Abstract
Hemolytic-uremic syndrome (HUS) is a thrombotic microangiopathy that is characterized by microangiopathic hemolytic anemia, thrombocytopenia, and renal failure. Excess complement activation underlies atypical HUS and is evident in Shiga toxin-induced HUS (STEC-HUS). This Spotlight focuses on new knowledge of the role of Escherichia coli-derived toxins and polyphosphate in modulating complement andcoagulation, andhowthey affect disease progression and response to treatment.Suchnewinsightsmayimpacton current and future choices of therapies for STEC-HUS.
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CITATION STYLE
Conway, E. M. (2015). HUS and the case for complement. Blood, 126(18), 2085–2090. https://doi.org/10.1182/blood-2015-03-569277
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