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- W2620789068 abstract "Atypical hemolytic uremic syndrome (aHUS) is a disease characterized by the triad of microangiopathic hemolytic anemia, thrombocytopenia and acute kidney injury. The histopathologic lesions of aHUS include thrombotic microangiopathy involving the glomerular capillaries and thrombosis involving arterioles or interlobar arteries. Extra-renal manifestations occur in up to 20% of patients. The majority of aHUS is caused by complement system defects impairing ordinary regulatory mechanisms. Activating events therefore lead to unbridled, ongoing complement activity producing widespread endothelial injury. Pathologic mutations include those resulting in loss-of-function in a complement regulatory gene (CFH, CFI, CD46 or THBD) or gain-of-function in an effector gene (CFB or C3). Treatment with the late complement inhibitor, eculizumab—a monoclonal antibody directed against C5—is effective." @default.
- W2620789068 created "2017-06-09" @default.
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- W2620789068 date "2017-06-01" @default.
- W2620789068 modified "2023-10-12" @default.
- W2620789068 title "Atypical Hemolytic Uremic Syndrome: A Brief Review" @default.
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- W2620789068 doi "https://doi.org/10.4081/hr.2017.7053" @default.
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