Simultaneous management of disordered phosphate and iron homeostasis to correct fibroblast growth factor 23 and associated outcomes in chronic kidney disease

Guillaume Courbon, Marta Martinez-Calle, Valentin David*

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

1 Scopus citations

Abstract

Purpose of reviewHyperphosphatemia, iron deficiency, and anemia are powerful stimuli of fibroblast growth factor 23 (FGF23) production and are highly prevalent complications of chronic kidney disease (CKD). In this manuscript, we put in perspective the newest insights on FGF23 regulation by iron and phosphate and their effects on CKD progression and associated outcomes. We especially focus on new studies aiming to reduce FGF23 levels, and we present new data that suggest major benefits of combined corrections of iron, phosphate, and FGF23 in CKD.Recent findingsNew studies show that simultaneously correcting iron deficiency and hyperphosphatemia in CKD reduces the magnitude of FGF23 increase. Promising therapies using iron-based phosphate binders in CKD might mitigate cardiac and renal injury and improve survival.SummaryNew strategies to lower FGF23 have emerged, and we discuss their benefits and risks in the context of CKD. Novel clinical and preclinical studies highlight the effects of phosphate restriction and iron repletion on FGF23 regulation.

Original languageEnglish (US)
Pages (from-to)359-366
Number of pages8
JournalCurrent opinion in nephrology and hypertension
Volume29
Issue number4
DOIs
StatePublished - Jul 1 2020

Keywords

  • anemia
  • cardiovascular disease
  • chronic kidney disease
  • iron
  • phosphate

ASJC Scopus subject areas

  • Internal Medicine
  • Nephrology

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