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The bone at the intersection of kidney and heart disease

Isaac Campos1, Christian Faul1

  • 1Division of Nephrology and Hypertension and Section of Mineral Metabolism, Department of Medicine, The University of Alabama at Birmingham, Birmingham, AL, USA.

Trends in Pharmacological Sciences
|December 6, 2021
PubMed

Insights

Systemic inflammation from kidney disease elevates fibroblast growth factor 23 (FGF23), harming the heart. Bone acts as a link, responding to kidney inflammation by secreting FGF23, worsening cardiac injury.

Area of Science:

  • Cardiovascular Medicine
  • Nephrology
  • Endocrinology

Background:

  • Systemic inflammation and elevated fibroblast growth factor 23 (FGF23) are linked to cardiac injury and mortality in kidney disease patients.
  • The interplay between kidney disease, inflammation, and heart health requires further mechanistic elucidation.

Purpose of the Study:

  • To investigate the mechanistic link between kidney disease, bone, and cardiac injury.
  • To explore the role of bone as a mediator in the progression of kidney disease-associated heart damage.

Main Methods:

  • The study proposes a mechanistic pathway involving kidney-derived factors and bone response.
  • Analysis focuses on the bone's role as a target for proinflammatory mediators from the damaged kidney.

Main Results:

  • Bone serves as a critical intermediary between the damaged kidney and the injured heart.
  • Bone responds to kidney-derived proinflammatory factors by increasing fibroblast growth factor 23 (FGF23) secretion.

Conclusions:

  • The bone-kidney-heart axis is a significant factor in the pathophysiology of kidney disease complications.
  • Targeting this axis may offer novel therapeutic strategies for mitigating cardiac injury in kidney disease.

Keywords:
chronic kidney diseasefibroblast growth factor 23inflammationleft ventricular hypertrophylipocalin 2

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