Does hepatitis C virus affect the reactivation of hepatitis B virus following renal transplantation?

BACKGROUND: Hepatitis B virus (HBV) is endemic in Taiwan. Transplantation followed by long-term immunosuppressive medications may precipitate HBV reactivation. Interference of hepatitis C virus (HCV) with HBV gene expression and replication has been confirmed in many studies involving non-transplant populations. This study investigates the incidence of HBV reactivation following renal transplantation and compares the clinical outcome, especially the liver outcome, of patients with or without HCV co-infection. METHODS: Fifty-one of 512 renal transplant recipients were positive for hepatitis B surface antigen before surgery, and were followed for 81.6+/-7.5 (4-120) months. Seventeen of 51 patients acquired HCV before transplantation and six patients acquired HCV after renal transplantation. RESULTS: At the end of this assessment, we had 28 patients who suffered HBV reactivation and another 23 patients who suffered no HBV reactivation. Initially, we found a significant difference of HCV carriage (P<0.05) between patients with (seven out of 28 or 25%) or without (21 out of 23 or 91.3%) HBV reactivation. Further inspection showed that 21 of the 28 patients without HCV co-infection and seven of the 23 patients with HCV co-infection suffered HBV reactivation. After comparison, we found a lower incidence of HBV reactivation in patients with HCV co-infection than in patients without HCV co-infection (P<0.05). In contrast to the latter, we found that patients with HCV co-infection suffering HBV reactivation tended to have a late onset of HBV reactivation (P<0.05). Otherwise, there was no difference in hepatitis severity, in terms of peak alanine aminotransferase, total bilirubin levels and hepatitis reactivation-related death, between these two groups of patients. Finally, a multivariable analysis also revealed that HCV carriage was indeed an independent variable leading to the reduced incidence of HBV reactivation in patients with HCV co-infection. CONCLUSION: HCV might affect the reactivation of HBV by decreasing the incidence or delaying the onset of HBV reactivation in renal transplant recipients carrying both HBV and HCV.

Impact of HCV infection on first cadaveric renal transplantation, a single center experience.

BACKGROUND: Controversy still persists regarding the impact of HCV infection on renal transplant recipients. This study aimed to evaluate the effect of anti-HCV antibody status on patients and grafts of renal transplants at a single center. METHODS: We examined 299 first cadaveric renal transplants performed between July 1981 and May 2000 at our hospital, including 129 patients with anti-HCV antibody positive (HCV+ group) and 170 patients with anti-HCV antibody negative (HCV- group). The HBsAg of the 299 patients were all negative throughout the follow-up period. Causes of graft failure and patient death were analyzed. Patient and graft cumulative survival were compared between HCV+ and HCV- groups. Multivariate analysis with Cox proportional hazard model were calculated for risk hazards of outcome. RESULTS: Overall cumulative patient survival was 97.72, 85.63 and 71.31% at 1, 10, and 15 yr, respectively, in the HCV+ group, compared with 95.02, 67.85 and 59.83% at 1, 10 and 15 yr, respectively, in the HCV- group (p = 0.014). The major cause of patient death in both groups was infection with 26.67% in HCV+ group and 60.87% in HCV- group. Cumulative graft survival in the HCV+ group revealed 92.26, 55.97 and 26.16% at 1, 10 and 15 yr, respectively, compared with 88.07, 58.34 and 58.32% at 1, 10 and 15 yr, respectively, in the HCV- group (p = 0.700). The major cause of graft failure was chronic allograft dysfunction (56.82%) in HCV+ group, and patient death (32.43%) in the HCV- group. Multivariate analysis of patient survival revealed anti-HCV antibody+ had lesser risk hazard (aRR: 0.30, p = 0.002), chronic hepatitis had higher risk hazard (aRR: 1.90, p = 0.135), male recipient had higher risk hazard (aRR: 2.18, p = 0.051), and older recipients (age >55) also had higher risk hazard (aRR: 4.21, p = 0.063). Analysis of graft survival revealed only older donors (age >35) had higher risk hazard (aRR: 1.90, p = 0.081). CONCLUSIONS: The study revealed that patients with anti-HCV antibody had higher incidence of chronic hepatitis, chronic allograft dysfunction and post-transplantation nephrotic syndrome. Graft survival tended lower in the very long time. However, patients with anti-HCV antibodies had better patient survival when compared with patients without HCV antibodies up to 15 yr follow up. Patients of hepatitis C group without clinical chronic hepatitis was associated with best patient survival.