October 1988, Volume 38, Issue 10

Short Reports


Qamar Jamal  ( Departments of Pathology, Jinnah Postgraduate Medical Centre, Karachi. )
Naeem A. Jafarey  ( Departments of Pathology, Jinnah Postgraduate Medical Centre, Karachi. )
Ali Jaffar Naqvi  ( Nephro-urology, Jinnah Postgraduate Medical Centre, Karachi. )

Since the introduction of percutaneous renal biopsies about 30 years ago, numerous clinicopathological studies have been reported from different parts of the world.1-6 Several small series have also been reported from Pakistan.7-9 This paper is a review of 1,508 percutaneous renal biopsies from March 1975 to March 1987.


One thousand five hundred and eight renal biopsies (1294 in adults and 214 in children 0-14 years ) were done in 1200 patients using the method of Kark et al.10 Of these 1,162 (77%) were adequate for diagnosis. The sections were routinely stained with haematoxylin. and eosin (H&E). Periodic Acid Schiff (PAS) and Improved Jones Methanamine Silver (JMS) stains were used to demonstrate any increase in the thickness of basement membrane of the glomeruli and congo red when amyloidosis was suspected. The lesions were classified according to the criteria described by Hepinstail.11
The ages of patients ranged from 6 months to 74 years and male to female ratio was 1.6: 1.

Tables-I and II show frequency of histological lesions in adults and children, respectively.
Of 948 biopsies in adults, 710 (7 5%) had primary and 220(23%) secondary glomerular lesions. In 18 (2%), lesions were advanced and could not be classified.
The most common lesions in both groups, viz., adults and children, were minimal change and proliferative glomerulonephritis. Their frequency in adults was 29% and 25% and in children 45% and 30%, respectively.
The next in frequency were chronic glomerulonephritis. (12% and 11% respectively) and chronic pyelonephritis (9% and 6.5% respec­tively).


The lesions most frequently encountered in the present series were minimal change disorders and proliferative glomerulonephritis followed by chronic glomerulonephritis and chronic pyelone­phritis. Nevertheless, frequency of amyloidosis and glomeruloscierosis were also noteworthy particularly in children (Table-I and II).
A higher frequency of minimal change disorder in adults and a lower frequency in children was observed in the present series as com­pared to the published data (P< 0.05) 1,2,5-6,8-9 (Tables-II and III).
The contrary was true for proliferative glomerulonephritis, viz., its frequency was less in adults and high in children as compared to the reported series (P <0.05)1-2,5-6,8-9 (Table II and III). Moreover chronic glomerulonephritis, quite prevalent in our series (both in adults and children), was reported only by Churg whereas chronic pyelonephritis was reported by none of them (Tables-Il and III).

Higher frequency of chronic, primary and secondary glomerular lesions in the present series could partly be due to the patients reporting late for. treatment and partly due to difference in the criteria for selection of biopsy cases. In the present series patients were randomly selected for biopsy. Thus the frequency of chronic pyelonephritis and glomerulonephritis in our series were similar to those of Huland and Busch12 who studied the biopsy findings of 161 paTtients of various glomerular diseases undergoing renal dialysis (44% and 31% vs 35% and 26%).
The purpose of this study was to establish the pattern of glomerular disease in Pakistan. Being based upon light microscopic findings and special staining techniques only, the pattern is liable to change with the use of more sophisticated diagnostic tools like immunohistochemical methods, immunofluorescence and electron mic­roscopy. We, however, assume that it would provide a baseline for future research work.


1. Kaxk, R.M., Pirani, C.L., Pollak, V.E. , Muehrcke, R.C., Blainey., J.D. The nephrotic syndrome in adults; a common disorder with many causes. Ann. Intern. Med., 1958; 49: 751.
2. Blainey, J.D., Brewer, DB., Haxdwicke, J. and Soothill, J.F. The nephrotic syndrome. Diagnosis by renal biopsy and biochemical and immuno­logical analysis related to the response to steroid therapy. Q.J. Med., 1960; 29:235.
3. McGovern, VJ. Persistent nephrotic syndrome; a renal biopsy study. Aust. Ann. Med., 1964; 13:306.
4. Pollak, V.E., Rosen, S., Pirani, C.L., Muehrcke, R.C. and Kark, R.M. Natural history of lipoid nephsosis and of membranous glomerulone­phritis. Ann. Intern. Med., 1968; 69:1171.
5. Churg, J.,Habib, R. and White, R.H.R. Pathology of the nephrotic syndrome in children. A report for the international study of kidney disease in children. Lancet, 1970; 1: 1299.
6. Blainey, J.D., Brewer, D.B. and Hardwicke, J. Protein uric glomerular disease in adults: cum­ulative life tables over twenty years Q.J. Med., 1986; 59: 557.
7. Dil, A.S., Naqvi, S.AJ. and Jafarey, N.A. A study of protein clearances in patients with nephrotic syndrome.JPMA., 1976; 26: 234.
8. Sadiq. S., Jafarey. N.A. and Naqvi, S.AJ. An analysis or percutaneous renal biopsies in fifty cases of nephiotic syndrome. JPMA., 1978; 28: 121.
9. Nagj, A.H., Naveed, l.A., Rashid, A.and Hussain, K.S. Primary proliferative glomerulonephritis. A clinicomorphological analysis. JPMA., 1983; 33:56.
10. Kark, R.M., Muehrcke, R.C.,Pollak,V..E,Pirani, C.L and Kiefer, J.H. An analysis of five hundred percutaneous renal biopsies. Arch Intern. Med., 1958; 101:439.
11. Hepinstall, R.H. Pathology of the kidney. 3rd ed. Boston, little Brown, 1983.
12. Huland, H. and Busch, R. Chronic pyelonephritis as a cause of end stage renal disease. J. Urol., 1982; 127 : 642.

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