Albumin Excretion Rate and Metabolic Modifications in Patients With Essential Hypertension

A prospective randomized, double-blind, doubledummy study investigated the effects of two angiotensin converting enzyme (ACE) inhibitors on urinary albumin excretion in nondiabetic patients with mild to moderate essential hypertension. At the end of a 4-week placebo run-in period, 36 patients were randomly allocated to receive a 12- week course of treatment with quinapril (10, 20, or 40 mg) once daily or Captopril (25, 50, or 75 mg) twice daily. Seventeen patients in each group completed the study. The mean change in mean blood pressure for patients taking quinapril (mean dose 32 mg/24 h) was -5 mm Hg (P = .002), and for patients taking Captopril (mean dose 132 mg/24 h), -9 mm Hg (P = .002). The baseline urinary albumin excretion rate in both groups was (mean ± EEM) 57 ± 7 µg/min. Fifteen patients in the quinapril group and 12 patients in the Captopril group had baseline albumin excretion rates of more than 20 µg/min. Mean urinary albumin excretion decreased in patients treated with quinapril from 55 to 33 µg/min (mean decrease 22 µg/min, 95% confidence interval [CI], 1 to 43 µg/min; P = .031) and with Captopril from 59 to 41 µg/min (mean decrease 18 µg/min, 95% CI, 3 to 32 µg/min; P = .025). No significant modifications were observed in serum lipid concentrations, serum and urinary electrolytes, and magnesium or phosphorus metabolism. Mean urinary calcium excretion decreased in the quinapril-treated group (from 219 to 188 mg/24 h; P = .023) but not in the Captopril group (from 264 to 267 mg/24 h). The mean variations in calcium excretion were significantly different between patients treated with quinapril (31 mg/ 24 h) and those receiving Captopril (-3 mg/24 h; P = .018). This study demonstrated that antihypertensive therapy with either quinapril or Captopril significantly reduced urinary albumin excretion in nondiabetic patients with mild to moderate hypertension. The administration of quinapril elicited a calcium-sparing effect, the significance of which is unknown. Am J Hypertens 1994;7:46-51