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10.4081/hr.2017.7053 http://scihub22266oqcxt.onion/10.4081/hr.2017.7053 C5472348!5472348!28626544     free     free     free       Hematol+Rep 2017 ; 9 (2): ä Nephropedia Template TP {{tp|p=28626544|t=2017. Atypical Hemolytic Uremic Syndrome: A Brief Review |pdf=|usr=}}{{28626544}} gab.com Text Atypical Hemolytic Uremic Syndrome: A Brief Review JO: Hematol Rep http://www.kidney.de/pget.php?&tw=1&pmid=28626544 #FOAvip 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. Twit Text FOAVip Atypical Hemolytic Uremic Syndrome: A Brief Review ????Hematol Rep http://www.kidney.de/pget.php?&tw=1&pmid=28626544 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28626544 #FOAvip English Wikipedia <ref>{{Cite pmid|28626544}}</ref> Atypical Hemolytic Uremic Syndrome: A Brief Review #MMPMID28626544 Zhang K; Lu Y; Harley KT; Tran MH Hematol Rep 2017[Jun]; 9 (2): ä PMID28626544show ga 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. äAtypical Hemolytic Uremic Syndrome: A Brief Review (epmc).pdf DeepDyve Pubget Overpricing