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Phosphate wasting disorders in adults.

G Marcucci1, L Masi1, S Ferrarì2

  • 1Metabolic Bone Diseases Unit, Department of Surgery and Translational Medicine, University of Florence, Florence, Italy.

Osteoporosis International : a Journal Established As Result of Cooperation Between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA
|July 18, 2018
PubMed
Summary

Phosphate wasting disorders, often caused by phosphatonins like FGF-23, lead to hypophosphatemia. Newer treatments targeting the FGF-23 pathway offer potential improvements over current therapies with limited efficacy.

Keywords:
FGF-23HypophosphatemiaOsteomalaciaPhosphate wasting disordersRicketsTreatment

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Area of Science:

  • Nephrology
  • Endocrinology
  • Metabolic Bone Disease

Background:

  • Phosphate wasting disorders are a significant cause of hypophosphatemia.
  • Recent advances have identified phosphatonins, such as FGF-23, as key regulators of phosphate homeostasis.
  • FGF-23, a bone-derived hormone, inhibits renal phosphate reabsorption and calcitriol synthesis.

Purpose of the Study:

  • To review phosphate metabolism and its regulators.
  • To discuss phosphate wasting disorders in adults, focusing on diagnosis and treatment.
  • To explore novel therapeutic strategies targeting the FGF-23 pathway.

Main Methods:

  • Literature review of phosphate metabolism and related disorders.
  • Analysis of current and emerging treatments for phosphate wasting conditions.
  • Focus on the role of FGF-23 in phosphate regulation and disease pathogenesis.

Main Results:

  • Current treatments for phosphate wasting disorders have limited efficacy and potential complications.
  • FGF-23 plays a critical role in regulating phosphate and vitamin D metabolism.
  • Targeting the FGF-23 pathway represents a promising avenue for new therapeutic interventions.

Conclusions:

  • Understanding FGF-23's role is crucial for managing hypophosphatemia.
  • Newer strategies targeting the FGF-23 pathway hold promise for improved treatment of phosphate wasting disorders.
  • Further research into FGF-23-targeted therapies is warranted.