The inferior impact of antibody‐mediated rejection on the clinical outcome of kidney allografts that develop de novo thrombotic microangiopathy

Background A ntibody‐mediated rejection ( AMR ) can induce and develop thrombotic microangiopathy ( TMA ) in renal allografts. A definitive AMR ( dAMR ) co‐presents three diagnostic features. A suspicious AMR ( sAMR ) is designated when one of the three features is missing. Methods Thirty‐two TMA cases overlapping with AMR ( AMR + TMA ) were studied, which involved 14 cases of sAMR + TMA and 18 cases of dAMR + TMA . Thirty TMA cases free of AMR features ( AMR − TMA ) were enrolled as control group. Results The ratio of complete response to treatment was similar between AMR − TMA and AMR + TMA group (23.3% vs. 12.5%, p = 0.33), or between sAMR + TMA and dAMR + TMA group (14.3% vs. 11.1%, p = 0.79). At eight yr post‐transplantation, the death‐censored graft survival ( DCGS ) rate of AMR − TMA group was 62.8%, which was significantly higher than 28.0% of AMR + TMA group (p = 0.01), but similar between sAMR + TMA and dAMR + TMA group (30.0% vs. 26.7%, p = 0.92). Overall, the intimal arteritis and the broad HLA (Human leukocyte antigens) mismatches were closely associated with over time renal allograft failure. Conclusion The AMR + TMA has inferior long‐term graft survival, but grafts with sAMR + TMA or dAMR + TMA have similar characteristics and clinical courses.