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Glucocorticoids (GCs) impair bone growth in children after kidney transplants by increasing FGF23. Blocking FGF23 signaling pathways, particularly FGFR3, may prevent this growth impairment.

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Area of Science:

  • Pediatric Nephrology
  • Endocrinology
  • Bone Biology

Background:

  • Renal transplantation (RTx) improves outcomes for children with chronic kidney disease.
  • Chronic immunosuppression with glucocorticoids (GCs) hinders bone growth and bone mineral density (BMD).
  • The precise mechanisms of GC-induced growth impairment remain unclear, but fibroblast growth factor 23 (FGF23) dysregulation is implicated.

Purpose of the Study:

  • To investigate the role of FGF23 in GC-induced growth impairment in pediatric RTx patients.
  • To explore the therapeutic potential of targeting the FGF23 pathway for growth recovery.

Main Methods:

  • Post hoc analysis of a randomized clinical trial comparing early GC withdrawal versus chronic GC treatment in prepubertal RTx children.
  • Preclinical studies in rats and mouse tibia explants to assess GC effects on FGF23, FGFR expression, and bone growth.
  • Pharmacological blockade of FGF23 receptors (FGFRs) in vitro and in vivo.

Main Results:

  • GC withdrawal correlated with improved growth, BMD, and lower plasma FGF23 levels.
  • GCs increased FGF23 expression in rats and decreased FGFR1 while increasing FGFR3 expression in mouse tibia explants.
  • Blocking FGF23 receptors (FGFRs) prevented GC-induced growth impairment in vitro and in vivo.

Conclusions:

  • GC treatment contributes to reduced longitudinal bone growth by upregulating FGF23 and FGFR3 expression.
  • The FGF23/Klotho/FGFR3 axis in the growth plate represents a potential therapeutic target for managing GC-induced growth impairment in children.