Inability of accumulated metabolic byproducts of uremia to alter the extent of warfarin binding in charcoal treated plasma.
The addition to charcoal treated normal and charcoal treated uremic plasma of four metabolites which accumulate during uremia--uric acid, beta -phenylpyruvic acid, guanidinosuccinic acid, and p-hydroxyphenylacetic acid--failed to produce a warfarin binding defect. Charcoal treatment corrected the warfarin binding defect in uremic plasma, however it diminished the extent of warfarin binding to normal plasma. These observations rule out the possibility that uric acid, beta -phenylpyruvic acid, guanidinosuccinic acid, or p-hydroxyphenylacetic acid contribute to the warfarin binding defect in uremia, and suggest that free fatty acids have no role in the warfarin binding defect.
D001798:Blood Proteins / Q000378:metabolism*; D002606:Charcoal / Q000494:pharmacology*; D006801:Humans; D066298:In Vitro Techniques; D011485:Protein Binding / Q000187:drug effects; D014511:Uremia / Q000097:blood*; D014859:Warfarin / Q000097:blood*
D001798:Blood Proteins; D002606:Charcoal; D014859:Warfarin