Pathophysiology of typical hemolytic uremic syndrome

Abstract

The typical form of hemolytic uremic syndrome (HUS) is associated with enterohemorrhagic ESCHERICHIA COLI (EHEC) infection. The disease process is initiated and perpetuated by interactions between the pathogen or its virulence factors and host cells, as well as the host response. During EHEC-associated HUS, alterations occurring at the intestinal mucosal barrier and in the circulation, as well as on endothelial cells and other target-organ cells, lead to cell activation and/or cytotoxicity, and trigger a prothrombotic state. This review summarizes current knowledge regarding the interactions of the pathogen and its virulence factors with cells in the intestine, bloodstream, kidney, and brain. Mechanisms of bacterial colonization, toxin circulation, and induction of target organ damage are discussed.