From January 1st, 2009 to June 30th, 2017, 83 D(HBsAg+)/R(HBsAg-) and 384 D(HBcAb+)/R(HBcAb-) patients were identified from 2071 living donor KTx in our transplant center, with a frequency of 4.0% and 18.5%, respectively. After propensity score matching 83 D(HBcAb+)/R (HBcAb-) were included in the control group. The baseline demographic, clinical, and immunological data of both groups, including donor and recipient, are summarized in Table 1. All baseline characters were comparable in both groups, including age, gender, cause of end stage renal failure, preemptive transplant rate, duration of dialysis, panel reactive antibody, induction therapy and initial immunosuppressants, except for a higher HLA mismatch was found in the D(HBsAg+)/R (HBsAg-) group (p=0.004). No evidence of abnormal liver enzymes, total bilirubin, coagulation dysfunction, or liver cirrhosis were noticed before surgery.
Pre-transplant and post-transplant HBV status
HBV serology of the experimental and control groups pre- and post-transplantation were summarized in Table 2. We identified 24 pre-transplant HBV DNA+ donors in the experimental group, and their pre-transplant median HBV DNA level was 1.20×103 IU/ml (range 5.86×10-4.04×106). In the control group, we did not use any prophylaxis treatment of HBV, meanwhile, in the experimental group, all recipients received prophylaxis treatment as following: HBIG alone (n=18, 21.7%), antiviral alone (n=41, 49.4%), and combination of HBIG and antiviral (n=24, 28.9%). HBIG was infused as a single dose of 2000 IU pre-transplantation, and antiviral treatment started on the first day post-transplantation. Among the 65 recipients (78.3%) who received antiviral prophylaxis, 49 received lamivudine, whereas 16 were on entecavir. Antiviral treatment duration was 1-3 months (due to the nature of retrospective study, the exact duration cannot be provided).
Two recipients in the experimental group showed seroconversion evidences: HBV DNA- to +, and HBsAg- to +, but none in control group, with a median follow-up of 36 months (range, 6–106 months) for the experimental group and 36 months (range, 4–107 months) for the control group (Table 2).
Post-transplant clinical outcomes and laboratory parameters
Post-transplant clinical complications indicated that the experimental group had a higher incidence of treatment failure and active liver injury rate than control group (Table 2). Most of the post-transplant laboratory parameters were comparable, except that the experimental group had lower total bilirubin level at 24 months post-transplant (p=0.021) (Table 3). Both groups had no significant differences on graft survival rate at 1 (98.8% vs. 100%, p=0.17), 3 (97.6% vs. 96.4%, p=0.84), and 5 years (97.6% vs. 95.2%, p=0.62), and no significant differences in patient survival rate at 1 (97.6% vs. 98.8%, p =0.15), 3 (97.6% vs. 98.8%, p=0.79), and 5 years (95.2% vs. 98.8%, p=0.68) was noticed.
Risk factors of treatment failure in the D(HBsAg+)/R(HBsAg-) group
To address the relative risk factors of treatment failure of D(HBsAg+) to R(HBsAg-) on HBV infection, the living donors’ and corresponding recipients’ pre-transplant HBV status and post-transplant treatment failure in the D(HBsAg+)/R(HBsAg-) group were therefore analyzed. From a clinical prospective, the definition of treatment failure would most likely to be HBV transmission (infection evidences), graft loss, severe complications et al. After reviewing recipients’ data, we observed a low rate of HBV DNA/HBsAg/HBeAg – to +, graft loss, clinical liver injury and death of the recipient, which make it inaccurate to elucidate the risk factors. Thus, we expanded our criteria to any evidence related to HBV, including HBV related antibody change. Potential factors were analyzed for the prognostic value of treatment failure including pre-transplant donor HBV DNA- vs +, pre-transplant recipient factors (including age, sex, HBsAb, HBeAb, and HBcAb status), HBV prophylactic regimens (including HBIG, antiviral treatment etc.). Logistic regression models were generated, and each model was evaluated by AIC and BIC. The logistic regression results demonstrated that pre-transplant HBV DNA+ donor and male recipient were the only two significant risk factors for treatment failure of recipients, on the contrary, pre-transplant HBcAb+ of the recipients was the only significant protective factor (Table4, 5).