Division of Nephrology, Department of Medicine, Mayo Clinic College of Medicine, Rochester, MN 55905, USA.
Nutrients. 2013 May 29;5(6):1913-36. doi: 10.3390/nu5061913.
The elderly chronic kidney disease (CKD) population is growing. Both aging and CKD can disrupt calcium (Ca2+) homeostasis and cause alterations of multiple Ca2+-regulatory mechanisms, including parathyroid hormone, vitamin D, fibroblast growth factor-23/Klotho, calcium-sensing receptor and Ca2+-phosphate product. These alterations can be deleterious to bone mineral metabolism and soft tissue health, leading to metabolic bone disease and vascular calcification and aging, termed CKD-mineral and bone disorder (MBD). CKD-MBD is associated with morbid clinical outcomes, including fracture, cardiovascular events and all-cause mortality. In this paper, we comprehensively review Ca2+ regulation and bone mineral metabolism, with a special emphasis on elderly CKD patients. We also present the current treatment-guidelines and management options for CKD-MBD.
老年慢性肾脏病(CKD)患者人群正在不断增加。衰老和 CKD 均可破坏钙(Ca2+)稳态,并导致多种 Ca2+调节机制发生改变,包括甲状旁腺激素、维生素 D、成纤维细胞生长因子 23/klotho、钙敏感受体和 Ca2+-磷酸盐产物。这些改变可能对骨矿物质代谢和软组织健康有害,导致代谢性骨病和血管钙化及衰老,即 CKD-矿物质和骨异常(MBD)。CKD-MBD 与不良临床结局相关,包括骨折、心血管事件和全因死亡率。本文全面综述了 Ca2+调节和骨矿物质代谢,并特别关注老年 CKD 患者。我们还介绍了 CKD-MBD 的现行治疗指南和管理选择。