Hypertension. 2005;45:198-202
Published online before print January 17, 2005, doi: 10.1161/01.HYP.0000154082.72286.2a
Published online before print January 17, 2005, doi: 10.1161/01.HYP.0000154082.72286.2a
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(Hypertension. 2005;45:198.)
© 2005 American Heart Association, Inc.
Scientific Contributions |
Reduction in Albuminuria Translates to Reduction in Cardiovascular Events in Hypertensive Patients
Losartan Intervention for Endpoint Reduction in Hypertension Study
From the Glostrup University Hospital (H.I., M.H.O., K.W.), Denmark; Steno Diabetes Centre (K.B.-J.), Gentofte, Denmark; Umeå University Hospital (L.H.L.), Sweden; Århus University Hospital (C.E.M.), Denmark; Sahlgrenska University Hospital/Östra (B.D.), Göteborg, Sweden; Weill Medical College of Cornell University (R.B.D.), New York, NY; Karolinska University Hospital (U.de F.), Stockholm, Sweden; Helsinki University Hospital (F.F., M.S.N.), Finland; University of Michigan (S.J.), Ann Arbor; Ullevaal University Hospital (S.E.K.), Oslo, Norway; Viborg Hospital (O.L.-P.), Denmark; Haukeland University Hospital (P.O.), Bergen, Norway; University of Alabama (S.O.), Birmingham; and Merck Research Laboratories (Y.W.), West Point, PA.
Correspondence to Hans Ibsen, Chief Physician, Medical Department M, Glostrup Hospital, DK-2600 Glostrup, Denmark. E-mail haib{at}glostruphosp.kbhamt.dk
Few data are available to clarify whether changes in albuminuria over time translate to changes in cardiovascular risk. The aim of the present study was to examine whether changes in albuminuria during 4.8 years of antihypertensive treatment were related to changes in risk in 8206 patients with hypertension and left ventricular hypertrophy in the Losartan Intervention For Endpoint reduction in hypertension (LIFE) study. Urinary albumin/creatinine ratio (UACR) was measured at baseline and annually. Time-varying albuminuria was closely related to risk for the primary composite end point (ie, when UACR decreased during treatment, risk was reduced accordingly). When the population was divided according to median baseline value (1.21 mg/mmol) and median year 1 UACR (0.67 mg/mmol), risk increased stepwise and significantly for the primary composite end point from those with low baseline/low year 1 (5.5%), to low baseline/high year 1 (8.6%), to high baseline/low year 1 (9.4%), and to high baseline/high year 1 (13.5%) values. Similar significant, stepwise increases in risk were seen for the components of the primary composite end point (cardiovascular mortality, stroke, and myocardial infarction). The observation that changes in UACR during antihypertensive treatment over time translated to changes in risk for cardiovascular morbidity and mortality was not explained by in-treatment level of blood pressure. We propose that monitoring of albuminuria should be an integrated part of the management of hypertension. If albuminuria is not decreased by the patient’s current antihypertensive and other treatment, further intervention directed toward blood pressure control and other modifiable risks should be considered.
Key Words: albuminuria • angiotensin antagonist • blood pressure • cardiovascular diseases
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