One Health Research Group, Faculty of Medicine, Universidad de Las Américas (UDLA), Antigua Vía a Nayón, Quito EC170124, Ecuador.
Nephrology Department, Hospital de Especialidades Eugenio Espejo, Av. Yahuachi s/n, Quito EC170403, Ecuador.
Toxins (Basel). 2021 Jan 3;13(1):26. doi: 10.3390/toxins13010026.
In patients with advanced chronic kidney disease (CKD), the accumulation of uremic toxins, caused by a combination of decreased excretion secondary to reduced kidney function and increased generation secondary to aberrant expression of metabolite genes, interferes with different biological functions of cells and organs, contributing to a state of chronic inflammation and other adverse biologic effects that may cause tissue damage. Several uremic toxins have been implicated in severe vascular smooth muscle cells (VSMCs) changes and other alterations leading to vascular calcification (VC) and early vascular ageing (EVA). The above mentioned are predominant clinical features of patients with CKD, contributing to their exceptionally high cardiovascular mortality. Herein, we present an update on pathophysiological processes and mediators underlying VC and EVA induced by uremic toxins. Moreover, we discuss their clinical impact, and possible therapeutic targets aiming at preventing or ameliorating the harmful effects of uremic toxins on the vasculature.
在晚期慢性肾脏病（CKD）患者中，尿毒症毒素的积累是由于肾功能下降导致排泄减少和代谢物基因异常表达导致生成增加的综合作用所致，干扰了细胞和器官的不同生物学功能，导致慢性炎症和其他不良生物学效应，可能导致组织损伤。几种尿毒症毒素与严重的血管平滑肌细胞（VSMCs）变化和其他导致血管钙化（VC）和早期血管老化（EVA）的改变有关。上述这些都是 CKD 患者的主要临床特征，导致他们的心血管死亡率异常高。本文介绍了尿毒症毒素诱导 VC 和 EVA 的病理生理过程和介质的最新进展。此外，我们还讨论了它们的临床影响以及可能的治疗靶点，旨在预防或改善尿毒症毒素对血管的有害影响。
