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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.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.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.Prevalence of low-renin status in therapy resistance. Blood pressure and hormonal responses to specific treatment. Numbers of adrenocortical adenomas and primary aldosteronism.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 ≤ 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.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.