In the most severe cases, extensive cortical necrosis ensues. Glomerular endothelial cell swelling, thrombotic occlusion of capillary lumens, tubular epithelial cell damage, mesangial expansion, and mesangiolysis have been observed (6). Fibrin thrombi are predominantly formed within small vessels, followed by ischemic damage. Endothelial cell damage is the hallmark of thrombotic microangiopathy found in D + HUS. The histopathologic features observed in HUS have been termed thrombotic microangiopathy, a term that also encompasses other conditions such as HUS not associated with a diarrheal prodrome (D − HUS) and thrombotic thrombocytopenic purpura (6). A hypothetical sequence of events from ingestion of the bacteria to the development of full-blown hemolytic uremic syndrome is proposed. The pathogenesis of the prothrombotic state leading to thrombocytopenia secondary to endothelial cell damage and platelet activation is also discussed.

Data on the inflammatory response of the host, including leukocytes and inflammatory mediators, are updated. coli-secreted proteins A, B, and D, the 60-MD plasmid, and enterohemolysin likely contribute to the pathogenesis.

Factors such as Shiga toxin, lipopolysaccharide, the adhesins intimin and E.

coli leads to hemolytic uremic syndrome remains unclear. Despite significant advances during the past decade, the exact mechanism by which Shiga toxin-producing E. The aim of this review is to examine recent advances in experimental and clinical research relevant to the pathogenesis of diarrhea-associated hemolytic uremic syndrome with special reference to histopathologic findings, virulence factors of Shiga toxin-producing Escherichia coli, the host response, and the prothrombotic state.

System shock 2 researching toxin a