Department of Pharmacodynamics, Medical University of Bialystok, Mickiewicza 2c, 15-222 Bialystok, Poland.
Department of Clinical Pharmacy, Medical University of Bialystok, Mickiewicza 2c, 15-222 Bialystok, Poland.
Oxid Med Cell Longev. 2020 Dec 29;2020:6656033. doi: 10.1155/2020/6656033. eCollection 2020.
Chronic kidney disease (CKD) occurrence is rising all over the world. Its presence is associated with an increased risk of premature death from cardiovascular disease (CVD). Several explanations of this link have been put forward. It is known that in renal failure, an array of metabolites cannot be excreted, and they accumulate in the organism. Among them, some are metabolites of tryptophan (TRP), such as indoxyl sulfate and kynurenine. Scientists have become interested in them in the context of inducing vascular damage in the course of chronic kidney impairment. Experimental evidence suggests the involvement of TRP metabolites in the progression of chronic kidney disease and atherosclerosis separately and point to oxidative stress generation as one of the main mechanisms that is responsible for worsening those states. Since it is known that blood levels of those metabolites increase significantly in renal failure and that they generate reactive oxygen species (ROS), which lead to endothelial injury, it is reasonable to suspect that products of TRP metabolism are the missing link in frequently occurring atherosclerosis in CKD patients. This review focuses on reports that shed a light on TRP metabolites as contributing factors to vascular damage in the progression of impaired kidney function.
慢性肾脏病（CKD）的发病率在全球范围内呈上升趋势。其存在与心血管疾病（CVD）导致的过早死亡风险增加有关。已经提出了几种解释这种关联的机制。众所周知，在肾功能衰竭时，许多代谢物无法排出体外，会在体内积累。其中一些是色氨酸（TRP）的代谢物，如吲哚硫酸酯和犬尿氨酸。科学家们对它们在慢性肾损伤过程中诱导血管损伤的能力产生了兴趣。实验证据表明，TRP 代谢物分别参与了慢性肾脏病和动脉粥样硬化的进展，并指出氧化应激的产生是导致这些情况恶化的主要机制之一。由于已知这些代谢物在肾功能衰竭时的血液水平显著增加，并且它们会产生导致内皮损伤的活性氧（ROS），因此有理由怀疑 TRP 代谢产物是 CKD 患者经常发生的动脉粥样硬化的缺失环节。本综述重点介绍了一些报告，这些报告揭示了 TRP 代谢物作为肾功能障碍进展中血管损伤的致病因素的作用。
