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Investigating FGF-23 concentrations and its relationship with declining renal function in paediatric patients with

Manish D Sinha1, Charles Turner, R N Dalton

  • 1Department of Paediatric Nephrology, Evelina Children’s Hospital, Guy’s and St Thomas’ NHS Foundation Trust, London, UK. manish.sinha@gstt.nhs.uk

Nephrology, Dialysis, Transplantation : Official Publication of the European Dialysis and Transplant Association - European Renal Association
|April 25, 2012
PubMed

Insights

Elevated fibroblast growth factor-23 (FGF-23) is common in children with chronic kidney disease (CKD). FGF-23 levels are primarily linked to declining glomerular filtration rate (GFR), not parathyroid hormone.

Area of Science:

  • Pediatric Nephrology
  • Endocrinology
  • Biochemistry

Background:

  • Fibroblast growth factor-23 (FGF-23) is implicated in mineral metabolism.
  • Understanding FGF-23 in pediatric chronic kidney disease (CKD) is crucial for management.

Purpose of the Study:

  • Investigate FGF-23 prevalence in pre-dialysis pediatric CKD Stages 3-5.
  • Examine the relationship between FGF-23 and renal dysfunction.
  • Identify key determinants of elevated FGF-23.

Main Methods:

  • Prospective observational study of 71 children with pre-dialysis CKD.
  • Measured FGF-23 levels, anthropometry, and routine laboratory parameters.
  • Analyzed FGF-23 concentrations against estimated glomerular filtration rate (eGFR) and other biomarkers.

Main Results:

  • 19.7% of patients had normal FGF-23 (< 50 ng/L); the majority had elevated levels.
  • FGF-23 concentrations showed a significant negative correlation with eGFR and 1,25 vitamin D3.
  • FGF-23 correlated positively with phosphate and its fractional excretion, but not with parathyroid hormone (PTH).
  • Multiple regression identified eGFR as the dominant determinant of FGF-23 levels.

Conclusions:

  • Elevated FGF-23 is prevalent in children with non-dialysis CKD.
  • Glomerular filtration rate (GFR) is the primary driver of FGF-23 elevation in this cohort.
  • These findings clarify the FGF-23-GFR relationship, independent of PTH and phosphate fluctuations.
Abstract

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