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Background: The aim of the present study was to investigate the impact of hepatitis C virus (HCV) infection on the long-term survival of renal transplant recipients., Methods: Outcomes and survivals among 325 patients who received renal allografts from July 1991 to September 2005 were compared between those known to have pretransplantation HCV infection (Group I, HCV+ group, n = 33) versus a matched cohort of those without this infection (Group II, HCV- control group, n = 33). Allograft performance, liver function, cholesterol, and glucose levels were determined both at transplantation and at a mean of postgrafting year 8. A one-way analysis of variance (ANOVA) statistical method was used for multivariate analysis., Results: Thirty-three patients (10.15%, 19 women and 14 men) were positive for HCV antibody. The mean follow-up period was 8 years (range, 0.5-14 years). The mean survival rates were similar in Groups I and II (96.6% and, 100%, respectively). Although the allograft survival rate was lower in Group I (84.8% vs 90.9%), the rejection rate among the HCV- group was 6%; only 1 patient died of hepatic failure. In spite of a significant rise in both total and direct bilirubin values (P < .01) in both groups, we failed to observe an adverse effect on graft survival. A significant rise in the fasting glucose level was seen in both HCV+ and HCV- patients., Conclusions: Chronic HCV infection before transplantation did not have a significant impact on graft survival or mortality compared with noninfected patients.

The number of patients on the kidney waiting list is increasing, creating a shortage of donor organs. To solve this problem, there is an interest in transplanting organs formerly considered marginal or undesirable. We performed seven (four living related, three cadaveric) kidney transplants from hepatitis B surface antigen (HBsAg)-positive donors. Hepatitis B e antigen (HBeAg) and hepatitis B virus (HBV) DNA were negative in the living donors and were unknown in cadaveric donors. Liver function tests were in the normal range in all of the donors. All of the recipients were HBsAg-negative and hepatitis B surface antibody (anti-HBs)-positive. Recipients receiving kidneys from cadaveric donors were given prophylactic lamivudine treatment postoperatively. Anti-HBs remained positive throughout the follow-up period in all but one patient with a cadaveric graft. None of the patients receiving a kidney from an HBsAg-positive donor developed clinical HBV infection in a mean follow-up period of 42.6 +/- 36.8 months (range: 16 to 121 months, median 30 months). Liver function tests remained in the normal ranges in all patients. All the grafts are still functioning with a mean serum creatinine level of 1.6 +/- 0.85 mg/dL. In conclusion, transplants from HBsAg-positive and HBeAg-/HBV DNA-negative donors seem to carry no risk to the recipients who are immune to HBV. Even cadaveric donors with HBsAg-positivity and unknown HBeAg/HBV DNA status can be used with caution in selected recipients without significantly affecting graft and patient outcome.