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Enalapril prevents clinical proteinuria in diabetic patients with low ejection fraction

S E Capes1, H C Gerstein, A Negassa

  • 1Department of Medicine, McMaster University, Hamilton, Ontario, Canada. scapes@fhs.csu.mcmaster.ca

Diabetes Care
|June 27, 2000
PubMed

Insights

Clinical proteinuria predicts heart failure hospitalization and mortality in patients with left ventricular dysfunction. Enalapril, an ACE inhibitor, helps prevent proteinuria in diabetic individuals with this condition.

Area of Science:

  • Nephrology
  • Cardiology
  • Clinical Trials

Background:

  • Clinical proteinuria is a known risk factor for end-stage renal disease and cardiovascular disease.
  • The role of proteinuria in patients with left ventricular (LV) dysfunction, and the impact of ACE inhibitors, remain unclear.

Purpose of the Study:

  • To investigate the prevalence and correlates of clinical proteinuria in patients with LV dysfunction.
  • To assess the predictive value of proteinuria for adverse cardiovascular outcomes.
  • To determine the efficacy of enalapril in preventing new-onset proteinuria.

Main Methods:

  • Analysis of data from the Studies of Left Ventricular Dysfunction (SOLVD) trials.
  • Assessment of baseline proteinuria, cardiovascular risk factors, and New York Heart Association (NYHA) class.
  • Evaluation of enalapril's effect on proteinuria development.

Main Results:

  • 3.2% of participants had baseline proteinuria, associated with higher blood pressure, diabetes prevalence, lower ejection fraction, and more severe heart failure.
  • Proteinuria independently predicted increased hospitalization for congestive heart failure (CHF) and mortality.
  • Enalapril significantly reduced proteinuria risk in diabetic patients but not in non-diabetic patients.

Conclusions:

  • Clinical proteinuria is an independent predictor of CHF hospitalization and mortality in patients with LV dysfunction.
  • Enalapril demonstrates a significant benefit in preventing clinical proteinuria among diabetic patients with LV dysfunction.
Abstract

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