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Hepatitis B virus infection in renal transplant recipients

Tak-Mao Chan, MD, FRCP
Anna SF Lok, MD
Section Editors
Daniel C Brennan, MD, FACP
Barbara Murphy, MB, BAO, BCh, FRCPI
Deputy Editors
Albert Q Lam, MD
Jennifer Mitty, MD, MPH


Hepatitis B virus (HBV) infection is a major risk factor for hepatic dysfunction after renal transplantation [1] because of the requirement for immunosuppressive therapies [2]. Although the incidence of HBV infection has declined among dialysis patients, the prevalence is still high in endemic areas.

This topic reviews the prognosis and management of HBV in end-stage renal disease (ESRD) patients who are undergoing renal transplantation. The serologic diagnosis of HBV infection and a general overview of management are provided elsewhere. (See "Diagnosis of hepatitis B virus infection" and "Hepatitis B virus: Overview of management".)


Incidence and prevalence — In endemic areas, a significant number of patients undergoing kidney transplantation are hepatitis B surface antigen (HBsAg) positive. The reported prevalence is approximately 15 percent of kidney transplant recipients in such locations [3]. The prevalence is much lower in areas in which HBV is less common.

Overall, the prevalence appears to be declining in most countries as a result of HBV vaccination programs in the general and dialysis patient population, as well as the result of strict precautions to prevent transmission of HBV infection in dialysis units. A national surveillance in the United States in 2002, for example, revealed that only 1 percent of dialysis patients was seropositive for HBsAg [4]. (See "Hepatitis B virus and dialysis patients".)

Risk factors for reactivation of HBV replication — Among HBsAg-positive patients, reactivation of HBV replication is variably defined by the appearance of HBV DNA in a patient who has had undetectable HBV DNA previously or by a >1 to 2 log increase in HBV DNA. Among HBsAg-negative, hepatitis B core antibody (anti-HBc)-positive patients, reactivation is defined by the reappearance of HBsAg or HBV DNA or an increase in HBV DNA in those with detectable HBV DNA prior to the start of immunosuppressive therapy.

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Literature review current through: Oct 2017. | This topic last updated: Mar 02, 2016.
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