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Increased homocysteine in heart failure: a result of renal impairment?

Nur Aksoy1, Mehmet Aksoy, Mahmut Cakmak

  • 1Department of Medical Laboratory, Vocational School of Higher Education for Health Services, University of Gaziantep, Gaziantep, Turkey. naksoy@gantep.edu.tr

Clinical Chemistry and Laboratory Medicine
|November 8, 2006
PubMed

Insights

In heart failure patients without coronary artery disease, impaired kidney function significantly elevates homocysteine levels. This suggests reduced renal clearance is a key factor in hyperhomocysteinemia.

Area of Science:

  • Cardiology
  • Nephrology
  • Biochemistry

Background:

  • Hyperhomocysteinemia is a potential risk factor in severe heart failure.
  • This study investigates homocysteine levels in heart failure patients without coronary artery disease.
  • Focus is on the interplay between homocysteine, left ventricular ejection fraction, and renal function.

Purpose of the Study:

  • To determine the relationship between plasma homocysteine concentration and renal function in heart failure patients.
  • To explore the association between homocysteine levels, left ventricular ejection fraction, and kidney function.
  • To identify predictors of elevated homocysteine in this patient cohort.

Main Methods:

  • Sixty-two advanced heart failure patients without significant coronary artery stenosis were studied.
  • Left ventricular ejection fraction was assessed.
  • Glomerular filtration rate was calculated using the Cockroft-Gault equation.

Main Results:

  • Elevated homocysteine (>or=15 micromol/L) was found in 22 patients.
  • Low glomerular filtration rate correlated with normal serum creatinine.
  • Glomerular filtration rate was the strongest independent predictor of homocysteine levels, with significant correlations also noted for age, disease duration, left ventricular ejection fraction, and serum creatinine.

Conclusions:

  • Impaired renal function contributes to elevated homocysteine levels in heart failure.
  • Reduced renal clearance is a significant pathophysiological mechanism for hyperhomocysteinemia in heart failure.
  • Kidney function is a critical determinant of homocysteine levels in heart failure patients.
Abstract

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