Nemcsik János, Kiss István, Tislér András
János Nemcsik, Department of Family Medicine, Semmelweis University, 1125 Budapest, Hungary.
World J Nephrol. 2012 Feb 6;1(1):25-34. doi: 10.5527/wjn.v1.i1.25.
Patients with chronic kidney disease (CKD) have an extremely poor cardiovascular outcome. Arterial stiffness, a strong independent predictor of survival in CKD, is connected to arterial media calcification. A huge number of different factors contribute to the increased arterial calcification and stiffening in CKD, a process which is in parallel with impaired bone metabolism. This coincidence was demonstrated to be part of the direct inhibition of calcification in the vessels, which is a counterbalancing effect but also leads to low bone turnover. Due to the growing evidence, the definition of "CKD mineral bone disorder" was created recently, underlining the strong connection of the two phenomena. In this review, we aim to demonstrate the mechanisms leading to increased arterial stiffness and the up-to date data of the bone-vascular axis in CKD. We overview a list of the different factors, including inhibitors of bone metabolism like osteoprotegerin, fetuin-A, pyrophosphates, matrix Gla protein, osteopontin, fibroblast growth factor 23 and bone morphogenic protein, which seem to play role in the progression of vascular calcification and we evaluate their connection to impaired arterial stiffness in the mirror of recent scientific results.
慢性肾脏病(CKD)患者的心血管预后极差。动脉僵硬度是CKD患者生存的一个强有力的独立预测指标,与动脉中层钙化有关。大量不同因素导致CKD患者动脉钙化增加和僵硬度增加,这一过程与骨代谢受损同时发生。这种巧合被证明是血管钙化直接抑制作用的一部分,这是一种平衡效应,但也会导致低骨转换。由于证据越来越多,最近提出了“CKD矿物质与骨异常”的定义,强调了这两种现象之间的紧密联系。在本综述中,我们旨在阐述导致动脉僵硬度增加的机制以及CKD中骨-血管轴的最新数据。我们概述了一系列不同因素,包括骨代谢抑制剂,如骨保护素、胎球蛋白-A、焦磷酸盐、基质Gla蛋白、骨桥蛋白、成纤维细胞生长因子23和骨形态发生蛋白,这些因素似乎在血管钙化进展中起作用,并且我们根据最近的科学结果评估它们与动脉僵硬度受损的关系。