Abstract
Introduction: Increased renal vascular resistance and microalbuminuria are associated with hypertensive target organ damage and may be predictors of hypertensive nephrosclerosis. Aim: We investigated changes in renal resistive index (RI) and urinary albumin excretion (UAE) in a group of patients with primary hypertension before and during long-term antihypertensive treatment. Methods: Thirty-two patients were randomized to receive antihypertensive treatment with either a calcium channel blocker (nifedipine GITS, up to 90 mg/day, n = 16) or an ACE inhibitor (lisinopril, up to 20 mg/day, n = 16), alone or in association with a diuretic (chlortalidone, 25 mg/day). Blood pressure, renal resistive index (by US Doppler) and UAE (mean of three nonconsecutive timed urinary collections, µg/min) were evaluated at baseline and over the course of 24 months of treatment. Results: Both regimens effectively lowered blood pressure (mean blood pressure from 123 ± 1.8 at baseline to 103 ± 1.5 mm Hg at 24 months in the lisinopril group and from 122 ± 1.9 at baseline to 104 ± 0.8 at 24 months in the nifedipine group, p < 0.001 for both groups). Overall, blood pressure decrease was associated with a reduction in UAE and no change in RI throughout the study. However, despite similar blood pressure reduction, the two regimens showed different specific effects. Lisinopril was associated with a significant decrease in both UAE (33.8 ± 16.2 at baseline and 9.1 ± 2.1 at 24 months, p < 0.01) and renal RI (0.61 ± 0.02 at baseline and 0.56 ± 0.04 at 24 months, p < 0.05) while nifedipine GITS did not significantly influence UAE (35.7 ± 12.2 at baseline and 31.2 ± 12.1 at 24 months, n.s.) or RI (0.61 ± 0.01 at baseline and 0.59 ± 0.02 at 24 months, n.s.). Conclusion: Effective blood pressure control over a long period of time reduces the severity of organ damage, namely UAE while maintaining renovascular resistance in patients with essential hypertension. Different classes of antihypertensive agents might convey additional specific renal protection beyond blood pressure control. These data could be useful in devising individualized therapeutic strategies in hypertensive patients at increased renal risk.
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