Reduction in Albuminuria Translates to Reduction in Cardiovascular Events in Hypertensive Patients

Hans Ibsen(Cornell University), Michael Hecht Olsen(Cornell University), Kristian Wachtell(Cornell University), Knut Borch‐Johnsen(Cornell University), Lars Lindholm(Cornell University), Carl Erik Mogensen(Cornell University), Björn Dahlöf(Cornell University), Richard B. Devereux(Cornell University), Ulf dé Fairé(Cornell University), Frej Fyhrquist(Cornell University), Stevo Julius(Cornell University), Sverre E. Kjeldsen(Cornell University), Ole Lederballe‐Pedersen(Cornell University), Markku S. Nieminen(Cornell University), Per Omvik(Cornell University), Suzanne Oparil(Cornell University), Ying Wan(Cornell University)
Hypertension
January 18, 2005
Cited by 563

Abstract

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.


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