Rituximab and hepatitis B reactivation in HBsAg-negative/anti-HBc-positive kidney transplant recipients

Juhan Lee, Junyong Park, Kyu Ha Huh, Beom Seok Kim, Myoung Soo Kim, Soon Il Kim, SangHoon Ahn, YuSeun Kim

Research output: Contribution to journalArticle

13 Citations (Scopus)

Abstract

Background. Hepatitis B virus (HBV) reactivation is a wellknown complication of immunosuppressive therapy. Although rituximab is increasingly used for desensitization of ABOincompatible or positive crossmatch kidney transplantation, the risk of HBV reactivation in hepatitis B surface antigen (HBsAg)-negative/hepatitis B core antibody (anti-HBc)-positive kidney transplant patients receiving rituximab desensitization remains undetermined. Methods. We analysed 172 resolved HBV patients who underwent living donor kidney transplantation between 2008 and 2014. Patients were divided into rituximab (n 49) or control (n 123) groups. All patients were observed for HBV reactivation, which was defined as the reappearance of hepatitis B surface antigen or HBV DNA. Results. During the follow-up period (median, 58 months; range, 4-95 months), five patients (10.2%) in the rituximab group and two patients (1.6%) in the control group experienced HBV reactivation (P0.003). In the rituximab group, two patients experienced HBV-related severe hepatitis, and one patient died due to hepatic failure. The median time fromrituximab desensitization to HBV reactivation was 11 months (range, 5-22 months). By contrast, no patients in the control group experienced severe hepatitis. The status of hepatitis B surface antibody was similar between groups. Rituximab desensitization [hazard ratio (HR), 9.18; 95% confidence interval (CI), 1.74-48.86; P0.009] and hepatitis B surface antibody status (HR, 4.74; 95% CI, 1.05-21.23, P0.04) were significant risk factors for HBV reactivation. Conclusions. Rituximab desensitization for incompatible kidney transplantation significantly increased the risk of HBV reactivation in HBsAg-negative/anti-HBc-positive patients. Therefore, closemonitoring of HBV DNA is required in these patients.

Original languageEnglish
Pages (from-to)722-729
Number of pages8
JournalNephrology Dialysis Transplantation
Volume32
Issue number4
DOIs
Publication statusPublished - 2017 Apr 1

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Hepatitis B Antibodies
Hepatitis B Surface Antigens
Hepatitis B
Hepatitis B virus
Kidney
Kidney Transplantation
Hepatitis
Rituximab
Transplant Recipients
Confidence Intervals
Control Groups
Living Donors
DNA
Liver Failure
Immunosuppressive Agents

All Science Journal Classification (ASJC) codes

  • Nephrology
  • Transplantation

Cite this

@article{dbaeb74e8796473db0877d616371177d,
title = "Rituximab and hepatitis B reactivation in HBsAg-negative/anti-HBc-positive kidney transplant recipients",
abstract = "Background. Hepatitis B virus (HBV) reactivation is a wellknown complication of immunosuppressive therapy. Although rituximab is increasingly used for desensitization of ABOincompatible or positive crossmatch kidney transplantation, the risk of HBV reactivation in hepatitis B surface antigen (HBsAg)-negative/hepatitis B core antibody (anti-HBc)-positive kidney transplant patients receiving rituximab desensitization remains undetermined. Methods. We analysed 172 resolved HBV patients who underwent living donor kidney transplantation between 2008 and 2014. Patients were divided into rituximab (n 49) or control (n 123) groups. All patients were observed for HBV reactivation, which was defined as the reappearance of hepatitis B surface antigen or HBV DNA. Results. During the follow-up period (median, 58 months; range, 4-95 months), five patients (10.2{\%}) in the rituximab group and two patients (1.6{\%}) in the control group experienced HBV reactivation (P0.003). In the rituximab group, two patients experienced HBV-related severe hepatitis, and one patient died due to hepatic failure. The median time fromrituximab desensitization to HBV reactivation was 11 months (range, 5-22 months). By contrast, no patients in the control group experienced severe hepatitis. The status of hepatitis B surface antibody was similar between groups. Rituximab desensitization [hazard ratio (HR), 9.18; 95{\%} confidence interval (CI), 1.74-48.86; P0.009] and hepatitis B surface antibody status (HR, 4.74; 95{\%} CI, 1.05-21.23, P0.04) were significant risk factors for HBV reactivation. Conclusions. Rituximab desensitization for incompatible kidney transplantation significantly increased the risk of HBV reactivation in HBsAg-negative/anti-HBc-positive patients. Therefore, closemonitoring of HBV DNA is required in these patients.",
author = "Juhan Lee and Junyong Park and Huh, {Kyu Ha} and Kim, {Beom Seok} and Kim, {Myoung Soo} and Kim, {Soon Il} and SangHoon Ahn and YuSeun Kim",
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Rituximab and hepatitis B reactivation in HBsAg-negative/anti-HBc-positive kidney transplant recipients. / Lee, Juhan; Park, Junyong; Huh, Kyu Ha; Kim, Beom Seok; Kim, Myoung Soo; Kim, Soon Il; Ahn, SangHoon; Kim, YuSeun.

In: Nephrology Dialysis Transplantation, Vol. 32, No. 4, 01.04.2017, p. 722-729.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Rituximab and hepatitis B reactivation in HBsAg-negative/anti-HBc-positive kidney transplant recipients

AU - Lee, Juhan

AU - Park, Junyong

AU - Huh, Kyu Ha

AU - Kim, Beom Seok

AU - Kim, Myoung Soo

AU - Kim, Soon Il

AU - Ahn, SangHoon

AU - Kim, YuSeun

PY - 2017/4/1

Y1 - 2017/4/1

N2 - Background. Hepatitis B virus (HBV) reactivation is a wellknown complication of immunosuppressive therapy. Although rituximab is increasingly used for desensitization of ABOincompatible or positive crossmatch kidney transplantation, the risk of HBV reactivation in hepatitis B surface antigen (HBsAg)-negative/hepatitis B core antibody (anti-HBc)-positive kidney transplant patients receiving rituximab desensitization remains undetermined. Methods. We analysed 172 resolved HBV patients who underwent living donor kidney transplantation between 2008 and 2014. Patients were divided into rituximab (n 49) or control (n 123) groups. All patients were observed for HBV reactivation, which was defined as the reappearance of hepatitis B surface antigen or HBV DNA. Results. During the follow-up period (median, 58 months; range, 4-95 months), five patients (10.2%) in the rituximab group and two patients (1.6%) in the control group experienced HBV reactivation (P0.003). In the rituximab group, two patients experienced HBV-related severe hepatitis, and one patient died due to hepatic failure. The median time fromrituximab desensitization to HBV reactivation was 11 months (range, 5-22 months). By contrast, no patients in the control group experienced severe hepatitis. The status of hepatitis B surface antibody was similar between groups. Rituximab desensitization [hazard ratio (HR), 9.18; 95% confidence interval (CI), 1.74-48.86; P0.009] and hepatitis B surface antibody status (HR, 4.74; 95% CI, 1.05-21.23, P0.04) were significant risk factors for HBV reactivation. Conclusions. Rituximab desensitization for incompatible kidney transplantation significantly increased the risk of HBV reactivation in HBsAg-negative/anti-HBc-positive patients. Therefore, closemonitoring of HBV DNA is required in these patients.

AB - Background. Hepatitis B virus (HBV) reactivation is a wellknown complication of immunosuppressive therapy. Although rituximab is increasingly used for desensitization of ABOincompatible or positive crossmatch kidney transplantation, the risk of HBV reactivation in hepatitis B surface antigen (HBsAg)-negative/hepatitis B core antibody (anti-HBc)-positive kidney transplant patients receiving rituximab desensitization remains undetermined. Methods. We analysed 172 resolved HBV patients who underwent living donor kidney transplantation between 2008 and 2014. Patients were divided into rituximab (n 49) or control (n 123) groups. All patients were observed for HBV reactivation, which was defined as the reappearance of hepatitis B surface antigen or HBV DNA. Results. During the follow-up period (median, 58 months; range, 4-95 months), five patients (10.2%) in the rituximab group and two patients (1.6%) in the control group experienced HBV reactivation (P0.003). In the rituximab group, two patients experienced HBV-related severe hepatitis, and one patient died due to hepatic failure. The median time fromrituximab desensitization to HBV reactivation was 11 months (range, 5-22 months). By contrast, no patients in the control group experienced severe hepatitis. The status of hepatitis B surface antibody was similar between groups. Rituximab desensitization [hazard ratio (HR), 9.18; 95% confidence interval (CI), 1.74-48.86; P0.009] and hepatitis B surface antibody status (HR, 4.74; 95% CI, 1.05-21.23, P0.04) were significant risk factors for HBV reactivation. Conclusions. Rituximab desensitization for incompatible kidney transplantation significantly increased the risk of HBV reactivation in HBsAg-negative/anti-HBc-positive patients. Therefore, closemonitoring of HBV DNA is required in these patients.

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DO - 10.1093/ndt/gfw455

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