Hemolytic uremic syndrome (HUS) is a severe disease characterized by the 
clinical triad of hemolytic anemia, thrombocytopenia, and acute renal failure. 
HUS exists in two forms: the atypical diarrhea-negative HUS, which is often 
associated with complement disorders, and the more frequent diarrheal-associated 
typical HUS, which is caused by infections with enterohemorrhagic ESCHERICHIA 
COLI. The virulence factors of the latter have been studied well, and Shiga 
toxin (Stx)2 is reported to represent the most important one. In contrast, risk 
factors on the host side have not been intensively studied until recently: 
Complement activation products have been detected in the serum and plasma of HUS 
patients, and an in vitro study could show that Stx2 not only damages the kidney 
directly but also indirectly via complement, in two ways. First, it activates 
complement, and second, it delays the functions of its control protein factor H 
on the cell surface, both known to damage the kidney.