Abstract
There is evidence of intravascular coagulation in accelerated hypertension and pre-eclamptic toxaemia, in all types of nephritis and in the haemolyticuraemia syndrome. The kidneys have a two-fold defence mechanism, namely mesangial cell phagocytosis and endothelial cell fibrinolytic activity. Intravascular coagulation occurs in all those types of shock that result in acute renal failure: more often than not the primary cause is endotoxinaemia.
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