Klotho, FGF23, and FGF receptors in chronic kidney disease: a yin–yang situation? | Zendy

Tilman B. Drüeke | Zendy

AI Assistant Blog Pricing

Home ZAIA Blog

Open Access

Klotho, FGF23, and FGF receptors in chronic kidney disease: a yin–yang situation?

Author(s) -

Tilman B. Drüeke

Publication year - 2010

Publication title -

kidney international

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 3.499

H-Index - 276

eISSN - 1523-1755

pISSN - 0085-2538

DOI - 10.1038/ki.2010.339

Subject(s) - klotho , endocrinology , medicine , parathyroid hormone , fibroblast growth factor 23 , kidney disease , hyperparathyroidism , secondary hyperparathyroidism , receptor , kidney , hypophosphatemia , calcium

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.

The content you want is available to Zendy users.

Already have an account? Click here to sign in.

Having issues? You can contact us here

Accelerating Research