Thrombotic microangiopathies (TMAs) are life-threatening clinical syndromes due to dysregulation of the complement and coagulation cascades.1 When a precipitant to endothelial injury persists (e.g., from infection, drug, autoimmunity, malignancy, or pregnancy), particularly in the setting of an acquired or genetic defect in complement and/or coagulation regulatory proteins, then alternative complement activity propagates abnormally without inhibition. Pathologically, this results in microvascular thrombosis with a predilection for glomeruli.
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Efe et al. (2021) studied this question.
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