Microangiopatia trombótica pós-transplante renal: características clínico-histológicas e prognóstico do enxerto renal

• Ano de defesa: 2018
• Autor(a) principal: Teixeira, Cinthia Montenegro [UNIFESP]
• Tipo de documento: Dissertação
• Tipo de acesso: Acesso aberto
• Idioma: por
• Instituição de defesa: Universidade Federal de São Paulo (UNIFESP)
• Palavras-chave em Português: Post-transplant; Thrombotic microangiopathy; Renal allograft; Microangiopatia trombótica; Transplante renal; Sobrevida do enxerto renal; Biopsia renal
• Link de acesso: https://sucupira.capes.gov.br/sucupira/public/consultas/coleta/trabalhoConclusao/viewTrabalhoConclusao.jsf?popup=true&id_trabalho=6635150; https://repositorio.unifesp.br/handle/11600/53184

Objective: To assess the incidence, clinical and histological features and prognosis of kidney or kidney-pancreas transplanted patients with Thrombotic microangiopathy (TMA). 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. Lesions were classified according to thrombi location and pattern of injury (with or without endothelial cell activation). 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%. The causes of TMA were infection (34%), acute rejection (16%), calcineurin inhibitor toxicity (13%), TMA recurrence (2%) and pregnancy (1%). 18% of the patients had several etiologies and in 17%, the TMA cause was undetermined. Glomerular TMA was the most prevalent lesion (50%). Endothelial cell activation was observed in 61% of the biopsies. 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- logrank test). There were no differences in allograft survival determined by hemolysis, time of onset, thrombi location or endothelial cell activation. Conclusion: Our results prove that post-transplant TMA is a rare but severe condition, regardless of its clinical and histological presentation. TMA had several etiologies, although ABMR was the only one associated to worse allograft outcomes.