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Evolving concepts in the pathogenesis of uraemic cardiomyopathy

Xiaoliang Wang1, Joseph I Shapiro2

  • 1Joan C. Edwards School of Medicine, Marshall University, Huntington, WV, USA.

Nature Reviews. Nephrology
|January 22, 2019
PubMed

Insights

Uraemic cardiomyopathy, cardiac issues in chronic kidney disease (CKD), involves diastolic dysfunction and left ventricular hypertrophy. Understanding its complex causes, including FGF23 and inflammation, is key to improving patient outcomes.

Area of Science:

  • Nephrology
  • Cardiology
  • Pathophysiology

Background:

  • Uraemic cardiomyopathy describes cardiac abnormalities in chronic kidney disease (CKD) patients.
  • Historically, it was a severe condition reversible by renal transplantation.
  • Currently, it's characterized by diastolic dysfunction, left ventricular hypertrophy, and fibrosis in CKD.

Purpose of the Study:

  • To review evolving concepts in uraemic cardiomyopathy pathogenesis.
  • To explore the roles of FGF23, inflammation, and oxidant stress.
  • To examine interactions with established mechanisms like pressure/volume overload and neurohormonal activation.

Main Methods:

  • Literature review focusing on recent advancements.
  • Analysis of established and emerging pathogenic factors.
  • Synthesis of information on FGF23, inflammation, oxidant stress, mineral metabolism, and cardiotonic steroids.

Main Results:

  • Uraemic cardiomyopathy is multifactorial, involving both traditional and novel pathways.
  • Fibroblast growth factor 23 (FGF23), inflammation, and oxidant stress play significant roles.
  • Established factors include pressure/volume overload, renin-angiotensin system activation, and abnormal mineral metabolism.

Conclusions:

  • Current treatments for uraemic cardiomyopathy offer modest improvements.
  • Further research into novel pathways like FGF23 is crucial for therapeutic development.
  • A comprehensive understanding of uraemic cardiomyopathy's complex etiology is needed to improve CKD patient cardiac outcomes.

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