ASN's Mission

ASN leads the fight to prevent, treat, and cure kidney diseases throughout the world by educating health professionals and scientists, advancing research and innovation, communicating new knowledge, and advocating for the highest quality care for patients.

learn more

Contact ASN

1401 H St, NW, Ste 900, Washington, DC 20005

email@asn-online.org

202-640-4660

The Latest on Twitter

Kidney Week

Abstract: FR-PO912

The Risk of Hepatitis B Virus Reactivation with Rituximab Desensitization in HBsAg-Positive Kidney Transplant Recipients

Session Information

Category: Transplantation

  • 1802 Transplantation: Clinical

Authors

  • Seo, Yuri, Asan medical center, Seoul, Korea (the Republic of)
  • Baek, Chung Hee, Asan Medical Center, Songpa-gu, SEOUL, Korea (the Republic of)
  • Park, Su-Kil, Asan Medical Center, Songpa-gu, SEOUL, Korea (the Republic of)
Background

Rituximab, as a powerful immunosuppressive agent, is used for ABO mismatched Kidney transplantation (KT) or flow cytometry positive patients. Because rituximab has elevated risk for hepatitis B virus (HBV) reactivation, antiviral prophylaxis is recommended for positive hepatitis B surface antigen (HBsAg(+)) recipients. The purpose of this study was to evaluate whether treatment with an antiviral agent is enough for preventing HBV reactivation in HBsAg(+) patients who had KT with rituximab desensitization.

Methods

The 128 patients who underwent KT from 2009 to 2016 identified as HBsAg(+) before KT in a single center were retrospectively analyzed. They were divided into two groups according to whether rituximab was used or not (29 patients in Rituximab(+) group, 99 patients in Rituximab(-) group). HBV reactivation was diagnosed by an increase in HBV DNA more than 2 log10 international units/mL or a detectable HBV DNA level when previously undetectable HBV DNA. In addition, HBV reactivation was compared between 500 mg and 200 mg in rituximab(+) group.

Results

Reactivation of HBV DNA was detected in 4 among 29 (13.79%) HBsAg(+) patients in rituximab(+) group and 20 among 99 (20.20%) HBsAg(+) patients in rituximab(-) groups (P=0.592). The 4 patients with HBV reactivation in rituximab(+) group had already taken antiviral agents since KT (Table1). LFT elevation was detected in 2 of the 4 patients that HBV DNA was reactivated. The elevated LFT or reactivated HBV DNA was spontaneously resolved without change of antiviral agents. The Number of HBV DNA reactivation was not lowered according to changing rituximab dose from 500 mg (1/8, 12.50%) to 200 mg (3/21, 14.29%) in rituximab(+) group.

Conclusion

When HBsAg(+) patients received KT, the use of Rituximab may not increase HBV reactivation. It is suggested that the usage of antiviral agents is efficient prophylaxis for HBV reactivation of HBsAg(+) recipients who had KT with rituximab desensitization.

Table 1. Time of DNA reactivation after KT in the 4 patients with HBV reactivation in rituximab(+) group (by year)
 Antiviral agentTime of DNA reactivation after KT
0-1 year1-2 year2-3 year3-4 year4-5 year
Patient 1entecavir  v  
Patient 2entecavir v   
Patient 3entecavir   v 
Patient 4telbivudine   v