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NDT Advance Access published online on January 3, 2006
Nephrology Dialysis Transplantation, doi:10.1093/ndt/gfk023
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© The Author [2005]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org
Received March 2, 2005
Accepted December 5, 2005

Original Article

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

Tzung-Hai Yen 1, Chiu-Ching Huang 2 *, Hsin-Hung Lin 2, Jeng-Yi Huang 3, Ya-Chun Tian 3, Chih-Wei Yang 3, Mai-Szu Wu 3, Ji-Tseng Fang 3, Chun-Chen Yu 3, Yang-Jen Chiang 4, and Sheng-Hsieh Chu 4

1 Department of Nephrology, Chang Gung Memorial Hospital, Taipei, Taiwan; Histopathology Unit, Cancer Research UK, London Research Institute, London, UK
2 Department of Medicine, China Medical University Hospital, Taichung, Taiwan
3 Department of Nephrology, Chang Gung Memorial Hospital, Taipei, Taiwan
4 Department of Urology, Chang Gung Memorial Hospital, Taipei, Taiwan

* To whom correspondence should be addressed.
Chiu-Ching Huang, E-mail: cch{at}www.cmuh.org.tw



  Abstract

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.

Keywords: co-infection; HBV; HCV; reactivation; renal transplantation.
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