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老年慢性肾脏病患者的钙调节与骨矿物质代谢。

Calcium regulation and bone mineral metabolism in elderly patients with chronic kidney disease.

机构信息

Division of Nephrology, Department of Medicine, Mayo Clinic College of Medicine, Rochester, MN 55905, USA.

出版信息

Nutrients. 2013 May 29;5(6):1913-36. doi: 10.3390/nu5061913.

Abstract

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.

摘要

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。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d7e/3725483/16fa1afdbd94/nutrients-05-01913-g001.jpg

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