title: Reduction in albuminuria translates to reduction in cardiovascular events in hypertensive patients: losartan intervention for endpoint reduction in hypertension study.
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.
authors.affiliation: Glostrup University Hospital, Denmark. haib@glostruphosp.kbhamt.dk <haib@glostruphosp.kbhamt.dk>
authors.forename: Hans
authors.initials: H
authors.lastname: Ibsen
authors.forename: Michael H
authors.initials: MH
authors.lastname: Olsen
authors.forename: Kristian
authors.initials: K
authors.lastname: Wachtell
authors.forename: Knut
authors.initials: K
authors.lastname: Borch-Johnsen
authors.forename: Lars H
authors.initials: LH
authors.lastname: Lindholm
authors.forename: Carl Erik
authors.initials: CE
authors.lastname: Mogensen
authors.forename: Björn
authors.initials: B
authors.lastname: Dahlöf
authors.forename: Richard B
authors.initials: RB
authors.lastname: Devereux
authors.forename: Ulf
authors.initials: U
authors.lastname: de Faire
authors.forename: Frej
authors.initials: F
authors.lastname: Fyhrquist
authors.forename: Stevo
authors.initials: S
authors.lastname: Julius
authors.forename: Sverre E
authors.initials: SE
authors.lastname: Kjeldsen
authors.forename: Ole
authors.initials: O
authors.lastname: Lederballe-Pedersen
authors.forename: Markku S
authors.initials: MS
authors.lastname: Nieminen
authors.forename: Per
authors.initials: P
authors.lastname: Omvik
authors.forename: Suzanne
authors.initials: S
authors.lastname: Oparil
authors.forename: Ying
authors.initials: Y
authors.lastname: Wan
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D000419:Albuminuria / Q000503:physiopathology*; D000959:Antihypertensive Agents / Q000627:therapeutic use*; D001262:Atenolol / Q000627:therapeutic use; D002318:Cardiovascular Diseases / Q000209:etiology*; D003404:Creatinine / Q000652:urine; D005260:Female; D006801:Humans; D006973:Hypertension / Q000188:drug therapy* / Q000652:urine*; D019808:Losartan / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged; D011237:Predictive Value of Tests; D016016:Proportional Hazards Models; D012307:Risk Factors; D012720:Severity of Illness Index
chemical_list: D000959:Antihypertensive Agents; D001262:Atenolol; D003404:Creatinine; D019808:Losartan