Case 1 -- Kidney biopsy after liver transplantation showing cyclosporine induced focal segmental sclerosis Contributed by Randhawa, Parmjeet, MD CLINICAL HISTORY: A 50 yr. old man transplanted 4 years ago for hepatitis C infection which subsequently recurred in the allograft liver. His immunosuppressive regime consisted of cyclosporine  and steroids. A renal biopsy was performed for 4+ proteinuria. Blood urea 70mg/dl, serum creatinine 2.5 mg/dl. DESCRIPTION OF FIGURES: A glomerulus showing mild increase in mesangial cellularity. A second glomerulus showing focal segmental sclerosis. A third glomerulus showing mild increase in mesangial matrix and cellularity confined to the polar region. Hyalin change is observed in the afferent arteriole (PAS stain). Renal tubules showing fine isometric vacuolization in the cytoplasm. Electron micrograph showing a glomerulus with mild increase in mesangial cellularity. No immune complex deposits are seen. Electron micrograph showing non-specific thickening of the glomerular basement membranes with incorporation of granular and filamentous cell debris. No immune complex deposits are seen. DISCUSSION OF CASE: Hepatitis C associated glomerular injury was the prime consideration in the differential diagnosis at the time of biopsy. Hepatitis C infection has been most commonly linked to membranoproliferative or cryoglobulinemic glomerulonephritis. However, in this case no immunoglobulin or cryoglobulin deposits were found by electron microscopy. Focal segmental sclerosis was the most important lesion found and provided an anatomic basis for the heavy proteinuria. The lesion was felt to be secondary to arteriolar hyalin change in the afferent arteriole, which in turn was most likely the result of chronic cyclosporine toxicity. The presence of prominent tubular vacuolization and a striped pattern of interstitial fibrosis supported the latter interpretation. There was no clinical evidence for other known causes of focal segmental glomerulosclerosis such as late stage glomerulonephritis, HIV infection, IV drug abuse, renal artery stenosis, reflux nephropathy or diabetes mellitus.  The possibility of idiopathic focal segmental glomerulosclerosis can not be definitely excluded. The cause of the mild increase in mesangial cellularity is uncertain. Presumably leakage of plasma proteins and lipids across the glomerular capillaries provided a stimulus for the proliferation of mesangial cells. DIAGNOSIS: Focal segmental glomerulosclerosis probably secondary to chronic cyclosporine therapy.

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