[Role of intravascular coagulation in the pathophysiology of the hemolytic-uremic syndrome].
Endothelial cell injury of capillaries and arterioles is considered to be the primary event in the hemolytic uremic syndrome. Intravascular coagulation increases the damaging processes. This intravascular coagulation can still be active after admission to the clinic. Several new data are available: prostacyclin deficiency can be present possibly due to the absence of a stimulating factor in plasma; the platelets are exhausted; an inhibitor of glomerular fibrinolysis has been demonstrated. A generally accepted therapy for HUS is still lacking.
D000990:Antithrombin III / Q000502:physiology; D002648:Child; D011464:Epoprostenol / Q000172:deficiency; D004903:Erythrocyte Aggregation; D005342:Fibrinolysis; D006463:Hemolytic-Uremic Syndrome / Q000503:physiopathology*; D006801:Humans; D010974:Platelet Aggregation
D000990:Antithrombin III; D011464:Epoprostenol
De rol van de intravasale stolling in de pathofysiologie van het hemolytisch-uremisch syndroom.