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Published on: June 24, 2018

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

Ekaterini Siomou1, Constantinos J Stefanidis

  • 1Department of Child Health, Medical School, University of Ioannina, Ioannina, Greece. stefanid@hol.gr

Nephrology, Dialysis, Transplantation : Official Publication of the European Dialysis and Transplant Association - European Renal Association
|August 1, 2012
PubMed

Insights

Fibroblast growth factor-23 (FGF-23) is elevated early in children with chronic kidney disease (CKD), preceding other mineral and bone disorder (CKD-MBD) markers. Targeting this FGF-23 axis may prevent bone deformities and growth issues in pediatric CKD.

Area of Science:

  • Pediatric Nephrology
  • Endocrinology
  • Mineral and Bone Metabolism

Background:

  • Chronic kidney disease (CKD) in children causes mineral and bone disorders (CKD-MBD), leading to skeletal abnormalities and growth issues.
  • Traditional understanding implicates vitamin D, parathyroid hormone (PTH), calcium (Ca), and phosphate (P) disturbances in CKD-MBD pathogenesis.
  • Emerging research highlights fibroblast growth factor-23 (FGF-23) as a critical regulator of phosphate and vitamin D metabolism.

Purpose of the Study:

  • To investigate the role of FGF-23 in the early stages of CKD-MBD in pediatric populations.
  • To determine if elevated FGF-23 levels precede other biochemical markers of CKD-MBD.
  • To explore FGF-23 as a potential therapeutic target for managing CKD-MBD in children.

Main Methods:

  • Analysis of FGF-23 levels in pediatric CKD patients.
  • Correlation of FGF-23 levels with serum Ca, P, and PTH concentrations.
  • Review of existing literature on FGF-23's role in mineral metabolism.

Main Results:

  • Elevated FGF-23 levels were observed early in pediatric CKD, prior to detectable abnormalities in serum Ca, P, or PTH.
  • Increased FGF-23 induces phosphaturia and suppresses vitamin D synthesis, contributing to negative phosphate balance.
  • FGF-23 acts independently of PTH in regulating phosphate homeostasis.

Conclusions:

  • The bone-kidney-parathyroid axis, mediated by FGF-23, is a crucial factor in pediatric CKD-MBD.
  • Early detection and therapeutic targeting of FGF-23 may be vital for preventing skeletal complications in children with CKD.
  • FGF-23 represents a promising novel therapeutic target even in the initial phases of pediatric CKD.

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