#5256 REACTIVATION OF HEPATITIS B VIRUS IN KIDNEY TRANSPLANT RECIPIENTS WITH RESOLVED INFECTION: A SINGLE-CENTER EXPERIENCE

Abstract

Abstract Background and Aims Patients with end-stage renal disease (ESRD) frequently present serologic evidence of previous contact with hepatitis B virus (HBV). Although uncommon, HBV reactivation after kidney transplantation (KT) may cause serious complications and adverse outcomes in these patients. However, data regarding risk factors for reactivation are still scarce. This study aims to describe a cohort of patients with resolved HBV infection who showed reactivation of the virus after KT. Method Retrospective cohort study including patients with resolved HBV infection who underwent KT between August 2007 and December 2021. Resolved HBV infection was defined as being seronegative to HB surface antigen (HBsAg) and seropositive to HB core antibody (HBcAb), regardless of HB surface antibody (HBsAb) status. HBV reactivation after KT was defined as seropositivity to HBsAg or presence of HBV-DNA in the serum (viraemia). Preemptive prophylactic entecavir was not used. Demographic and clinical data were collected from the electronic records. Results A total of 104 patients (70.2% male) were included with a mean age of 52±10 years. Prior to KT, 93.3% were seropositive to HBsAb. Seropositivity to other viruses was present in 18 patients: human immunodeficiency virus (HIV) alone in 5 patients, hepatitis C virus (HCV) alone in 11 patients and coinfection in 2 patients. Deceased-donor KT was performed in 94.2% and only 9 patients had had a previous KT. Rituximab was used as induction immunosuppressive therapy in 13 patients. Median follow-up time after KT was 75 months (IQR 37-115). HBV reactivation occurred in 6 patients with a median time after KT of 5 months (IQR 3-11.5). At reactivation diagnosis, median HBsAg titer was 83.2 (IQR 34-784.5; reference range < 1) and median viral load was 6.7 × 106 copies/mL (IQR 0.4 × 106-378 × 106). Only one patient presented seropositivity to HBsAg without viraemia. Half of these patients were seropositive to HBsAb prior to KT and became seronegative at reactivation diagnosis. No liver enzyme elevation was registered at reactivation diagnosis. Donor HBcAb status, coinfection with HIV or HCV, Rituximab use and recipient HBsAb status were not associated to HBV reactivation after KT. Two patients with HBV reactivation lost kidney graft function and 2 died during follow-up. Conclusion Hepatitis B virus reactivation is possible after kidney transplantation and may pose major adjustments to the treatment, namely the immunosuppressive therapy. Careful monitoring of hepatitis B virus serology and viraemia could be particularly useful in early diagnosis and prompt approach to its reactivation. Larger and multi-center studies are warranted to identify specific risk factors in this population and prevent reactivation.