Bleeding in renal failure: a possible role of vascular prostacyclin (PGI2).
Specimens of venous tissues from a group of 25 patients with chronic uremia and 7 patients with acute renal failure generated significantly higher PGI2-like (platelet aggregation inhibiting) activity than venous tissues from 30 normal subjects. After repeated washings, when this activity could barely be detected in the controls, pronounced inhibitory activity was still evident in samples containing venous tissues from uremic patients. Both prolonged bleeding times and increased PGI2-like activity returned to normal in 4 acute uremic patients on restoration of their renal function. These findings may be relevant to the pathogenesis of bleeding in renal failure.
D058186:Acute Kidney Injury / Q000378:metabolism; D000328:Adult; D001095:Arachidonic Acids / Q000378:metabolism; D001760:Bleeding Time; D001792:Blood Platelets / Q000378:metabolism; D011464:Epoprostenol / Q000096:biosynthesis*; D005260:Female; D006470:Hemorrhage / Q000209:etiology*; D006801:Humans; D007676:Kidney Failure, Chronic / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D011449:Prostaglandin Endoperoxides / Q000096:biosynthesis; D011453:Prostaglandins / Q000096:biosynthesis*; D014511:Uremia / Q000097:blood / Q000150:complications / Q000378:metabolism*; D014680:Veins / Q000378:metabolism*
D001095:Arachidonic Acids; D011449:Prostaglandin Endoperoxides; D011453:Prostaglandins; D011464:Epoprostenol