LONG-TERM THERAPY WITH AN ACE-INHIBITOR, TEMOCAPRIL, REDUCES MICROALBUMINURIA IN ESSENTIAL-HYPERTENSION

The present study was conducted to prospectively evaluate whether a ne w ACE inhibitor, temocapril, could modify urinary microalbumin excreti on rate (UAE) in a group of hypertensive outpatients who had no eviden ce of renal impairment. Sixty-three outpatients (32 men and 31 women; mean age, 59.9 +/- 1.5 yr) with essential hypertension entered the stu dy, all having been treated for at least 6 mo with dihydropyridine cal cium-channel blockers (CCBs: nitrendipine, nisoldipine, or amlodipine) . Their blood pressures (BPs) had been controlled to adequate levels w ith the CCBs. None had overt proteinuria (determined by Albustix) or a bnormal serum creatinine levels. After 3 mo of baseline observation un der the previous treatment, the subjects were randomly divided into tw o groups. In group A (n=31), the previously used CCBs were switched to temocapril, 2 to 4 mg once daily far 12 mo, and BP was controlled at a level equivalent to that during CCB treatment. In group B (n=32), th e subjects were maintained on their previous treatment for a further 1 2 mo. The effect of temocapril on BP appeared to be clinically similar to that of the previously used CCBs, but it significantly decreased U AE as compared with the previous therapy. In group A, UAE decreased si gnificantly (p < 0.01) from the baseline value of 38.9 +/- 5.1 mg/g cr eatinine (Cr) to 22.2 +/- 4.2 and 25.3 +/- 5.6 mg/g Cr at the 6th and 12th months of temocapril therapy, respectively. In contrast, in group B UAE was unchanged (baseline 39.8 +/- 6.6 mg/g Cr; 6 mo, 44.6 +/- 6. 8; 12 mo, 45.9 +/- 7.7). In group A, 17 of 31 patients (54.8%) had abn ormal UAE levels (greater than or equal to 29.5 mg/g Cr) during previo us therapy with CCBs, but 6 mo after switching to temocapril 25 of the se patients (80.6%) had normal UAE (<29.5 mg/g Cr). In group B, 15 of 32 patients (46.9%) had abnormal UAE levels during the observation per iod, and these abnormal UAE levels remained unchanged; 17 of the 32 pa tients (53.1%) had abnormal UAE levels after a further 6 mo of continu ed CCBs therapy. We conclude that long-term therapy with temocapril ma y provide renal protection by reducing UAE even in hypertensive patien ts with no evidence of renal impairment.