Lichtenwalner D M, Suh B, Lichtenwalner M R
J Clin Invest. 1983 May;71(5):1289-96. doi: 10.1172/jci110879.
An organic compound that inhibits drug binding in uremia has been isolated from the sera of chronic renal failure patients, and its chemical structure has been determined. Addition of the compound to normal human sera in vitro resulted in drug binding defects similar to those seen in uremia. The purification of this substance was accomplished by n-butyl chloride extraction of acidified (pH 3.0) uremic sera followed by column chromatography, thin-layer chromatography, and paper electrophoresis. From analytical studies including ultraviolet and fluorescence spectroscopy, gas chromatography, chemical ionization and electron impact mass spectrometry, and proton nuclear magnetic resonance spectroscopy, the chemical structure of the uremic binding inhibitor was deduced to be 2-hydroxybenzoylglycine. This confirms the hypothesis that the drug binding defect in uremia is due to the accumulation of endogenous metabolic products rather than an intrinsic structural defect in albumin.
从慢性肾衰竭患者的血清中分离出一种可抑制尿毒症中药物结合的有机化合物，并确定了其化学结构。在体外将该化合物添加到正常人血清中会导致与尿毒症中所见类似的药物结合缺陷。该物质的纯化是通过用正丁基氯萃取酸化（pH 3.0）的尿毒症血清，然后进行柱色谱、薄层色谱和纸电泳来完成的。通过包括紫外和荧光光谱、气相色谱、化学电离和电子轰击质谱以及质子核磁共振光谱在内的分析研究，推断出尿毒症结合抑制剂的化学结构为2-羟基苯甲酰甘氨酸。这证实了以下假设，即尿毒症中的药物结合缺陷是由于内源性代谢产物的积累，而非白蛋白的内在结构缺陷。
