Published online before print September 25, 2006, doi: 10.1161/01.HYP.0000244082.26293.2d
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(Hypertension. 2006;48:870.)
© 2006 American Heart Association, Inc.
Original Articles |
Predictors of Angiotensin-Converting Enzyme Inhibitor–Induced Reduction of Urinary Albumin Excretion in Nondiabetic Patients
From the St Antonius Hospital (R.M.A.v.d.W., H.W.T.P.), Department of Cardiology, Nieuwegein; Departments of Nephrology (R.T.G., P.E.d.J.) and Clinical Pharmacology (W.H.v.G.), University Medical Center Groningen, Groningen; University Medical Center Groningen (P.v.d.H., D.J.v.V., A.A.V.), Department of Cardiology, Groningen; and the Department of Internal Medicine (F.B.), Erasmus University Medical Center, Rotterdam, The Netherlands.
Correspondence to Ruud M.A. van de Wal, St Antonius Hospital, Department of Cardiology, Koekoekslaan 1, 3435 CM, Nieuwegein, The Netherlands. E-mail r.wal{at}antonius.net
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 (ßstandardized=0.161; P=0.006), urinary sodium excretion (ßstandardized=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 (ßstandardized=–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.
Key Words: randomized, controlled trial • albumin • urine • ACE inhibitor • hypertension • sodium
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