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Fibroblast growth factor 23 and calcium phosphate homeostasis after pediatric renal transplantation

Michael van Husen1, Anja Lehnhardt, Ann-Katrin Fischer

  • 1Pediatric Nephrology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. mhusen@uke.de

Pediatric Transplantation
|May 5, 2012
PubMed

Insights

Fibroblast growth factor 23 (FGF23) is elevated in children after kidney transplant (PRT), particularly those with impaired kidney function. FGF23 appears to be a sensitive indicator of calcium-phosphate imbalance post-transplant.

Area of Science:

  • Nephrology
  • Endocrinology
  • Pediatric Medicine

Background:

  • Fibroblast growth factor 23 (FGF23) regulates phosphate homeostasis and is elevated in chronic kidney disease (CKD).
  • Limited data exist on FGF23 levels following pediatric renal transplantation (PRT).

Purpose of the Study:

  • To investigate FGF23 levels and their association with bone metabolism parameters in children post-PRT.
  • To compare FGF23 levels in children post-PRT with healthy controls and assess its role in CKD and hypophosphatemia.

Main Methods:

  • Analysis of serum calcium, phosphate, vitamin D metabolites, alkaline phosphatase, parathyroid hormone (PTH), and FGF23 in 57 children post-PRT and 11 controls.
  • Assessment of estimated glomerular filtration rate (eGFR) and correlation with FGF23 and other bone metabolism markers.
  • Multivariate analysis to identify factors associated with FGF23 levels.

Main Results:

  • FGF23 and PTH levels were significantly elevated in children post-PRT compared to controls.
  • Highest FGF23 levels were observed in children with eGFR < 60 mL/min/1.73 sqm, with elevated levels present even in early CKD stages (CKD2T).
  • eGFR, PTH, calcium, and phosphate were significantly associated with FGF23; in hypophosphatemic patients, phosphate was associated with FGF23, not PTH.

Conclusions:

  • FGF23 is increased in children after PRT, especially with chronic allograft dysfunction.
  • FGF23 may serve as a more sensitive marker of disturbed calcium-phosphate homeostasis than PTH in pediatric kidney transplant recipients.

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