title: Enalapril prevents clinical proteinuria in diabetic patients with low ejection fraction.
abstract: OBJECTIVE
  Clinical proteinuria is a risk factor for both end-stage renal disease and cardiovascular disease. The prevalence of clinical proteinuria, its correlates and predictive value, and the effect of ACE inhibitors in preventing clinical proteinuria in diabetic and nondiabetic patients with left ventricular (LV) dysfunction are unknown.
  
  
  METHODS
  The Studies of Left Ventricular Dysfunction (SOLVD) trials were analyzed to determine the baseline distribution of clinical proteinuria and related cardiovascular risk factors, the effect of baseline proteinuria on the risk of hospitalization for congestive heart failure (CHF) and mortality, and the effect of enalapril in preventing new clinical proteinuria.
  
  
  RESULTS
  A total of 5,487 out of 6,797 SOLVD participants (81%) were assessed for proteinuria at baseline. A total of 177 patients (3.2%) had baseline proteinuria. These patients had significantly higher systolic (137 vs. 125 mmHg, P < or = 0.001) and diastolic (83 vs. 77 mmHg, P < or = 0.001) blood pressure levels, a higher prevalence of diabetes (41 vs. 18%, P < or = 0.001), a lower ejection fraction (26.2 vs. 27.3%, P < or = 0.05), and greater degree of CHF (New York Heart Association [NYHA] class III/IV in 22 vs. 10%, P < or = 0.001) than patients without baseline proteinuria. Patients with baseline proteinuria also had higher rates of hospitalization for CHF (relative risk 1.81 [95% CI 1.37-2.41], P = 0.0001) and mortality (1.73 [1.34-2.24], P = 0.0001). Enalapril prevented clinical proteinuria in diabetic patients (0.38 [0.17-0.81], P = 0.0123) but not in nondiabetic patients (1.43 [0.77-2.63], P = 0.2622) without baseline proteinuria.
  
  
  CONCLUSIONS
  Clinical proteinuria is an independent predictor of hospitalization for CHF and mortality in diabetic and nondiabetic patients with LV dysfunction. Enalapril significantly reduces the risk of clinical proteinuria in diabetic patients with LV dysfunction.
authors.affiliation: Department of Medicine, McMaster University, Hamilton, Ontario, Canada. scapes@fhs.csu.mcmaster.ca
authors.forename: S E
authors.initials: SE
authors.lastname: Capes
authors.forename: H C
authors.initials: HC
authors.lastname: Gerstein
authors.forename: A
authors.initials: A
authors.lastname: Negassa
authors.forename: S
authors.initials: S
authors.lastname: Yusuf
mesh_terms: D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use*; D001794:Blood Pressure; D004311:Double-Blind Method; D004656:Enalapril / Q000627:therapeutic use*; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D011507:Proteinuria / Q000517:prevention & control*; D018487:Ventricular Dysfunction, Left / Q000188:drug therapy / Q000503:physiopathology* / Q000652:urine; D016277:Ventricular Function, Left
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D004656:Enalapril