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

作者：Siomou Ekaterini; Stefanidis Constantinos J^*

来源：Nephrology Dialysis Transplantation, 2012, 27(12): 4259-4262.

DOI：10.1093/ndt/gfs315

• calcium
• children
• chronic kidney disease
• CKDmineral and bone disorder
• fibroblast growth factor-23
• parathyroid hormone
• phosphate
• vitamin D

Disturbances in mineral and bone metabolism in children with chronic kidney disease (CKD) lead to specific abnormalities of skeletal homeostasis called CKDmineral 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 bonekidneyparathyroid endocrine axis mediated by FGF-23 should be a novel therapeutic target in clinical practice, even in early stages of CKD in children.

• 出版日期2012-12