Venous tissues from 15 patients with renal failure (five acute and 10 chronic) generated significantly higher PGI2-like (platelet aggregation inhibitory) activity than venous tissues from 10 normal subjects. The longer the bleeding times, the higher the values for PGI2-like activity found in these patients. Both bleeding times and PGI2-like activity values returned to normal in three acute uraemic patients on restoration of their renal function. Two additional patients with acute renal failure and greatly prolonged bleeding times were under aspirin treatment at the moment of this study: venous specimens from neither of them generated measurable amounts of PGI2-like material. Malondialdehyde formation in platelets from 12 patients with chronic renal failure and prolonged bleeding times was significantly lower than in platelets from 11 controls. The defect was evident with each of the three stimuli used, i.e., collagen, arachidonic acid and thrombin. It is concluded that prostaglandin metabolism in platelets and in the vessel wall from uraemic patients is impaired in different ways, both contributing to the impaired primary haemostasis in these patients.
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine