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- W52926311 abstract "Microvascular endothelial cell injury plays a central role in the pathogenesis of a set of diseases known as endotheliopathies. Typically, such diseases demonstrate prominent renal manifestations since the kidneys are richly vascularized. Morphologically, endotheliopathies classically demonstrate features of thrombotic microangiopathy on renal biopsy and include diseases such as hemolytic uremic syndrome (HUS), thrombotic thrombocytopenic purpura (TTP), and preeclampsia. Recent advances have elucidated several mechanisms by which endothelial injury may occur leading to the development of endotheliopathies. More specifically, direct cytotoxic endothelial injury is caused by exposure to Shiga or Shiga-like toxins following gastroenteritis in classic HUS, while atypical HUS has been traced to endothelial perturbation due to overactivation of the alternative complement pathway. In TTP, abrogated ADAMTS13 activity leads to the accumulation of uncleaved large multimers of von Willebrand factor, which in turn causes inappropriate platelet aggregation and endothelial damage. In preeclampsia, soluble circulating factors likely derived from the placenta act as antagonists to the glomerular endothelial cell microenvironment, inciting endothelial cell injury. Understanding the molecular mechanisms by which these diseases develop and progress will greatly aid in the design and implementation of effective treatments specific to each endotheliopathy." @default.
- W52926311 created "2016-06-24" @default.
- W52926311 creator A5029617371 @default.
- W52926311 creator A5048109211 @default.
- W52926311 date "2014-01-01" @default.
- W52926311 modified "2023-10-14" @default.
- W52926311 title "Endotheliopathies: Hemolytic Uremic Syndrome, Thrombotic Thrombocytopenic Purpura, and Preeclampsia" @default.
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