TABLE 6.

Hyperaldosteronism – screening and diagnosis

i) Plasma aldosterone and plasma renin activity (see ii below for conversion factors) should be measured under standardized conditions, including the collection of morning samples taken from patients in a sitting position after resting at least 15 min. Antihypertensive drugs may be continued, with the exception of aldosterone antagonists, angiotensin receptor blockers, beta-adrenergic antagonists and clonidine.
ii) Renin, aldosterone and ratio conversion factors:
A. To estimate:	B. From:	Multiply (B) by:
Plasma renin concentration (ng/mL)	Plasma renin activity (ng/mL/h)	0.206
Plasma renin activity (g/L/s)	Plasma renin activity (ng/mL/h)	0.278
Plasma aldosterone concentration (pmol/L)	Plasma aldosterone concentration (ng/dL)	28
iii) Definition of a positive screening test: plasma aldosterone to renin activity ratio greater than 550 pmol/L/ng/mL/h (or 140 pmol/L/ng/L when renin is measured as renin mass or concentration).
iv) Manoeuvres to demonstrate autonomous hypersecretion of aldosterone:
a) saline loading tests (2 L of normal saline over 4 h, with primary aldosteronism defined as failure to suppress plasma aldosterone to less than 280 pmol/L, or oral sodium 300 mmol/day for three days, with primary aldosteronism defined as failure to suppress plasma aldosterone to less than 240 pmol/L);
b) fludrocortisone suppression test (oral sodium loading plus oral fludrocortisone 0.25 mg/day for 2 days) positive for primary aldosteronism: plasma aldosterone level of 140 pmol/L or greater in upright and/or supine positions;
c) a plasma aldosterone to plasma renin activity ratio greater than 1400 pmol/L/ng/mL/h, with a plasma aldosterone level greater than 440 pmol/L; and
d) captopril suppression test (primary aldosteronism defined as failure to suppress plasma aldosterone level to less than 240 pmol/L 2 h after 25 mg of oral captopril).
v) Differentiating potential causes of primary aldosteronism:
a) For patients with established primary aldosteronism, attempts to differentiate potential causes should be made and may include localization with adrenal computed tomography scan (standard: 3 mm contiguous cuts) or magnetic resonance imaging (where available), or assessment of plasma aldosterone level before (supine) and after 2 h to 4 h of upright posture.
b) For patients with established primary aldosteronism and negative imaging studies, selective adrenal venous sampling should be considered, because it may be the only way to reliably differentiate unilateral from bilateral overproduction of aldosterone. Adrenal venous sampling should be conducted in centres with experience in performing this diagnostic technique.

Reproduced with permission of the Canadian Hypertension Education Program