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Abstract
We have evaluated pH, chloride, calcium and several endogenous aromatic acids as possible
causes of the impaired binding of drugs by plasma albumin in renal failure. Changes
in pH, chloride and calcium over the range found in renal failure had minimal or no
effects on the binding of [14C]salicylate, a model probe which binds to both of the
major drug-binding loci of human albumin. Hippurate and indoxyl sulfate were weak
inhibitors of binding by normal plasma. Ortho-hydroxy-hippurate was undetectable or
minimally elevated, except among patients with elevated plasma salicylate concentration.
Although plasma hippurate and indoxyl sulfate concentrations were elevated markedly
in patients with renal failure, inhibition of salicylate binding was significantly
correlated only with the concentration of indoxyl sulfate. Addition of hippurate and
indoxyl sulfate separately and together to normal plasma showed that these ligands
could account for only 15% of the impaired binding of salicylate by azotemic plasma.
The retained solutes which account for most of this binding defect remain to be identified.
This uremic disorder (and perhaps others) is due not to a single chemical but to the
additive effect of a family of chemicals.