Urinary
albumin excretion is a predictor for cardiovascular mortality and morbidity. We investigated which parameters determine baseline urinary
albumin excretion in nondiabetic subjects, without renal disease. In addition, we evaluated the parameters that predict the
albuminuria-lowering efficacy of an
angiotensin-converting enzyme inhibitor. In this substudy of the Prevention of Renal and Vascular Endstage Disease Intervention Trial, 384 microalbuminuric patients were included. Patient and biochemical characteristics were obtained at baseline and after 3 months of double-blinded, randomized treatment (
fosinopril 20 mg or placebo). Mean age was 51.1+/-11.5 years, and 65.6% were male. Median urinary
albumin excretion was 22.2 mg per 24 hours. At baseline, mean arterial pressure (beta(standardized)=0.161; P=0.006), urinary
sodium excretion (beta(standardized)=0.154; P=0.011), and estimated renal function were independently associated with
albumin excretion. In these predominantly normotensive to prehypertensive subjects,
fosinopril reduced
albumin excretion by 18.5% versus a 6.1% increase on placebo after 3 months (P<0.001).
Fosinopril use and blood pressure reduction independently predicted the change in urinary
albumin excretion. Baseline urinary
albumin excretion independently predicted the antialbuminuric effect of
fosinopril (beta(standardized)=-0.303; P<0.001). In conclusion, at baseline,
sodium intake and blood pressure were positively associated with urinary
albumin excretion.
Fosinopril reduced
albuminuria more than might be expected from its blood pressure-lowering effect alone, and this effect was more outspoken in subjects with higher baseline
albumin excretion. Based on our data, we hypothesize that
angiotensin-converting enzyme inhibition may result in superior cardiovascular protection when compared with other blood pressure-lowering agents in subjects with higher baseline levels of
albuminuria.