Diarrhoea-associated haemolytic uraemic syndrome (D+ HUS) is usually caused
by verotoxin-producing Escherichia coli. Histology shows endothelial swell
ing with localised thrombus. Activation of coagulation and fibrinolysis als
o occurs. These facts, combined with the knowledge that recovery usually fo
llows within weeks, led us to hypothesise that verotoxin causes localised e
ndothelial cell activation but not injury. Markers of endothelial cell acti
vation and injury were measured serially in 30 children with acute D+ HUS,
healthy children, and children receiving chronic dialysis. Interpretation o
f markers was complicated by the renal dysfunction characteristic of D+ HUS
. Nevertheless there was no evidence for endothelial cell injury, as solubl
e tissue factor levels were not increased and soluble thrombomodulin levels
were lower than dialysed controls (P < 0.001). In the acute phase, soluble
vascular cell adhesion molecule levels were raised above normal (P < 0.001
), but were lower than dialysed controls (P < 0.001), and soluble E-selecti
n levels were not significantly increased compared with normal controls (P
= 0.2). Hence, there was no evidence for endothelial cell damage or endothe
lial cell activation by the time children reached hospital; but this study
did not exclude the possibility that endothelial cell activation occurred p
rior to hospital admission.