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Phosphate and FGF-23.

Harald Jüppner1

  • 1Endocrine Unit and Pediatric Nephrology Unit, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts, USA.

Kidney International
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PubMed
Summary
This summary is machine-generated.

Fibroblast growth factor (FGF)-23 is a key regulator of phosphate and vitamin D. In chronic kidney disease (CKD), FGF-23 rises, but its effectiveness diminishes, leading to adverse effects.

Keywords:
FGF-23PTHphosphate and calcium homeostasis

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Area of Science:

  • Endocrinology
  • Nephrology
  • Mineral Metabolism

Background:

  • Fibroblast growth factor (FGF)-23 is a critical regulator of serum phosphate and calcitriol (1,25(OH)2D3) levels.
  • Secreted by osteocytes and osteoblasts, FGF-23 responds to phosphate load and calcitriol levels.
  • In chronic kidney disease (CKD), elevated FGF-23 serves as an early biomarker of impaired renal phosphate handling.

Purpose of the Study:

  • To elucidate the role of FGF-23 in the pathogenesis and progression of chronic kidney disease.
  • To understand the adaptive and maladaptive functions of FGF-23 in CKD.
  • To explore potential therapeutic strategies targeting FGF-23 in CKD.

Main Methods:

  • Review of existing literature on FGF-23 in human and animal models of CKD.
  • Analysis of FGF-23's impact on phosphate excretion, calcitriol metabolism, and parathyroid hormone (PTH) secretion.
  • Investigation of the mechanisms underlying FGF-23 resistance in advanced CKD, including Klotho co-receptor expression.

Main Results:

  • FGF-23 levels increase progressively with CKD severity, rising significantly in end-stage renal disease.
  • Elevated FGF-23 initially promotes phosphate excretion but becomes less effective as kidney function declines.
  • Reduced Klotho expression in late CKD leads to FGF-23 resistance.
  • High FGF-23 concentrations in late CKD are associated with adverse outcomes like left ventricular hypertrophy, accelerated CKD progression, and mortality.

Conclusions:

  • FGF-23 plays a crucial adaptive role in maintaining normophosphatemia in early CKD.
  • In advanced CKD, FGF-23 resistance impairs its phosphaturic effect, contributing to disease progression.
  • Therapeutic interventions aimed at lowering phosphate levels in early CKD may mitigate FGF-23 elevation and its detrimental off-target effects, potentially improving patient outcomes.