Impaired platelet thromboxane production in renal failure.
Platelet aggregation and thromboxane B2 production, in response to adenosine diphosphate, were significantly impaired in 7 undialyzed or inadequately dialyzed patients with renal failure when compared to adequately dialyzed individuals or normal subjects. In 1 patient, platelet aggregation and thromboxane synthesis were corrected after adequate hemodialysis. The defect in both platelet aggregation and thromboxane production was induced in normal platelets incubated with uremic platelet-poor plasma. These findings suggest that the uremic platelet defect may be due, in part, to a plasma factor that inhibitors platelet thromboxane synthesis. Further, adequate dialytic therapy may reverse this defect.
D058186:Acute Kidney Injury / Q000097:blood*; D000328:Adult; D000368:Aged; D005260:Female; D006801:Humans; D007676:Kidney Failure, Chronic / Q000097:blood*; D008297:Male; D008875:Middle Aged; D010974:Platelet Aggregation; D006435:Renal Dialysis; D013928:Thromboxane A2 / Q000096:biosynthesis / Q000097:blood; D013929:Thromboxane B2 / Q000096:biosynthesis / Q000097:blood; D013931:Thromboxanes / Q000096:biosynthesis*
D013931:Thromboxanes; D013929:Thromboxane B2; D013928:Thromboxane A2