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

Abstract

Background: Fibroblast growth factor-23 (FGF-23) is a novel regulator of phosphate metabolism; however, the clinical knowledge is limited in children with chronic kidney disease (CKD) who are at risk of developing mineral bone disorder. Methods: This prospective study over 2 years investigated the development of bone mass and bone turnover in relation to serum FGF-23 in children with CKD. Thirteen patients, 4–15 years, were included with a median corrected glomerular filtration rate (GFR) of 38 (range 7–74) mL/min/1.73 m². Results: Median FGF-23 was 127 RU/mL at baseline and 70 RU/mL at follow-up. Five patients had FGF-23 levels exceeding the upper reference limit of 141 RU/mL for healthy children. No correlation with age or puberty was found. FGF-23 was inversely correlated with GFR, r = −0.73 (p <0.05). Four of the five patients within CKD stages 4–5 (GFR <30 mL/min/1.73 m²) had elevated FGF-23 levels and two patients with end-stage renal disease had markedly high levels of FGF-23 (1333 and 1700 RU/mL). One of these patients was transplanted after 1 year, which normalized FGF-23 to 70 RU/mL at follow-up. FGF-23 was significantly associated with PTH, r = 0.69 (p <0.01). FGF-23 correlated with osteocalcin, but not with other markers of bone turnover. Total body bone mineral density (BMD) was not correlated with FGF-23, however, the lumber spine BMD Z-score correlated with FGF-23 at baseline, r = 0.61 (p <0.05). Conclusions: Although a small study group, this prospective study suggests that FGF-23 is associated with GFR, PTH, and lumbar spine BMD in pediatric patients with various degrees of CKD.

Key Words::

• Bone turnover
• DXA
• osteocalcin
• osteoprotegerin
• pediatric
• phosphate
• renal osteodystrophy

Acknowledgements

We thank all the patients and parents for participating in this study. We are grateful to the staff at the Pediatric Uronephrological Center and the Göteborg Pediatric Growth Research Center, and we also thank Christina Linnér and Cecilia Halling Linder for excellent technical assistance. We acknowledge the expert statistical advice of Anders Pehrsson. This study was supported by grants from the Swedish Research Council, the Swedish Society of Medicine, the County Council of Östergötland, and the Swedish Association for Kidney Patients, and the Göteborg Medical Society.

Declaration of interest: The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.