Institut National de la Santé et de la Recherche Médicale (Inserm) Equipe Région-Inserm-12, UFR (Unité de Formation et de Recherche) de Médecine et de Pharmacie, Université de Picardie Jules Verne, Amiens, France.
Kidney Int. 2010 Dec;78(11):1057-60. doi: 10.1038/ki.2010.339.
Secondary hyperparathyroidism in chronic kidney disease (CKD) develops in response to disturbances in calcium and phosphate metabolism associated with CKD, including FGF23 and klotho. FGF23 activates its receptor FGFR1, splice variant IIIC, in the parathyroid gland via a klotho-dependent mechanism and suppresses parathyroid hormone (PTH) secretion. Klotho also may regulate PTH secretion in an FGF23-independent mode, by modulating parathyroid Na+/K+-ATPase activity. The persistence of hyperparathyroidism with progressing CKD despite high serum FGF23 is indicative of FGF23 resistance.
慢性肾脏病（CKD）中的继发性甲状旁腺功能亢进症是对与 CKD 相关的钙和磷代谢紊乱的反应，包括 FGF23 和 klotho。FGF23 通过依赖 klotho 的机制在甲状旁腺中激活其受体 FGFR1、剪接变体 IIIC，并抑制甲状旁腺激素（PTH）的分泌。klotho 还可以通过调节甲状旁腺 Na+/K+-ATPase 活性，以不依赖于 FGF23 的模式调节 PTH 的分泌。尽管血清 FGF23 水平升高，但 CKD 进展时仍存在甲状旁腺功能亢进症表明存在 FGF23 抵抗。
