Pretransplant hepatitis C virus infection - A predictor of proteinuria after renal transplantation

Background. Reports have suggested that hepatitis C virus (HCV)-infected kidney recipients may develop de novo glomerular lesions caused by the virus. We studied the relationships between pretransplantation anti-HCV antibodies and the occurrence of proteinuria and the link with short-and long-term patient and graft survival. Methods. A total of 322 consecutive renal recipients treated at a single center from 1989 to 1994 whose sera were routinely assayed for anti-HCV antibodies at the time of transplantation were analyzed. The risks of persistent proteinuria (>1 g/day), graft loss, or death were estimated by Kaplan-Meier analysis. The relationship between clinical variables and each outcome was examined by Cox multivariate regression analysis. Results. Before transplantation, 9.6% of the recipients were anti-HCV antibody positive. Persistent proteinuria developed in 13.6% recipients. The presence of anti-HCV antibodies was strongly associated with proteinuria (relative risk [RR]=5.36, 95% confidence interval [CI]=2.49-11.51). Proteinuria occurred more frequently in second grafts (RR=2.64, 95% CI=1.10-6.29). The number of HLA-A,B mismatches was an independent risk factor (RR=1.55, 95% CI=1.10-2.19). Recipient age (RR=0.80, 95% CI=0.63-1.02) and duration of dialysis (RR=0.86, 95% CI=0.77-0.96) were protective factors. Histology of biopsies from 26/44 recipients with proteinuria showed that de novo glomerular lesions were more frequent in HCV-positive patients, although the difference was not significant. One-and five-year graft survival rates were significantly worse in patients with proteinuria (90.7% and 41.1%) than in patients without it (95.6% and 91.8%) (P<0.00001). Despite the strong association between HCV infection and proteinuria, patient and graft survival rates in anti-HCV-positive and anti-HCV-negative recipients were similar. Conclusions. The presence of anti-HCV antibodies before renal transplantation seems to be a major risk factor of proteinuria after transplantation. This may be due to glomerular lesions caused by HCV. However, anti-HCV has no impact on B-year patient and graft survival.