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Uremic Toxins and Platelet Function
Herbert I. Horowitz, MD
Arch Intern Med. 1970;126(5):823-826.
Abstract
The hemostatic abnormalities in patients with uremia are related to acquired functional platelet defects. Evidence derived from dialysis, in vitro studies with cell-free uremic plasma, and the ingestion or infusion of uremic metabolities indicate that one or more dialyzable toxins are responsible for altering the function of intrinsically normal platelets. Urea, creatinine, methylguanidine, phenol and phenolic acids, and guanidinosuccinic acid (GSA) have been proposed for this role. These substances affect platelet aggregation, platelet factor 3 activation induced by adenosine diphosphate (ADP), platelet ultrastructure, and bleeding time. Only guanidinosuccinic acid and perhaps the phenolic compounds thus far meet the most rigid criteria for toxins affecting platelet function. A toxin which competitively limits internal platelet transformation in response to exogenous adenosine diphosphate could account for the hemostatic abnormalities found in renal failure.
Author Affiliations
Bronx, NY
From the Department of Medicine, Bronx-Lebanon Hospital Center, Bronx, NY.
Footnotes
Received for publication June 22, 1970; accepted July 7.
Read before the session entitled "Hematologic Disorders" (Allen J. Erslev, MD, chairman) of the Symposium on Uremic Toxins sponsored by the National Institute of Arthritis and Metabolic Diseases, Monterey, Calif, March 18, 1970.
Reprint requests to Department of Medicine, Bronx-Lebanon Hospital Center, Bronx, NY 10456 (Dr. Horowitz)
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