Niwa T, Ise M, Miyazaki T
Department of Clinical Laboratory, Nagoya University Branch Hospital, Japan.
Am J Nephrol. 1994;14(3):207-12. doi: 10.1159/000168716.
In uremia there is a marked elevation of serum levels of indoxyl sulfate due to its decreased renal clearance. Indoxyl sulfate is synthesized in the liver from indole which is produced by bacteria in the intestines. To determine the role of indoxyl sulfate in the progression of chronic renal failure, we administered indole, the precursor of indoxyl sulfate, to subtotally nephrectomized uremic rats. The oral administration of indole increased the serum levels of creatinine and blood urea nitrogen and decreased creatinine, inulin, and p-aminohippuric acid clearances. The glomerular sclerosis index in the indole-treated rats was higher than in the control uremic rats. After oral administration, indole could not be detected in the urine, but large amounts of its metabolite, indoxyl sulfate. Thus, indole administration stimulated glomerular sclerosis in a uremic model through the production of indoxyl sulfate.
在尿毒症中，由于硫酸吲哚酚的肾脏清除率降低，其血清水平显著升高。硫酸吲哚酚由肠道细菌产生的吲哚在肝脏中合成。为了确定硫酸吲哚酚在慢性肾衰竭进展中的作用，我们将硫酸吲哚酚的前体吲哚给予行次全肾切除术的尿毒症大鼠。口服吲哚会增加血清肌酐和血尿素氮水平，并降低肌酐、菊粉和对氨基马尿酸清除率。吲哚处理组大鼠的肾小球硬化指数高于对照尿毒症大鼠。口服后，尿液中检测不到吲哚，但能检测到大量其代谢产物硫酸吲哚酚。因此，在尿毒症模型中，吲哚给药通过产生硫酸吲哚酚刺激肾小球硬化。
