Objective (95% CI, specificity 97.5% (95% CI, LR+ 34.7 (95% CI,

Abstract-The objective of the study was to assess the factors related to the occurrence of microalbuminuria during the follow-up of a young adult group with essential hypertension that had not been previously treated. Normo-albuminuric essential hypertensives, Ͻ50 years old, who had not been previously treated with antihypertensive drugs and who did not have diabetes mellitus were included. After the initial evaluation, patients were treated using only nonpharmacological measures (nϭ62), ␤-blockers (nϭ38), ACE inhibitors (nϭ64), calcium channel blockers (nϭ8), and several classes (nϭ15). Measurements were taken for office blood pressure, biochemical profile, and 24-hour urinary albumin excretion at the beginning of the study and were measured yearly during an average of 2.7Ϯ1.2 years of follow-up. Among the 187 patients included, 22 (11,7%) developed microalbuminuria (progressors, 4.4/100 patients/y). No differences were present between progressors and those who remained normo-albuminuric (nonprogressors) in terms of age, gender, body mass index, disease duration, blood pressure values, biochemical profile, familial history of diabetes or hypertension, smoking habits, or the presence of EKG left ventricular hypertrophy. The group with the lowest progression rate was the patients treated with ACE inhibitors (nϭ5; 2.9/100 patients/y), followed by the diet group (nϭ5; 3.3/100 patients/y) and the ␤-blockers group (nϭ5; 4.1/100 patients/y). When we excluded patients treated with calcium channel blockers or those who changed over time between different classes of treatment, no significant differences in the incidence of microalbuminuria were observed among the groups. Progressors showed higher slopes of fasting glucose (4.78Ϯ11.4 versus 0.50Ϯ6.8 mg/y, PϽ0.02) and uric acid (0.58Ϯ0.93 versus 0.05Ϯ1.10 mg/y, PϽ0.03) compared with the slopes of nonprogressors. Both the slopes for glucose and systolic blood pressure over time were associated independently with the slope of the logarithm of urinary albumin excretion when adjusted for age, gender, and treatment groups. Cox proportional hazard model for progression of microalbuminuria showed that baseline urinary albumin excretion (risk ratio [RR]ϭ1.06; confidence interval [CI] 95%, 1.01 to 1.11), slope for systolic blood pressure (RRϭ1.11; CI 95%, 1.03 to 1.20), and slope for glucose (RRϭ1.08; CI 95%, 1.03 to 1.14) were independently associated to the development of microalbuminuria. In conclusion, in a group of young adults with essential hypertension that had not been previously treated, the main factors influencing the occurrence of microalbuminuria during antihypertensive treatment were the values of microalbuminuria at baseline and the slopes for systolic blood pressure and fasting glucose. icroalbuminuria is now considered a marker of cardiovascular and renal risk in diabetic 1 and nondiabetic elderly subjects. 2 In hypertension, although the prevalence of microalbuminuria is variable and depends on the characteristics of the population studied, a clustering of cardio...

beta1-AR expression levels were higher in circulating lymphocytes from hypertensive patients (2-DeltaDeltaCt = 2.135 +/- 0.4252*, vs. control group), but this difference was not observed when these patients were treated with blockers of the renin-angiotensin system. beta1-AR levels directly correlated (r2 = 0.5711, P = 0.0185) with urinary albumin excretion in microalbuminuric patients, which relates alterations of this receptor to cardiovascular risk. An inverse correlation was observed between the expression levels of beta2-AR and diastolic blood pressure (r2 = 0.2078, P = 0.0031), suggesting that beta2-AR levels in lymphocytes mirror their expression in vascular cells, in which beta2-AR-mediated relaxation regulates vascular resistance. mRNA levels for GRK3 were inversely correlated with systolic and diastolic blood pressure (day, night and 24 h), which suggests a protective role for GRK3 in the regulation of human blood pressure, as supported by previous findings in transgenic mice.