Treatment-related reductions in microalbuminuria (MAU) are associated with a reduced incidence of cardiovascular events and a reduction in progression to end-stage renal disease in hypertensive patients, but if reduction in MAU correlates with regression of left ventricular hypertrophy (LVH) is still insufficiently studied. Our goal was to assess changes in the level of microalbuminuria and its relationship with regression of LVH during antihypertensive treatment.Design and method:
443 patients with microalbuminuria and LVH were treated with losartan 50–100 mg plus hydrochlorothiazide 12.5–25 mg (219 patients) or amlodipine 5–10 mg o.i.d. (224 patients) during follow-up period of 12 months. Albumin-creatinine ratio was measured in the first morning void urine prior to treatment and 4 weeks after treatment. After 4 weeks of losartan-based combination therapy patients were divided according to reduction in albumin-creatinine ratio on 2 groups: <50% from baseline (1st group) and >50% from baseline (2nd group).Results:
Reduction in albumin-creatinine ratio after 4 weeks of treatment in the 1st group was 28% (from 11.8 ± 7.3 to 8.4 ± 3.8 mg/mmol) (p > 0.05) and in the 2nd group was 71% (from 10.9 ± 4.2 to 3.2 ± 1.6 mg/mmol, p < 0.05). In the 1st group office systolic blood pressure (BP) decreased from 166 ± 4/91 ± 3 to 133 ± 3/79 ± 2 mmHg (p < 0.01) and in the 2nd group from 163 ± 5/93 ± 2 to 131 ± 4/80 ± 1 mmHg (p < 0.05), respectively. Decrease of LVMI was significantly higher after 1 year of treatment in the 2nd group as compared with the 1st group (-19.4 ± 4.1% vs -6.5 ± 3.2%, respectively (p < 0.01). In a multiple regression model, significant relationship between reduction in microalbuminuria and decrease of LVMI was found, independent of office systolic and diastolic BP changes, age and sex (p < 0.01).Conclusions:
There is a strong relationship between reduction in albumin-creatinine ratio and regression of LVH in hypertensive patients. Reduction in microalbuminuria after 4 weeks of treatment predicts further regression of left ventricular hypertrophy in hypertensive patients.