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.

• Authors: Ekaterini Siomou, Constantinos J Stefanidis
• Journal: Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association (Nephrol Dial Transplant) Vol. 27 Issue 12 Pg. 4259-62 (Dec 2012) ISSN: 1460-2385 [Electronic] England
• PMID: 22848110 (Publication Type: Journal Article, Comment)

Chemical References

• FGF23 protein, human
• Fibroblast Growth Factors
• Fibroblast Growth Factor-23

Topics

• Female
• Fibroblast Growth Factor-23
• Fibroblast Growth Factors (blood)
• Humans
• Kidney (physiopathology)
• Male
• Renal Insufficiency, Chronic (blood, physiopathology)