Background and objectivesThrombotic microangiopathies constitute a diagnostic and therapeutic challenge. Secondary thrombotic microangiopathies are less characterized than primary thrombotic microangiopathies (thrombotic thrombocytopenic purpura and atypical hemolytic and uremic syndrome). The relative frequencies and outcomes of secondary and primary thrombotic microangiopathies are unknown.Design, setting, participants, & measurementsWe conducted a retrospective study in a four-hospital institution in 564 consecutive patients with adjudicated thrombotic microangiopathies during the 2009–2016 period. We estimated the incidence of primary and secondary thrombotic microangiopathies, thrombotic microangiopathy causes, and major outcomes during hospitalization (death, dialysis, major cardiovascular events [acute coronary syndrome and/or acute heart failure], and neurologic complications [stroke, cognitive impairment, or epilepsy]).ResultsWe identified primary thrombotic microangiopathies in 33 of 564 patients (6%; thrombotic thrombocytopenic purpura: 18 of 564 [3%]; atypical hemolytic and uremic syndrome: 18 of 564 [3%]). Secondary thrombotic microangiopathies were found in 531 of 564 patients (94%). A cause was identified in 500 of 564 (94%): pregnancy (35%; 11 of 1000 pregnancies), malignancies (19%), infections (33%), drugs (26%), transplantations (17%), autoimmune diseases (9%), shiga toxin due to Escherichia coli (6%), and malignant hypertension (4%). In the 31 of 531 patients (6%) with other secondary thrombotic microangiopathies, 23% of patients had sickle cell disease, 10% had glucose-6-phosphate dehydrogenase deficiency, and 44% had folate deficiency. Multiple causes of thrombotic microangiopathies were more frequent in secondary than primary thrombotic microangiopathies (57% versus 19%; P<0.001), and they were mostly infections, drugs, transplantation, and malignancies. Significant differences in clinical and biologic differences were observed among thrombotic microangiopathy causes. During the hospitalization, 84 of 564 patients (15%) were treated with dialysis, 64 of 564 patients (11%) experienced major cardiovascular events, and 25 of 564 patients (4%) had neurologic complications; 58 of 564 patients (10%) died, but the rates of complications and death varied widely by the cause of thrombotic microangiopathies.ConclusionsSecondary thrombotic microangiopathies represent the majority of thrombotic microangiopathies. Multiple thrombotic microangiopathies causes are present in one half of secondary thrombotic microangiopathies. The risks of dialysis, neurologic and cardiac complications, and death vary by the cause of thrombotic microangiopathies.

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The incidence of acute kidney injury (AKI) in infective endocarditis (IE), its risk factors and consequences on patient and renal survival remain debated. Methods: Patients hospitalized for a first episode of IE (possible or definite according to modified Duke criteria) between 2013 and 2016 were included. The primary endpoint was to determine risk factors for early AKI (E-AKI) during the first week of management of IE. Results: A total of 276 patients were included: 220 (79.7%) had definite IE and 56 (20.3%) had possible IE. E-AKI occurred in 150 patients (53%). IE due to Staphylococcus aureus (OR 3.41; 95% CI 1.83-6.39; p < 0.01), history of diabetes (OR 2.34; 95% CI 1.25-4.37; p < 0.01), peripheral arterial disease (OR 2.59; 95% CI 1.07-6.23; p < 0.05), immunological manifestations (OR 3.11; 95% CI 1.31-7.39; p = 0.01), and use of norepinephrine (OR 3.44; 95% CI 1.72-7.02; p < 0.01) were associated with E-AKI. In subgroup analysis, infectious disease consultation was associated with a lower risk of AKI at day 7 (OR 0.41; 95% CI 0.16-0.88; p = 0.04). E-AKI was associated with 1-year mortality (OR 1.65; 95% CI 1.03-2.64; p = 0.04) and chronic kidney disease progression (OR 2.23; 95% CI 1.30-3.82; p < 0.01).Conclusions: E-AKI is common in IE and often associated with non-modifiable variables. Multidisciplinary management should be mandatory, and awareness of AKI diagnosis and etiological explorations should be raised.