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

Autor: Teixeira CM; Nephrology Division, Federal University of São Paulo, São Paulo, Brazil., Tedesco Silva Junior H; Nephrology Division, Federal University of São Paulo, São Paulo, Brazil., Moura LAR; Pathology Division, Hospital do Rim, Federal University of São Paulo, São Paulo, Brazil., Proença HMS; Pathology Division, Hospital do Rim, Federal University of São Paulo, São Paulo, Brazil., de Marco R; Immunogenetics Institute, AFIP, São Paulo, Brazil., Gerbase de Lima M; Immunogenetics Institute, AFIP, São Paulo, Brazil., Cristelli MP; Nephrology Division, Federal University of São Paulo, São Paulo, Brazil., Viana LA; Nephrology Division, Federal University of São Paulo, São Paulo, Brazil., Felipe CR; Nephrology Division, Federal University of São Paulo, São Paulo, Brazil., Medina Pestana JO; Nephrology Division, Federal University of São Paulo, São Paulo, Brazil.
Jazyk: angličtina
Zdroj: PloS one [PLoS One] 2020 Jan 10; Vol. 15 (1), pp. e0227445. Date of Electronic Publication: 2020 Jan 10 (Print Publication: 2020).
DOI: 10.1371/journal.pone.0227445
Abstrakt: Introduction: Thrombotic microangiopathy (TMA) in post-transplant setting has heterogeneous clinical manifestations.
Methods: 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.
Results: 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.
Conclusions: 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.
Competing Interests: I have read the journal's policy and the authors of this manuscript have the following competing interests: Dr. HTS reports grants and personal fees from NOVARTIS, grants and personal fees from PFIZER, grants and personal fees from SANOFI and grants from QUARK, outside the submitted work. This does not alter our adherence to PLOS ONE policies on sharing data and materials. All the other authors declared no relevant competing interests.
Databáze: MEDLINE
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