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Clinical and pathological features of thrombotic microangiopathy influencing long-term kidney transplant outcomes
Clinical and pathological features of thrombotic microangiopathy influencing long-term kidney transplant outcomes
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Clinical and pathological features of thrombotic microangiopathy influencing long-term kidney transplant outcomes
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Clinical and pathological features of thrombotic microangiopathy influencing long-term kidney transplant outcomes
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Clinical and pathological features of thrombotic microangiopathy influencing long-term kidney transplant outcomes
Clinical and pathological features of thrombotic microangiopathy influencing long-term kidney transplant outcomes
Journal Article

Clinical and pathological features of thrombotic microangiopathy influencing long-term kidney transplant outcomes

2020
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Overview
Thrombotic microangiopathy (TMA) in post-transplant setting has heterogeneous clinical manifestations. We retrospectively studied data of 89 patients with post-transplant TMA, which was characterized by thrombi in at least one glomerulus and/or arteriole. Systemic TMA was defined by thrombocytopenia and microangiopathic anemia and early onset TMA, when occurred less than 90 days post transplant. The cumulative incidence was 0.93%. The majority of the recipients were young (mean age 39 years), female (52%) and Caucasian (48%) with primary kidney disease of unknown etiology (37%). Early TMA occurred in 51% of the patients and systemic TMA, in 25%. Underlying precipitating factors were: infection (54%), acute rejection (34%), calcineurin inhibitor toxicity (13%) and pregnancy (3%). 18% of the patients had several triggers. Glomerular TMA was observed in 50% of the biopsies and endothelial cell activation, in 61%. The 1-year patient survival was 97% and corresponding graft survival, 66%. Allograft survival was inferior when acute antibody mediated rejection (ABMR) occurred (with 41%; without 70%, p = 0.01), however no differences were determined by hemolysis, time of onset, thrombi location or endothelial cell activation. Our results suggest that post-transplant TMA is a rare but severe condition, regardless of its clinical and histological presentation, mainly when associated to ABMR.