Summary
Diarrhoea-associated haemolytic uraemic syndrome (D+ HUS) is usually caused by verotoxin
producing Eschericia coli. We hypothesized that verotoxin binding to glomerular endothelial cells causes localised
endothelial cell activation and thus activation of coagulation and reduction of fibrinolytic
potential. We also proposed that treatment with fresh frozen plasma or dialysis would
not affect these changes. Markers of activation of coagulation and fibrinolysis were
measured in 30 children with acute D+ HUS serially, in healthy children and in children
on dialysis.
In acute D+ HUS, levels of thrombin-antithrombin III complex and prothrombin fragment
1+2 were significantly increased (p <0.001). The source of thrombin generation was
unclear. Factor Xlla levels were increased in patients and controls with renal failure.
Factor VIIa levels were not significantly raised in children with acute D+ HUS. D-dimers
were increased, but fibrinolytic potential as measured by fibrin plate was reduced.
Levels of plasminogen activator inhibitor antigen and activity and tissue plasminogen
activator antigen were increased.
Neither peritoneal dialysis nor administration of blood products, the most common
treatments, altered parameters of coagulation or fibrinolysis.
