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

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.

• Authors: Tilman B Drüeke
• Journal: Kidney international (Kidney Int) Vol. 78 Issue 11 Pg. 1057-60 (Dec 2010) ISSN: 1523-1755 [Electronic] United States
• PMID: 21076444 (Publication Type: Journal Article, Comment)

Chemical References

• FGF23 protein, human
• Parathyroid Hormone
• Receptors, Fibroblast Growth Factor
• Phosphorus
• Fibroblast Growth Factors
• Fibroblast Growth Factor-23
• Glucuronidase
• Klotho Proteins
• Sodium-Potassium-Exchanging ATPase
• Calcium

Topics

• Animals
• Calcium (metabolism)
• Chronic Disease
• Fibroblast Growth Factor-23
• Fibroblast Growth Factors (metabolism)
• Glucuronidase (metabolism)
• Humans
• Hyperparathyroidism, Secondary (etiology, metabolism)
• Kidney (metabolism)
• Kidney Diseases (complications, metabolism)
• Klotho Proteins
• Parathyroid Glands (metabolism)
• Parathyroid Hormone (metabolism)
• Phosphorus (metabolism)
• Receptors, Fibroblast Growth Factor (metabolism)
• Sodium-Potassium-Exchanging ATPase (metabolism)