No abstract

No abstract

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. Key Words: albuminuria Ⅲ angiotensin antagonist Ⅲ blood pressure Ⅲ cardiovascular diseases A ssessment of small amounts of urinary albumin excretion, so-called microalbuminuria, has become an integrated marker of cardiovascular risk in diabetic as well as nondiabetic populations. [1][2][3][4] We published data recently from a large group of patients with essential hypertension and ECG-verified left ventricular hypertrophy (LVH) from the Losartan Intervention For Endpoint reduction in hypertension (LIFE) study showing a 4-to 5-fold increase in risk for cardiovascular events from the lowest to the highest decile of baseline urinary albumin excretion rate. 3 In another publication from the same hypertensive population, we showed that high urinary albumin excretion rate was related to LVH and was independent of age, blood pressure, diabetes, race, serum creatinine, or smoking. 5 This suggested cardiac organ damage was paralleling increased renal albumin excretion rate, which itself was most likely a marker of generalized hypertensionrelated damage to the peripheral vasculature. 6,7 Although baseline level of urinary albumin excretion is a powerful risk predictor, there are no data from a comprehensive study population to clarify whether a reduction in albuminuria during antihypertensive treatment relates to a ...

The increase in SUA over 4.8 years in the LIFE study was attenuated by losartan compared with atenolol treatment, appearing to explain 29% of the treatment effect on the primary composite end point. The association between SUA and events was stronger in women than in men with or without adjustment of FRS.

New-onset diabetes could be strongly predicted by a newly developed risk score using baseline serum glucose concentration (non-fasting), body mass index, serum high-density lipoprotein cholesterol concentration, systolic blood pressure and history of prior use of antihypertensive drugs. Independently of these risk factors, fewer hypertensive patients with left ventricular hypertrophy developed diabetes mellitus if they were treated with losartan than if they were treated with atenolol.