Aasim Ahmad  ( Department of Medicine, The Aga Khan University Hospital, Karachi. )
Jawed Akhtar  ( Department of Medicine, The Aga Khan University Hospital, Karachi. )

Renal transplant is now the accepted mode of treatment of end stage renal disease (ESRD)¹. The major causes of ESRD being diabetes mellitus, hypertension, glomerulonephritis, polycystic kidney disease and other/unknown². The most common glomerular disease in renal allograft biopsies is transplant glomerulopathy³, i.e., those lesions related to transplant rejections. Other glomerulonephropathies (GN) also occur which are recurrences of GN the original disease which caused ESRD, diseases related to the donor and those without any explanation called denovo GN. One hundred five well documented cases of denovo occurrence of membranous GN in renal allograft have been reported in medical literature. We present a case from Pakistan where ap­proximately 1,000 transplanted patients are being fol­lowed-up.

A 48 year old male was diagnosed as having ESRD secondary to hypertension. He received a renal allograft from a living non- related donor. For immunosuppres­sion he was on azathioprine 100 mg, prednisolone 10 mg and cycloporin 160 mg daily and hypertension was controlled by atenolol 100 mg and prazocin 8 mg daily. He remained well for three year post transplant when he noticed bilateral oedema of feet which gradually in­creased. There were no symptoms relating to his urinary tract and his urinary output remained unchanged. On examination, he had bilateral pitting pedal oedema extending upto mid calf but did not have fever, pallor, jaundice orlymphadenopathy. His jugular venous pressure was not raised and blood pressure was 140/80 mmHg. His cardiovascular, respiratory, CNS and abdominal examinations were normal. His right lower quadrant graft area was non-tender and without a bruit. The investigations revealed proteinuria of > 4gm/24 hours with a normal microscopy, serum al­bumin of 1.8 gm/dl and fasting cholesterol of 320 mg/dl. His creatinine rose to 2.1 mg/dl from his baseline post-transplant level of 1.6 mg/dl. The electrolyte, cyclosporin levels, ESR, autoimmune profile and hepatitis B profile did not reveal any abnormality.A lower pole renal transplant biopsy was done under ultrasound guidance and the specimen was subjected to light microscopy, immunofluorescence and electron micros­copy. On light microscopy it showed swelling of glomerular epithelial cells and thickening of basement membrane, on silver stains the basement membrane was thick and demonstrated “spike” formation. There was no evidence of acute or chronic rejection or cyclosporine toxicity. Immunofluoresceure revealed anti-JgG 3+ granular staining along capillary walls and anti-C3 patchy 1+ granular staining along capillary walls. Electron midroscopy (Figure 1 and 2)


revealed irregularly thick­ened basement membrane with dense deposit dis­tributed along the subepithelial aspects; these were separated and occasionally surrounded by basement membrane extensions. Epithelial foot processes demonstrated effacement and the tubules showed mild degenerative change (Figure 3).

Apart from transplant glomerulonephropathies recurrence of glomerulonephritis in a renal allograft occur in 6-9% of cases⁴ and these have different mor­phological forms like diffuse proliferative, crescentric, membranous and focal sclerosis^5-7. The most common gI omerular lesion which occurs denovo is membranous GN (MGN) the reported incidence in the West being 2-9%3. MGN may occur between four months to six years following transplant with a mean Of 21 months⁸. The diagnosis is suspected when nephrotic syndrome is not associated with obvious clinical features of rejection, while renal function is either normal or slightly decreased. It is confirmed by excluding recurrence of GN and by the histological picture. The denovo MGN progress to renal failure more rapidly than the idiopathic form³ and the graft survival is poor⁹. There is no relationship with the type of graft, age, sex, race and antigen matching. To the best of our knowledge this is the first case of denovo membranous glomerulonephropathy in a renal allograft reported from Pakistan.

We are extremely thankful to Prof S.A.J. Naqvi, Nephrologist, Jinnah Postgraduate Medical Centre for his advice and opinion. We are also thankful to Mr. Sulaiman his help in preparing this manuscript.

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