IMMUNE-COMPLEX GLOMERULONEPHRITIS IN PATIENTS COINFECTED WITH HUMAN-IMMUNODEFICIENCY-VIRUS AND HEPATITIS-C VIRUS

Human immunodeficiency virus-associated nephropathy (HIVAN), character ized by heavy proteinuria, rapidly progressive renal failure, ''collap sing'' glomerulopathy, and tubulointerstitial abnormalities, is the mo st common finding in HIV-infected patients undergoing a renal biopsy a nd predominantly affects blacks. We describe the clinical features and renal pathologic findings of 12 intravenous drug users (IVDUs) coinfe cted with HIV and hepatitis C virus (HCV) who were selected for renal biopsy because they presented with features different from typical HIV AN, including hypertension, microscopic hematuria, and cryoglobulinemi a, There were seven black and five Hispanic patients. Eleven patients had immune complex glomerulonephritis (ICGN); one had glomeruloscleros is with immune complex deposits. Ten individuals had evidence of past hepatitis B viral infection, but none had persistent hepatitis B surfa ce antigenemia. No other underlying cause for immune complex glomerulo nephritis was identified. Renal biopsy showed membranoproliferative gl omerulonephritis in five patients, mesangial proliferative glomerulone phritis in five, membranous nephropathy in one, and ''collapsing'' glo merulopathy with immune complex deposits in one. Hepatitis C virus RNA was detected by reverse transcription-polymerase chain reaction (RT-P CR) in the renal tissue and/or serum of nine of the 11 patients tested , and also in the renal biopsy tissue of four of eight patients with c linical and pathologic features of typical HIVAN without immunofluores cence evidence of immune complex deposits. One patient presented with renal failure, five patients developed end-stage renal disease (ESRD) requiring hemodialysis (mean time, 6.5 months), and six had stable ren al function after a mean follow-up of 29.1 months (range, 2 to 72 mont hs). Liver function abnormalities were present in seven of the 12 indi viduals, including four of the six patients who developed renal failur e. These findings indicate that in some patients coinfected with HIV a nd HCV, the development of ICGN may dominate the clinical course of th e disease. The occurrence of ICGN among black patients at risk for HIV AN may be related to the relatively high prevalence of HCV infection a mong IVDUs in this group. (C) 1997 by the National Kidney Foundation, Inc.