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Novel markers of left ventricular hypertrophy in uremia

Hironori Nakamura1, Masanori Tokumoto, Masahide Mizobuchi

  • 1Washington University Medical School, St. Louis, Mo., USA.

American Journal of Nephrology
|February 5, 2010
PubMed

Insights

Elevated phosphorus contributes to left ventricular hypertrophy (LVH) in chronic kidney disease. Sevelamer carbonate, combined with enalapril, reduced LVH and cardiomyocyte growth, suggesting its therapeutic potential.

Area of Science:

  • Nephrology
  • Cardiology
  • Pathology

Background:

  • Left ventricular hypertrophy (LVH) is a common complication in chronic kidney disease (CKD).
  • Elevated serum phosphorus is a suspected risk factor for LVH in CKD patients.

Purpose of the Study:

  • To investigate the effect of sevelamer carbonate on LVH and left ventricle (LV) remodeling in a rat model of CKD.
  • To determine if sevelamer carbonate provides additional benefits beyond enalapril in managing LVH.

Main Methods:

  • 5/6 nephrectomized rats were treated with enalapril or enalapril plus sevelamer carbonate for 4 months.
  • Left ventricular weight, cardiomyocyte size, and protein expression (cyclin D2, PCNA, p27) were assessed.
  • Cell proliferation markers (Ki67, phosphohistone H3) were evaluated in interstitial cells and cardiomyocytes.

Main Results:

  • Uremia increased LV weight and cardiomyocyte size; enalapril and enalapril + sevelamer blunted LV weight increase.
  • Only enalapril + sevelamer significantly reduced cardiomyocyte size increase.
  • Enalapril + sevelamer counteracted uremia-induced decreases in p27 expression and interstitial cell proliferation markers.

Conclusions:

  • Left ventricular remodeling in uremia involves cardiomyocyte hypertrophy and interstitial cell proliferation, not cardiomyocyte proliferation.
  • p27 and cyclin D2 are implicated in LVH development.
  • Serum phosphorus is an independent risk factor for LVH and cardiomyocyte size in CKD.
Abstract

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