title: HUS and the case for complement.
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 and coagulation, and how they affect disease progression and response to treatment. Such new insights may impact on current and future choices of therapies for STEC-HUS.
authors.affiliation: Centre for Blood Research, Life Sciences Institute, Department of Medicine, Faculty of Medicine, University of British Columbia, Vancouver, BC, Canada.
authors.forename: Edward M
authors.identifier: http://orcid.org/0000-0003-0081-0305
authors.initials: EM
authors.lastname: Conway
mesh_terms: D001777:Blood Coagulation; D003167:Complement Activation; D003165:Complement System Proteins / Q000235:genetics / Q000276:immunology*; D004927:Escherichia coli Infections / Q000097:blood / Q000150:complications* / Q000235:genetics / Q000276:immunology; D006463:Hemolytic-Uremic Syndrome / Q000097:blood / Q000235:genetics / Q000276:immunology* / Q000382:microbiology*; D006801:Humans; D009154:Mutation; D011122:Polyphosphates / Q000276:immunology; D054323:Shiga-Toxigenic Escherichia coli / Q000276:immunology*
chemical_list: D011122:Polyphosphates; D003165:Complement System Proteins