*Purpose: Owing to limited organ availability, ABO-incompatible living kidney transplantation (ABO-ILKT) has been used extensively. Various forms of preconditioning therapies have been used alone or in combination. We examined the association of response to rituximab and incidence of antibody-mediated rejection (AMR) in preconditioning of rituximab and plasmapheresis (PP) without posttransplant plasmapheresis.

*Methods: We selected 225 patients who underwent ABO-ILKT between January 2005 and December 2015 at our institute. We excluded 110 patients owing to the following reasons: lack of data on lymphocyte subsets during the perioperative period, no use of rituximab, and positive DSA. The remaining 115 patients were divided into two groups based on the response to rituximab: well-response (n = 75) or poor-response (n = 40). The rituximab well-response and poor-response patient were defined as the patient whose CD19+ cells were non-detected (0%) and detected on the day of transplantation (2-5 days (median 3days) after rituximab administration), respectively. Rituximab was administered as a single dose (200 mg) within 2-5 d (median 3 d) prior to the operation. All patients underwent PP before surgery to reduce anti-A/B antibody to less than or equal to the titer of <1:32

*Results: Poor-response recipients had much higher CD19⁺ cells even after transplantation than well-response recipients. Univariate analysis indicated that rituximab response was a potential significant risk factor of AMR. A multivariate analysis indicated that rituximab response and anti-A/B blood antibody titer after PP were both significant risk factors of AMR (p=0.036, 0.045, respectively).The occurrence of AMR was higher in the poor-response group than in the well-response group (22.5% vs. 8.0%; p=0.028). The 14-day, 3-month and 1-year cumulative incidence of AMR was 2.7%, 5.3% and 8.0% in the well-response group, and 17.5%, 20.0% and 22.5% in the poor-response group after ABO-ILKT (p=0.022, log-rank test). In pathological findings, C4d and MVI (g + ptc) were higher in the poor response group than in the well response group. The patient and graft survival were not significantly different between the two groups. However, graft survival 1 month after transplantation was lower in the poor-response group. There is no significant difference in incidence of infection and complication after transplantation between two groups. No patients with febrile neutropenia was observed in rituximab poor-response group.

*Conclusions: The response to rituximab was significantly associated with the incidence of AMR. In our preconditioning protocol using antibody removal therapy and rituximab without postoperative apheresis, enough CD19 depletion by rituximab may be important to suppress AMR in ABO-ILKT.

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