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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.

Introduction Thrombotic microangiopathy (TMA) represents a spectrum of disorders characterized by thrombosis that affect small arterial vessels. Pregnancy is a potential trigger to acute episodes of TMA, which in turn, although rare, are associated with high maternal and perinatal morbidity and mortality. In renal transplant (RT) setting, fertility is increased by restoration of renal function, meanwhile RT patients are more susceptible to gestational complications, such as TMA syndromes. Objectives The aim of this study was to report our experience with RT recipients who developed TMA in allograft during pregnancy. Methods We describe four cases of pregnant RT recipients with TMA diagnosed by allograft biopsy, due to acute allograft dysfunction, at Hospital do Rim between 2011 and 2015. Their clinical and laboratory data were collected and are highlighted here. Results At conception, the average age was 21 ± 4 years. Their obstetric history revealed previous abortions in two patients and one previous uncomplicated pregnancy in another patient. All patients had chronic hypertension before conception and one patient also had preexisting proteinuria greater than 0.5 g. At the time of the confirmation of pregnancy, 75% of the patients were being maintained on immunosuppressive therapy with prednisone, tacrolimus and azathioprine, while one patient was receiving prednisone, tacrolimus and everolimus. The mean interval time of RT to pregnancy was 25 (9–45) months and the average baseline creatinine was 1.1 (0.9–1.4). The TMA diagnosis was established in the 14th week of gestation on average, and it was associated with thrombocytopenia and microangiopathic hemolytic anemia in only one patient. Moreover, concomitant acute cellular rejection (AR) occurred in one patient, and superimposed urinary tract infection in another. Except for the patient who had AR, in all cases the calcineurin inhibitor was withdrawn. Three patients developed preeclampsia with HELLP (hemolysis, elevated liver enzymes and low platelets) syndrome. The mean gestational term at delivery was 23 ± 2 weeks and these resulted in two abortions and two stillbirths. Over a 6 month follow-up period post pregnancy, there was one case of graft loss and all patients had increased proteinuria and creatinine levels – median creatinine = 4.3 (1.5–11); median proteinuria = 1.1 (0.6–1.9). Conclusions Since HELLP syndrome was very prevalent in these cases we suggest that the TMA diagnosis demands careful surveillance for gestational hypertension complications. Apart from the poor pregnancy outcomes, TMA in pregnant RT patients is associated with deterioration of graft function.