Hepatitis C virus infection in kidney transplant recipients

To determine the prevalence and significance of hepatitis C virus infection in kidney transplant recipients, paired serum samples collected from 100 renal allograft recipients on admission for kidney transplantation and 1 yr after transplantation were tested for antibody to hepatitis C virus with second-generation enzyme immunoassay and recombinant immunoblot assay and for hepatitis C virus RNA with reverse transcription–polymerase chain reaction. Before kidney transplantation, hepatitis C virus antibody was detected with second-generation enzyme immunoassay in 18 patients (12 second-generation recombinant immunoblot assay–positive, 6 second-generation recombinant immunoblot assay–indeterminate). Nine of 12 second-generation recombinant immunoblot assay–positive and 2 of 6 second-generation recombinant immunoblot assay–indeterminate samples were hepatitis C virus RNA positive. In addition, 7 of 82 patients who had no detectable antibody on second-generation enzyme immunoassay or second-generation recombinant immunoblot assay were hepatitis C virus RNA positive. After kidney transplantation, hepatitis C virus antibody was detected in 19 patients (12 second-generation recombinant immunoblot assay–positive, 7 second-generation recombinant immunoblot assay–indeterminate, 14 seropositive for hepatitis C virus antibody). Eleven of 12 patients with second-generation recombinant immunoblot assay–positive results and 4 of 7 with second-generation recombinant immunoblot assay–indeterminate results were positive for hepatitis C virus RNA. Hepatitis C virus RNA was present in 28 patients 1 yr after kidney transplantation. Six patients appeared to have acquired active hepatitis C virus infection 1 yr after kidney transplantation (seroconverted to hepatitis C virus RNA positivity). We found no correlation between the presence of hepatitis C virus markers in the pretransplant and posttransplant sera and clinical/biochemical parameters or clinical outcome. Hepatitis C virus infection was clinically silent in most patients. Semiquantitation of serum hepatitis C virus RNA in 25 patients with hepatitis C virus infection showed that the hepatitis C virus RNA titer remained the same (n = 12) or increased at least 10-fold (n = 12), and only 1 patient had a decrease in serum hepatitis C virus RNA level. These data suggest that (a) the prevalence of hepatitis C virus infection is high in kidney transplant recipients, (b) active hepatitis C virus replication may be present in the absence of hepatitis C virus antibody, (c) many of these patients who are second-generation enzyme immunoassay–positive but second-generation recombinant immunoblot assay–indeterminate are hepatitis C virus RNA positive, (d) hepatitis C virus infection is usually clinically silent during the initial follow-up period and (e) antirejection immunosuppression may enhance hepatitis C virus replication. (HEPATOLOGY 1993;18:1027-1031).