Institute for Physiology and Pathophysiology, Johannes Kepler University Linz, Linz, Austria.
Department of Internal Medicine and Cardiology, Campus Virchow-Klinikum.
Curr Opin Nephrol Hypertens. 2019 Jul;28(4):289-296. doi: 10.1097/MNH.0000000000000507.
Chronic kidney disease (CKD) facilitates a unique environment to strongly accelerate vascular calcification - the pathological deposition of calcium-phosphate in the vasculature. These calcifications are associated with the excessive cardiovascular mortality of CKD patients.
Vascular calcification is a multifaceted active process, mediated, at least partly, by vascular smooth muscle cells. These cells are able to transdifferentiate into cells with osteo/chondrogenic properties, which exert multiple effects to facilitate vascular tissue mineralization. As the understanding of the underlying pathophysiology increases, first therapeutic concepts begin to emerge.
This brief review provides an overview on the so far known mechanisms involved in the initiation and progression of vascular calcification in CKD.
慢性肾脏病（CKD）为血管钙化提供了一个独特的强加速环境 - 钙磷在脉管系统中的病理性沉积。这些钙化与 CKD 患者过高的心血管死亡率相关。
血管钙化是一个多方面的活跃过程，至少部分由血管平滑肌细胞介导。这些细胞能够转分化为具有成骨/软骨特性的细胞，这些细胞发挥多种作用以促进血管组织矿化。随着对潜在病理生理学的认识不断增加，初步的治疗概念开始出现。
本文简要综述了目前已知的 CKD 中血管钙化起始和进展的相关机制。
