who presented with nephrotic syndrome. Maximum

cases were of secondary amyloidosis in which tuberculosis and chronic

respiratory infections were common.

8. Nephrotic syndrome was the commonest presentation for both primary and

secondary glomerular diseases.

9. Out of 75 cases which included both primary and secondary glomerular diseases,

64 cases showed correlation of pathological findings with clinical and laboratory

parameters.

10. The clinical examination, laboratory findings including biochemical tests were

very much helpful in arriving the histopathological diagnosis.

11. Immunofluorescence was done in selected cases where there was difficulty in

diagnosis by light microscopy.

 SUMMARY

Our results showed that among 75 cases which were reviewed in 3 years

which included one year retrospective and two years prospective study , there

were 59 cases (78.66%) of primary glomerular diseases. The maximum cases in

these diseases were of FSGS accounting for 15 cases (25.42%) followed by

MESPGN 13 cases (22.03%), MPGN accounting for 9 cases (15%) and MN were

9 cases (15%).

Minimal change disease was commonly found in less than 10 years of age,

accounting for 4 cases (6.66%) and was commonly seen in males.

A total of 12 cases due to secondary glomerular diseases were reviewed

among which 7 cases (58.33%) were of renal amyloidosis and 5 cases (45.45%)

were of lupus nephritis.

Out of 75 cases which included both primary and secondary glomerular

diseases, 64 cases showed correlation of pathological findings with clinical and

laboratory parameters.

Among the secondary glomerular diseases renal amyloidosis was commonly

seen in adults 40-60 years with male predominance with high creatinine and urea

levels with nephrotic range proteinuria >3.5gm/kg and nephrotic syndrome .

 All the cases were associated with chronic inflammatory states in which

tuberculosis, bronchiactasis, and rheumatoid arthritis were common.

Lupus nephritis was commonly seen in adult females, who clinically

presented with joint pains, rashes, and positive biochemical tests like ANA, Anti

ds DNA. There were 5 cases out of 12 secondary glomerular diseases in which 4

cases showed Diffuse proliferative GN ( WHO grade IV ) by light microscopy

and confirmed by Immunofluorescence which shows full house positivity of IgG,

IgA, IgM and C3 and one case of Membranous nephropathy ( WHO grade V ).

Special stains were used and were helpful in arriving at a better

histopathological diagnosis.

Immuunofluorescence was done in selected cases and was helpful in

confirmation of the diagnosis.

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 PROFORMA

A clinicopathological study of renal biopsies in glomerular diseases conducted in

BLDEA’S Shri B. M. Patil medical college.

Serial No: Date:

Name: I P/OP No:

Age/sex HPR No:

Chief complaints:

Past history

Personal history

Family history

General physical examination

Vital signs / Vital parameters

Systemic examination

1) Per abdomen
2) Respiratory
3) Cardiovascular
4) Central nervous

Clinical diagnosis

Laboratory parameters

I) Routine Hematological Investigations

1) Hb
2) TC,DC,ESR

II) Biochemical Data

1) Blood Urea
2) Serum Creatinine
 3) Total proteins
4) Albumin

III) Urine findings

1) urine routine and microscopy
2) 24 hrs urinary protein estimation

IV) Serological test

1) C3, C4, ( complement )
2) ANCA
3) ANA
4) Anti GBM antibodies

Histopathological examination:

Light microscopy:

1. TOTAL NUMBER OF GLOMERULI

2. GLOMERULAR SIZE

3. CAPILLARY WALL/GBM

4. GLOMERULAR CELLULARITY

5. MESANGIAL CELLS

6. BOWMAN’S CAPSULE/SPACE

7. TUBULOINTERSTITIAL CHANGES

8. VASCULAR CHANGES

Impression :

Immunofluorescence findings :

Final diagnosis:
 Master Chart

S.No. HPR.No Age/Sex Clinical History Lab Inves. Clinical Diag. LM Diag. IF - Findings. Final Diag.
.
1 1136/05 10Y/M Facial puffiness, Alb 3+ MPGN, IgA Inadequate IgG ++, C3 & Diffuse proli.
Pedal edema C3-88 nephropathy for opinion IgM negative GN
2 1192/05 23Y/M Sepsis with renal Alb 3+ FSGS Amyloidosi ------------ Amyloidosis
failure Creat-4.6 s of kidney
of kidney
3 1196/05 11Y/F Facial puffiness, Alb 3+ FSGS MPGN C3 in sclerotic FSGS
pedal edema Creat-2.7 tufts
4 1228/05 65Y/M Subdural ---------- --------- ATN -------------- ATN
hematoma
5 1178/05 65Y/M Head injury TP/Alb- ATN ATN with ------------- ATN with
7.1/3.0 nephritis nephritis
6 1434/05 10Y/F Facial puffiness, Alb 3+ MCNS FSGS -------------- FSGS
pedal edema Creat-1.0 FSGS
7 13/06 35Y/F Facial puffiness, Alb 3+ FSGS FSGS ---------------- FSGS
pedal edema MN
8 40/06 2Y/M Facial puffiness, Alb 4+ Congenital Inadequate ---------------- Inadequate for
pedal edema NS for opinion opinion
9 109/06 40Y/M Proteinuria with Alb 3+, C3- MPGN FSGS IgM(+),C3(+) FSGS
renal failure 113 FSGS

10 454/06 45Y/M K/C/O Pulm.TB Alb 3+ Amyloidosis -------------- Amyloidosis

Of kidney Amyloidosi of kidney
s
of kidney
11 143/06 30Y/M Facial puffiness Alb 4+ FSGS FSGS IgG,IgM&C3 MesPGN
negative

65
12 299/06 42Y/M Blunt injury, Alb 4+ RPGN Diff proli --- ------------ Diff proli GN
facial puffiness GN
13 958/06 36Y/M Hydronephrosis Alb 2+ ARF Inadequate -------------- Inadequate for
for opinion opinion
14 767/06 32Y/M Nephrotic Alb 4+ MN IgA IgA 3+&C3 2+ IgA Neph.
syndrome nephropaty with sclerosis
15 908/06 72Y/M Facial puffiness Alb 4+ ARF Apple green
Amyloidosi bifrengence Amyloidosis
s of kidney
of kidney
16 1266/06 17Y/M Facial puffiness --- MPGN Crescentic C3 3+ Crescentic
GN GN
17 641/06 8Y/M Facial puffiness ----- MPGN MCD --------------- MCD
18 1278/06 18Y/M Facial puffiness Creat.0.9 NS MCD IgM + FSGS
19 1424/06 11Y/M Swelling face , Alb 2+ NS FSGS -------- FSGS
edema feet
20 1388/06 56Y/M Facial puffiness Alb 4+ FSGS MPGN C3-2+,IgG -1+ MPGN
pedal edema
21 1419/06 9Y/F Nephrotic Alb 4+ FSGS FSGS ------------- FSGS
syndrome
22 1568/06 28Y/F Nephrotic Alb 4+ FSGS MesPGN IgG,IgM.&C3 MesPGN
syndrome MPGN NEG
23 52/07 16Y/F Nephrotic Alb 4+ FSGS MesPGN IgG,IgM.&C3 MesPGN
syndrome NEG
24 145/07 38Y/M Facial puffiness, Alb 4+ FSGS Amyloidosi IgG,IgM.&C3 Diffuse
edema feet s NEG mesangial
of kidney hypercellularit
y
25 206/07 35Y/F Facial puffiness Alb 4+ FSGS FSGS ----------------- FSGS
edema feet MN
26 412/07 12Y/F Nephrotic Alb 4+ SLE with Lupus ------------- Lupus
syndrome ANA/DsDN renal nephritis nephritis (V)
A-+VE involvement (V)
27 481/07 16Y/M Nephrotic Alb 4+ FSGS MesPGN IgM 3+, MesPGN with
syndrome MCNS MCD
28 486/07 23Y/M Fever with joint ANA –VE Secondary MPGN ------------- MPGN
pains Alb 4+ GD

29 493/07 17Y/F Fever with joint ANA SLE Lupus -------------- Lupus
pains +VE,C3 low nephritis nephritis (IV)
(IV)
30 590/07 38Y/M Facial puffiness, TP/Alb- FSGS MN -------------- MN
edema feet 7.1/3.0 MN
31 618/07 35Y/F Facial puffiness, Alb 4+ FSGS MPGN C3-3+, MPGN
edema feet C3-low MPGN
32 633/07 11Y/M Nephrotic Protein FSGS FSGS ---------------- FSGS
syndrome traces MCNS
33 692/07 62Y/F Facial puffiness, ------------- Nephrotic Amyloidosi -------------- Amyloidosis
edema feet syndrome s of kidney
of kidney
34 748/07 30Y/F Facial puffiness, Alb 4+ FSGS MesPGN IgM 3+ MesPGN
edema feet MPGN
35 749/07 22Y/M Facial puffiness, ----------- FSGS MN IgG3+,C3-2+ MN
edema feet IgA
36 713/07 26Y/F Facial puffiness, Alb 4+ FSGS MesPGN --------------- MesPGN
edema feet MCNS
37 786/07 28Y/M Facial puffiness, Alb 4+ FSGS MesPGN IgM3+ MesPGN
edema feet
38 1071/07 55Y/M Nephrotic Alb 4+ Amyloidosis MPGN IgG 3+,faint C3 MPGN
syndrome of kidney
39 838/07 25Y/M Facial puffiness, Creat-1.0 MPGN MN ---------------- MN
edema feet
40 702/07 27Y/F ARF Alb 4+ MPGN MesPGN IgG,IgM.&C3 MesPGN
C3low FSGS NEG
41 785/07 31Y/M Facial puffiness, Alb 3+ MPGN MesPGN ------------- MesPGN
edema feet Creat-1.6 FSGS
42 888/07 55Y/F Nephrotic Alb 3+ FSGS MN ------------- MN
syndrome Creat-1.2 MN
43 900/07 36Y/F Nephrotic Alb 4+ FSGS MesPGN -------------- MesPGN
syndrome Creat-1.0 MN
44 914/07 35Y/M Facial puffiness Alb 4+ FSGS MPGN -------------- MPGN
Creat-2.8 MN
45 976/07 25Y/M Facial puffiness, Alb 4+ MPGN Global IgG,IgM&C3+v Chr. GN
edema feet Creat-1.8 MN sclerosis e
46 1000/07 70Y/M Type 2 DM Creat-2.7 MPGN MPGN C3-3+ MPGN
47 1117/07 65Y/M Facial puffiness, Alb 4+ FSGS Global ------------- Global
edema feet Creat-4.2 sclerosis sclerosis
48 1155/07 2Y/F Snake bite Urine ARF Cortical ------------- Cortical
protein – necrosis necrosis
8:1
49 1203/07 15Y/F Snake bite Alb 2+ Cortical Cortical --------------- Cortical
Creat-4.8 necrosis necrosis necrosis
50 1283/07 28Y/M Facial puffiness Alb 4+ Crescentic Crescentic IgG 3+ Crescentic
edema feet ANA-ve GN GN GN
51 1285/07 28Y/M Facial puffiness Alb 4+ FSGS MesPGN -------------- MesPGN
edema feet Creat-1.0
52 1357/07 30Y/F Pedal edema Creat-4.0 Nephrotic MPGN IgA3+,IgG2+ Diffuse GN
syndrome FSGS with IgA
nephropathy
53 1363/07 48Y/M Facial puffiness, Alb 4+ FSGS FSGS IgG 3+ MN
edema feet Creat-1.0 MN
54 1635/07 23Y/F Nephrotic Alb 4+ FSGS FSGS ------------- MesPGN
syndrome MesPGN
55 1414/07 25Y/M Facial puffiness, Alb 4+ FSGS MesPGN IgG,IgM.&C3 MesPGN
edema feet Creat-1.7 negative
56 1415/07 7Y/F Facial puffiness, Alb 3+ MCNS FSGS --------------- FSGS
edema feet Creat-0.8
57 1456/07 48Y/F Facial puffiness, Alb 3+ FSGS FSGS --------------- FSGS
edema feet Creat-0.6
58 1457/07 20Y/M Pulm.Kochs 3 Alb 3+ Amyloidosis Amyloidosi -------------- Amyloidosis
years of kidney s of kidney
of kidney
59 1540/07 32Y/M Facial puffiness, Alb 3+ Amyloidosis MN -------------- MN
edema feet of kidney
60 1541/07 50Y/M Facial puffiness, Alb 3+ FSGS MesPGN IgG,IgM.&C3 MesPGN
edema feet negative
61 19/08 27Y/M Facial puffiness, Alb 3+ FSGS MPGN --------------- MPGN
edema feet
62 22/08 12Y/M Facial puffiness, Alb 3+ FSGS MesPGN IgM 2+ MCD
edema feet
63 33/08 28Y/F Joint pains Alb 4+ SLE Lupus IgG3+,IgM2+,Ig Lupus
,rashes ANA/DsDN nephritis A3+ nephritis (IV)
A-+ve (IV)
64 92/08 17Y/M Edema feet Alb 3+ FSGS MesPGN IgM + MesPGN

65 133/08 12Y/M Facial puffiness, Alb 3+ SLE Lupus IgG3+,IgM2+,Ig Lupus

edema feet ANA/DsDN nephritis A3+ nephritis (IV)
A-+ve (IV)
66 240/08 45Y/M Facial puffiness, Alb 3+ FSGS Amyloidosi ----------------- Amyloidosis
edema feet Creat-0.8 s of kidney
Of kidney
67 262/08 50Y/M Facial puffiness, Alb 3+ ARF ATN IgM + Chr.GN
edema feet Creat-3.6
68 284/08 45Y/F Facial puffiness, Alb 3+ FSGS FSGS IgG3+ MN
edema feet Creat-0.8
69 227/08 50Y/M Edema feet Alb 3+ FSGS MN IgG2+ MN
Creat-2.8 MN
70 381/08 41Y/M Edema feet Alb 3+ FSGS FSGS IgM2+ FSGS
Creat-5.0
71 392/08 17Y/F Joint pains Alb 4+ SLE Lupus IgG3+,IgM2+,Ig Lupus
,rashes ANA/DsDN nephritis A3+ nephritis (IV)
A-+ve (IV) C32+
72 512/08 23Y/M Facial puffiness, Alb 3+ FSGS MPGN C3-3+ MPGN
edema feet Creat-1.8 MPGN
73 565/08 60Y/M COAD Alb 4+ FSGS Amyloidosi ------------------ Amyloidosis
s of kidney
Of kidney
74 641/08 16Y/M Hematuria Alb 4+ FSGS Crescentic ------------------- Crescentic
RPGN GN GN
75 653/08 28Y/M Facial puffiness, Alb 4+ Nephrotic FSGS ------------------- FSGS
edema feet Creat-1.2 syndrome
 KEY TO MASTER CHART

M - Male

F - Female

LM - Light microscopy

IF - Immunofluorescence

Alb - Albumin

Crea - Creatinine

C3 - Complement

ANA - Anti nuclear antibody

ATN - Acute tubular necrosis

FSGS - Focal segmental glomerulosclerosis

MesPGN - Masangioproliferative glomerulonephritis

MPGN - Membranoproliferative glomerulonephritis

MN - Membranous nephropathy

AMY - Amyloidosis

NS - Nephrotic syndrome

SLE - Systemic lupus erythematosus

ARF - Acute renal failure

MCD - Minimal change disease

LN - Lupus nephritis

71