Complement contributes to the pathogenesis of Shiga toxin–associated hemolytic uremic syndrome

Complement is activated during Shiga toxin–producing Escherichia coli –associated hemolytic uremic syndrome (STEC-HUS). There is evidence of complement activation via the alternative pathway in STEC-HUS patients as well as from in vivo and in vitro models. Ozaki et al. demonstrate activation of the mannose-binding lectin (MBL) pathway in Shiga toxin–treated mice expressing human MBL2, but lacking murine Mbl s. Treatment with anti–human MBL2 antibody was protective, suggesting that MBL pathway activation also contributes to Shiga toxin–mediated renal injury.