FGF-23 in children with CKD: a new player in the development of CKD–mineral and bone disorder

Abstract

Disturbances in mineral and bone metabolism in children with chronic kidney disease (CKD) lead to specific abnormalities of skeletal homeostasis called CKD–mineral and bone disorder (CKD-MBD). These disturbances should be diagnosed and managed appropriately to prevent bone deformities and disturbed growth. Changes in the vitamin D and parathyroid hormone (PTH), and the subsequent alterations in calcium (Ca) and phosphate (P) homeostasis are considered responsible for the development of CKD-MBD. Recently, a phosphaturic hormone, the fibroblast growth factor-23 (FGF-23), has been reported as a key regulator of P and vitamin D metabolism. A number of recent studies in paediatric populations have documented that the FGF-23 levels are increased early in CKD, before any abnormalities in serum Ca, P or PTH are apparent. The elevated FGF-23 levels result in a negative P balance to maintain P homeostasis, inducing phosphaturia, independently of PTH, and suppressing vitamin D synthesis. Therefore, the bone–kidney–parathyroid endocrine axis mediated by FGF-23 should be a novel therapeutic target in clinical practice, even in early stages of CKD in children.

calcium, children, chronic kidney disease, CKD–mineral and bone disorder, fibroblast growth factor-23, parathyroid hormone, phosphate, vitamin D