Department of Pediatrics, University Children's Hospital Rostock, Germany.
Kidney Blood Press Res. 2013;37(1):68-83. doi: 10.1159/000343402. Epub 2013 Mar 18.
The term chronic kidney disease-mineral bone disorder has been coined recently to highlight that the disturbed mineral and bone metabolism is a major contributor to vascular calcification and finally cardiovascular disease. This syndrome is characterized by clinical, biochemical and/or histological findings, i.e. i) biochemical alterations in the homeostasis of calcium, phosphate and their key player parathyroid hormone (PTH), Fibroblast growth factor-23 (FGF-23), klotho and vitamin-D, ii) the occurrence of vascular and/or soft tissue calcification, and iii) an abnormal bone structure and/or turnover. Apart from the combined and synergistic action of "traditional" and uremia-related risk factors, promoters and inhibitors of calcification have to be considered as well. This review will focus on the disturbed mineral metabolism as the triggering force behind distortion of vascular integrity and cardiovascular malfunction in CKD patients.
近年来,“慢性肾脏病-矿物质和骨异常”这一术语被提出,以强调矿物质和骨代谢紊乱是血管钙化、最终导致心血管疾病的主要因素。该综合征的特征在于临床、生化和/或组织学发现,即 i)钙、磷及其关键调控因子甲状旁腺激素(PTH)、成纤维细胞生长因子 23(FGF-23)、klotho 和维生素 D 的体内平衡发生生化改变,ii)血管和/或软组织钙化的发生,以及 iii)异常的骨结构和/或转换。除了“传统”和尿毒症相关危险因素的联合和协同作用外,钙化的促进剂和抑制剂也必须被考虑。这篇综述将重点讨论矿物质代谢紊乱,作为 CKD 患者血管完整性受损和心血管功能障碍的触发因素。