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A prospective study of fibroblast growth factor-23 in children with chronic kidney disease

Per Magnusson1, Sverker Hansson, Diana Swolin-Eide

  • 1Bone and Mineral Metabolic Unit, Division of Clinical Chemistry, Department of Clinical and Experimental Medicine, Faculty of Health Sciences at Linköping University, Linköping, Sweden. per.magnusson@lio.se

Scandinavian Journal of Clinical and Laboratory Investigation
|November 26, 2009
PubMed

Insights

Fibroblast growth factor-23 (FGF-23) is linked to kidney function and bone health in children with chronic kidney disease (CKD). Higher FGF-23 levels correlate with lower GFR and altered bone density, highlighting its role in pediatric CKD mineral bone disorder.

Area of Science:

  • Pediatric Nephrology
  • Endocrinology
  • Mineral and Bone Metabolism

Background:

  • Fibroblast growth factor-23 (FGF-23) is a key regulator of phosphate metabolism.
  • Limited clinical data exists on FGF-23 in pediatric chronic kidney disease (CKD) patients at risk for mineral bone disorder.

Purpose of the Study:

  • To investigate the relationship between serum FGF-23 levels, bone mass, and bone turnover in children with CKD over a 2-year period.

Main Methods:

  • Prospective study involving 13 pediatric CKD patients (ages 4-15) with a median GFR of 38 mL/min/1.73 m(2).
  • Serum FGF-23 levels, bone mineral density (BMD), and bone turnover markers were assessed over 2 years.

Main Results:

  • Median FGF-23 levels decreased from 127 to 70 RU/mL during follow-up.
  • Elevated FGF-23 levels were observed in 5 patients, particularly those with advanced CKD (stages 4-5) and end-stage renal disease.
  • FGF-23 showed an inverse correlation with GFR (r = -0.73) and a positive association with parathyroid hormone (PTH) (r = 0.69).
  • Lumbar spine BMD Z-score correlated with FGF-23 at baseline (r = 0.61).

Conclusions:

  • FGF-23 is associated with GFR, PTH levels, and lumbar spine BMD in pediatric CKD patients.
  • These findings suggest FGF-23 plays a significant role in the pathophysiology of mineral bone disorder in children with CKD.
Abstract

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