Institute of Musculoskeletal Sciences, Oxford University, Oxford, UK.
University of Colorado Health Sciences Center, Denver, CO, USA.
J Bone Miner Res. 2020 Dec;35(12):2313-2317. doi: 10.1002/jbmr.4155. Epub 2020 Sep 15.
Chronic kidney disease (CKD) disturbs mineral homeostasis, leading to mineral and bone disorders (MBD). CKD-MBD is a significant problem and currently available treatment options have important limitations. Phosphate retention is thought to be the initial cause of CKD-MBD but serum phosphate remains normal until the late stages of CKD, due to elevated levels of the phosphaturic hormone fibroblast growth factor-23 (FGF-23), and parathyroid hormone (PTH). Reduction of 1,25-dihydroxy-vitamin D (1,25[OH] D) concentration is the next event in the adaptive response of the homeostatic system. We argue, and provide the rationale, that calcium retention which takes place concurrently with phosphate retention, could be the reason behind the hysteresis in the response of PTH. If indeed this is the case, intermittent administration of PTH in early CKD could prevent the hysteresis, which arguably leads to the development of secondary hyperparathyroidism, and provide the platform for an effective management of CKD-MBD. © 2020 American Society for Bone and Mineral Research (ASBMR).
慢性肾脏病(CKD)扰乱了矿物质的体内平衡,导致矿物质和骨代谢紊乱(MBD)。CKD-MBD 是一个重大问题,目前可用的治疗方法存在重要的局限性。磷酸盐潴留被认为是 CKD-MBD 的初始原因,但由于磷转运蛋白成纤维细胞生长因子 23(FGF-23)和甲状旁腺激素(PTH)水平升高,血清磷酸盐在 CKD 晚期之前仍保持正常。1,25-二羟维生素 D(1,25[OH]D)浓度的降低是体内平衡系统适应性反应的下一个事件。我们认为并提供了理由,即与磷酸盐潴留同时发生的钙潴留可能是 PTH 反应滞后的原因。如果情况确实如此,在 CKD 早期间歇性给予 PTH 可能会防止滞后,这可能导致继发性甲状旁腺功能亢进的发展,并为 CKD-MBD 的有效管理提供平台。© 2020 美国骨骼与矿物质研究学会(ASBMR)。