In haemolytic uraemic syndrome there is evidence of intravascular haemolysis owing to microangiopathy with fragmentation of red cells, a low serum haptoglobin concentration and a marginally raised serum indirect bilirubin concentration. Patients with this syndrome differ from those with other causes of renal failure in their ability to mount a reticulocyte response. The platelet count is reduced by consumption in microthrombi. There is no association with autoimmune haemolytic anaemia.
Most of the children who present with this condition have an infection with an organism producing a toxin acting on vascular endothelial cells, commonly E. coli O157. A smaller number will have an inherited abnormality of the complement system.
The latter will usually progress to chronic renal failure and a small proportion of children who suffer from diarrhoea-associated HUS will also develop CRF.
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