C3 and hemolytic-uremic syndrome: Our experimental studies were consistent with data from patients with Stx-associated HUS showing podocyte foot process impairment associated with glomerular C3 deposition [19,20], and support the hypothesis that the complement system plays a role in HUS and, in particular, that the activation of C3 and the generation of C3a also have a major effect on glomerular damage in HUS.