title: Prevalence of primary hyperaldosteronism assessed by aldosterone/renin ratio and spironolactone testing.
abstract: Recent studies have suggested that primary hyperaldosteronism may be present in more than 10% of patients with hypertension. We aimed to estimate the prevalence in unselected patients in primary care, and investigate the influence of current drug treatment upon the aldosterone/renin ratio (ARR) and its prediction of blood pressure response to spironolactone. We measured blood pressure, plasma electrolytes, renin activity and aldosterone in 846 patients with hypertension. Spironolactone 50 mg was prescribed for one month to patients with blood pressure > or = 130/85 mmHg and ARR > or = 400. The primary outcome measure was to discover the proportion of patients with plasma aldosterone > or = 400 pmol/l and ARR > or = 800 and either an adrenal adenoma on computed tomography scan or a systolic blood pressure response to spironolactone > or = 20 mmHg. Only one patient had an adenoma, and only 16 (1.8%) had both a plasma aldosterone > or = 400 pmol/l and ARR > or = 800. By contrast, 119 patients (14.1%) had an elevated ARR but normal plasma aldosterone. In 69 patients out of the 119 who received spironolactone, blood pressure fell by 26/11 mmHg. These patients were normokalaemic but had uncontrolled hypertension despite multiple drugs. The response to spironolactone was best predicted by a low plasma renin, < or = 0.5 pmol/ml/h (<10 mU/l), despite treatment with an ACE inhibitor. We concluded that adrenal adenomas are an uncommon cause of hypertension. In the absence of hypokalaemia, a low plasma renin is a sufficient and simple way of detecting spironolactone-responders among patients with resistant hypertension. Only patients with both hypokalaemia and low plasma renin, measured while the patient is off beta blockade, require measurement of aldosterone. A plasma aldosterone >400 pmol/l together with renin activity < or = 0.5 pmol/ml/h should trigger further investigations for an adrenal adenoma.
authors.affiliation: Clinical Pharmacology Unit, Addenbrooke's Hospital, Cambridge.
authors.forename: Sue
authors.initials: S
authors.lastname: Hood
authors.forename: John
authors.initials: J
authors.lastname: Cannon
authors.forename: Roger
authors.initials: R
authors.lastname: Foo
authors.forename: Morris
authors.initials: M
authors.lastname: Brown
mesh_terms: D000236:Adenoma / Q000150:complications; D000310:Adrenal Gland Neoplasms / Q000150:complications; D000368:Aged; D000450:Aldosterone / Q000097:blood*; D001794:Blood Pressure / Q000187:drug effects; D005260:Female; D006801:Humans; D006929:Hyperaldosteronism / Q000097:blood / Q000175:diagnosis / Q000453:epidemiology*; D006973:Hypertension / Q000209:etiology; D008297:Male; D008875:Middle Aged; D000451:Mineralocorticoid Receptor Antagonists / Q000494:pharmacology; D012083:Renin / Q000097:blood*; D013148:Spironolactone / Q000494:pharmacology
chemical_list: D000451:Mineralocorticoid Receptor Antagonists; D013148:Spironolactone; D000450:Aldosterone; D012083:Renin