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FGF23 from bench to bedside.

Csaba P Kovesdy1, L Darryl Quarles2

  • 1University of Tennessee Health Science Center, Memphis, Tennessee; and Memphis Veterans Affairs Medical Center, Memphis, Tennessee ckovesdy@uthsc.edu.

American Journal of Physiology. Renal Physiology
|February 12, 2016
PubMed
Summary
This summary is machine-generated.

Elevated fibroblast growth factor-23 (FGF23) in chronic kidney disease (CKD) is linked to poor outcomes. FGF23 may directly harm the heart and kidneys, but its role needs more study.

Keywords:
boneheartkidney

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Area of Science:

  • Nephrology
  • Cardiology
  • Endocrinology

Background:

  • Fibroblast growth factor-23 (FGF23) is associated with adverse outcomes in chronic kidney disease (CKD).
  • FGF23 regulates phosphate and vitamin D homeostasis.
  • Emerging evidence links FGF23 to cardiovascular and renal pathophysiology in CKD.

Purpose of the Study:

  • To explore the pathophysiological mechanisms by which FGF23 may negatively impact cardiovascular and renal systems in CKD.
  • To investigate the potential direct and indirect effects of FGF23 on cardiac and renal function.

Main Methods:

  • Review of existing literature on FGF23, CKD, and cardiovascular/renal outcomes.
  • Analysis of proposed mechanisms involving FGF receptor/α-klotho complexes.
  • Discussion of FGF23's role in renin-angiotensin-aldosterone system activation, sodium retention, and left ventricular hypertrophy (LVH).

Main Results:

  • Elevated FGF23 levels correlate strongly with adverse outcomes across all stages of CKD.
  • FGF23 may exert direct myocardial effects and indirect renal effects via FGF receptor/α-klotho pathways.
  • Proposed mechanisms include activation of the renin-angiotensin-aldosterone system, altered soluble α-klotho, and increased sodium retention, potentially leading to LVH.

Conclusions:

  • The precise role of FGF23 in CKD pathophysiology, particularly concerning cardiovascular and renal adverse outcomes, requires further investigation.
  • FGF23's contribution could be causal or correlational (an innocent bystander) in processes like chronic inflammation leading to LVH.
  • Modulation of FGF23 as a clinical target in CKD necessitates a deeper understanding of its complex mechanisms.