Protective mechanisms harnessing against injurious heme and preventing kidney damage in STEC-HUS: toward new therapies?

Abstract

Hemolytic uremic syndrome can be initiated by Escherichia coli infections (Shiga-toxin-producing enterohemorrhagic Escherichia coli hemolytic uremic syndrome). When hemoglobin and heme released from ruptured erythrocytes interact with the kidney cells, this can result in platelet activation, vascular inflammation and occlusion, and kidney injury. Pirschel et al. now report that in the absence of protective mechanisms against free hemoglobin and heme, heme-induced kidney injury can be exacerbated. Therapeutic strategies should therefore also target heme-mediated deleterious effects in (severely ill) patients with Shiga-toxin-producing enterohemorrhagic Escherichia coli hemolytic uremic syndrome.