Custom Search


Monday 01 November 2004

Low-renin status in therapy-resistant hypertension: a clue to efficient treatment.

By: Eide IK, Torjesen PA, Drolsum A, Babovic A, Lilledahl NP.

J Hypertens 2004 Nov;22(11):2217-26

OBJECTIVE: Therapy resistance is an enduring problem in clinical hypertension. Our aims were to estimate: (1) the contribution of a low-renin status in therapy resistance; (2) whether such status could give a clue to more successful treatment; and (3) the contribution by adrenal cortical adenomas and by primary aldosteronism. SETTING: Patients were referred from general and internal medicine practices following written invitations and included consecutively. Participants were examined and followed-up on an outpatient basis. DESIGN AND INTERVENTIONS: Patients were divided according to renin status. Low-renin patients were treated with an aldosterone inhibitor in a prospective, randomized, placebo-controlled, double-blind, cross-over study. MAIN OUTCOME MEASURES: Prevalence of low-renin status in therapy resistance. Blood pressure and hormonal responses to specific treatment. Numbers of adrenocortical adenomas and primary aldosteronism. RESULTS: In 90 treatment-resistant hypertensive, 67% had plasma renin activity (PRA) below 0.5 nmol/l per hour. Of the 60 low-renin patients, 38 were studied on a fixed combination of amiloride and hydrochlorothiazide. Three weeks' treatment reduced blood pressure by 31/15 mmHg compared to placebo (P < or = 0.0001). Serum aldosterone and plasma renin activity increased substantially during active treatment. Through the subsequent 6-12 months of open treatment, seven patients (18%) showing an escape phenomenon had their high blood pressure effectively treated by extra amiloride. Of the 60 low-renin patients, eight had adrenal adenoma. CONCLUSION: A low-renin status characterized two-thirds of patients with treatment-resistant hypertension, who could be treated efficiently by aldosterone inhibition. Patients with an escape phenomenon (18%) could effectively be treated by increasing the aldosterone inhibitor. Low-renin hypertensives had high prevalence of adrenocortical adenomas and primary aldosteronism.

Use of this site is subject to the following terms of use