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Shiga toxin-associated hemolytic uremic syndrome: advances in pathogenesis and therapeutics

Petruzziello-Pellegrini, Tania N.a,b,c; Marsden, Philip A.a,b,c,d

Current Opinion in Nephrology and Hypertension: July 2012 - Volume 21 - Issue 4 - p 433–440
doi: 10.1097/MNH.0b013e328354a62e
RENAL PATHOPHYSIOLOGY: Edited by Orson W. Moe and Susan Quaggin

Purpose of review 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.

Recent findings 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.

Summary 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:

© 2012 Lippincott Williams & Wilkins, Inc.