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Published on: November 10, 2021
Klotho, FGF23, and FGF receptors in chronic kidney disease: a yin-yang situation?
1Institut 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. tilman.drueke@inserm.fr
Abstract:
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.
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