Diarrhea-associated hemolytic uremic syndrome (HUS) caused by Shiga toxin-producing Escherichia coli (STEC) continues to be an important public health threat worldwide. Specific therapies are lacking and patient care remains largely supportive. This review discusses the lessons learned from recent events and summarizes key advances made toward understanding the basic mechanisms involved in the pathogenesis of typical HUS.
The recent German outbreak of a hybrid organism resulted in an unprecedented number of HUS cases and drastically changed the face of typical (diarrhea-associated) HUS. New findings on the roles of complement and the CXCR4/SDF-1 pathway in HUS pathogenesis are summarized and novel therapeutic strategies are highlighted.
A better understanding of STEC-mediated HUS underlies improved therapeutic approaches. New studies of the mechanistic basis of the disease, together with patient-based studies, have led to key findings with important clinical implications.
aDepartment of Laboratory Medicine and Pathobiology, University of Toronto
bKeenan Research Centre, Li KaShing Knowledge Institute, St. Michael's Hospital
cDepartment of Medicine, University of Toronto
dRenal Division, Department of Medicine, St. Michael's Hospital, Toronto, Ontario, Canada
Correspondence to Philip A. Marsden, Li KaShing Knowledge Institute, Saint Michael's Hospital, 209 Victoria Street, Room 522, Toronto, ON M5B 1C6, Canada. Tel: +1 416 847 1734; e-mail: email@example.com