What is the aldosterone-to-renin ratio and why is it important?

The aldosterone-to-renin ratio screens for primary aldosteronism by detecting autonomous aldosterone secretion with suppressed renin. A ratio above the laboratory threshold combined with an absolute aldosterone above 10–15 ng/dL is a positive screen and triggers confirmatory testing.

Does posture affect aldosterone results?

Yes. Aldosterone rises when upright due to volume shifts that activate renin. Standardise collection posture — either upright after at least 2 hours of walking or supine after overnight rest — and document it, as posture affects both aldosterone and renin and thus the ratio.

Should antihypertensive medications be stopped before testing?

Ideally yes, when medically safe. ACE inhibitors, angiotensin receptor blockers, diuretics, beta-blockers, and especially mineralocorticoid receptor antagonists alter aldosterone and renin and can mask or mimic primary aldosteronism. Guidelines recommend a 2–4 week wash-out, using non-interfering agents like verapamil or hydralazine to control blood pressure in the interim.

Why must potassium be corrected before the test?

Hypokalaemia suppresses aldosterone synthesis, so low potassium can produce a false-negative screen. Correct serum potassium to above 4.0 mmol/L before sampling to avoid missing primary aldosteronism.

What does a high aldosterone with high renin indicate?

High aldosterone with high renin suggests secondary aldosteronism — a physiological response to volume depletion, heart failure, cirrhosis, or renal artery stenosis. The aldosterone-to-renin ratio remains normal or low, distinguishing it from primary aldosteronism.

Can aldosterone be measured in chronic kidney disease?

Yes, but interpretation is more complex. Advanced renal impairment reduces renin clearance and can raise the aldosterone-to-renin ratio without true primary aldosteronism. Absolute aldosterone and clinical judgement guide decisions in this population.

What happens after a positive aldosterone screen?

A positive screen (elevated ratio and absolute aldosterone) is not a diagnosis. Confirmatory testing — saline infusion, oral sodium loading, fludrocortisone suppression, or captopril challenge — follows to document non-suppressible aldosterone, then adrenal imaging and, in many cases, adrenal vein sampling to distinguish unilateral from bilateral disease before deciding on surgery or medical therapy.

BML-ADR-023adrenal stressUSA

Aldosterone, LC/MS/MS

The Aldosterone, LC/MS/MS Test quantifies serum aldosterone using liquid chromatography–tandem mass spectrometry, the reference standard for steroid measurement. It is central to screening and diagnosing primary aldosteronism, the commonest secondary cause of hypertension, and to evaluating hypoaldosteronism.

Biomarkers

Blood (serum)

Sample

3–5 business days

Turnaround

Fasting

What is the Aldosterone test?

The Aldosterone, LC/MS/MS Test quantifies serum aldosterone using liquid chromatography–tandem mass spectrometry, the reference standard for steroid hormone measurement. It is ordered when practitioners suspect dysregulation of the renin–aldosterone axis: primary aldosteronism in hypertensive patients, secondary aldosteronism in conditions of volume depletion or renal artery stenosis, or hypoaldosteronism in salt-wasting syndromes and hyperkalaemia. Primary aldosteronism, once considered rare, is now recognised in 5–10 per cent of hypertensive populations and up to 20 per cent of those with resistant hypertension. Early detection matters because PA carries excess cardiovascular and renal morbidity beyond the degree of blood pressure elevation, and targeted treatment — surgery for unilateral adenoma or mineralocorticoid receptor antagonists for bilateral hyperplasia — improves outcomes. The aldosterone result is paired with renin (plasma renin activity or direct renin concentration) to calculate the aldosterone-to-renin ratio, the screening test of choice, and absolute aldosterone guides decisions on confirmatory suppression testing and subtype classification.

What does the Aldosterone test measure?

ALDO(Aldosterone)

Range: Upright (2 h standing): approximately 3–35 ng/dL; supine (morning): approximately 1–16 ng/dL. Position-dependent and assay-specific.Optimal: Optimal aldosterone is context-dependent: in a patient with hypertension and suppressed renin, a screening aldosterone above 10–15 ng/dL warrants confirmatory testing for PA; in hypotension and salt-wasting, undetectable or inappropriately low aldosterone suggests adrenal insufficiency or hypoaldosteronism.ng/dL / pmol/L

Aldosterone is the principal mineralocorticoid secreted by the zona glomerulosa of the adrenal cortex. Its synthesis is regulated by the renin–angiotensin system, serum potassium, and, to a lesser extent, adrenocorticotrophic hormone. Aldosterone acts on the distal convoluted tubule and collecting duct to promote sodium reabsorption and potassium excretion, thereby maintaining plasma volume, blood pressure, and electrolyte homoeostasis. Circulating concentrations vary with posture, sodium intake, and time of day, rising in the upright position due to volume shifts that activate renin.

Aldosterone measurement is central to diagnosing primary aldosteronism (PA), the commonest cause of secondary hypertension, and to distinguishing it from other causes of hypokalaemia and renin–angiotensin dysregulation. Liquid chromatography–tandem mass spectrometry quantifies aldosterone with greater specificity than immunoassay, reducing interference from structurally related steroids and improving diagnostic accuracy in borderline or treated patients. The test is interpreted with renin — the aldosterone-to-renin ratio screens for PA, and absolute aldosterone guides confirmatory testing.

Why is the Aldosterone test ordered?

Screening for primary aldosteronism in patients with hypertension and spontaneous or diuretic-induced hypokalaemia
Evaluation of resistant hypertension (blood pressure uncontrolled on three agents including a diuretic) or early-onset or severe hypertension
Investigation of hypertension with an incidentally discovered adrenal mass
Work-up of unexplained hyperkalaemia or salt-wasting, where low or inappropriately normal aldosterone suggests hypoaldosteronism or adrenal insufficiency
Assessment of secondary aldosteronism in states of volume depletion (heart failure, cirrhosis, nephrotic syndrome) or renovascular hypertension
Follow-up of patients treated for primary aldosteronism to document biochemical remission or adequate medical suppression
Paediatric investigation of severe hypertension or suspected congenital adrenal hyperplasia with mineralocorticoid pathway involvement

Sample collection and turnaround

Sample type

Blood (serum)

Fasting required

Collection method

Venipuncture at patient service centre

Turnaround

3–5 business days

Collection notes

Phlebotomy via Quest. Standardise posture: either upright after at least 2 hours of ambulation (mid-morning) or supine after overnight recumbency, documented on the request. Correct hypokalaemia to >4.0 mmol/L before sampling. Ideally withdraw interfering antihypertensive agents (ACE inhibitors, ARBs, diuretics, beta-blockers, spironolactone) for 2–4 weeks when medically safe, maintaining blood-pressure control with non-interfering agents (verapamil, hydralazine, alpha-blockers); document all medications. Note dietary sodium intake if known. Morning collection preferred.

Specimen requirements

Minimum 1.0 mL serum, separated and frozen within 30 minutes if not analysed immediately. Aldosterone is stable frozen at –20°C for months. Ship frozen on dry ice if referred.

What can affect Aldosterone results?

variablePosture and sodium intake

Aldosterone rises in the upright position and with sodium restriction; standardise collection posture (upright after 2 hours ambulation or supine after overnight recumbency) and document dietary sodium, as both alter both aldosterone and renin and affect the ratio.

variableAntihypertensive medications (ACE inhibitors, ARBs, diuretics, beta-blockers)

Renin–angiotensin–aldosterone axis drugs alter aldosterone and renin in opposing directions and can mask or mimic PA. Guidelines recommend withdrawing interfering agents for 2–4 weeks before screening when safe; mineralocorticoid receptor antagonists must be stopped, while verapamil, hydralazine, and alpha-blockers are preferred for blood-pressure control during the wash-out.

reducesHypokalaemia

Low serum potassium suppresses aldosterone synthesis, so uncorrected hypokalaemia can false-negative the screen. Correct potassium to above 4.0 mmol/L before testing.

variableChronic kidney disease

Advanced renal impairment reduces renin clearance and alters the aldosterone-to-renin ratio, complicating interpretation. Absolute aldosterone and clinical context guide decisions in this population.

elevatesPregnancy and oral contraceptives

Oestrogen increases hepatic synthesis of angiotensinogen, raising renin and secondary aldosterone; physiological elevations in pregnancy are normal, but the ratio may be uninterpretable for PA screening.

variableTime of day and stress

Aldosterone shows a diurnal rhythm (highest in the morning) and ACTH can acutely stimulate secretion. Standardise collection time and avoid sampling during acute illness or stress when possible.

What do Aldosterone results mean?

Elevated

Primary aldosteronism (unilateral adenoma or bilateral adrenal hyperplasia), glucocorticoid-remediable aldosteronism, or secondary aldosteronism (renal artery stenosis, renin-secreting tumour, heart failure, cirrhosis). An aldosterone-to-renin ratio above the laboratory threshold (commonly ≥20–30 when aldosterone is in ng/dL and renin in ng/mL/h, though cut-offs vary) with an absolute aldosterone ≥10–15 ng/dL is a positive screen; confirmatory suppression testing (saline infusion, oral sodium loading, fludrocortisone suppression, or captopril challenge) follows before imaging and subtype differentiation.

Normal

A normal aldosterone with a normal or elevated renin rules out primary aldosteronism in most cases. Interpretation depends on the clinical question: in a normotensive patient with normal potassium, normal aldosterone is reassuring; in resistant hypertension, re-evaluate if interfering medications were not withdrawn or if sampling conditions were suboptimal.

Reduced

Hypoaldosteronism (primary adrenal insufficiency, isolated aldosterone deficiency, congenital adrenal hyperplasia affecting the mineralocorticoid pathway) or suppression by exogenous mineralocorticoids. Low or inappropriately normal aldosterone in the setting of hyperkalaemia, salt-wasting, or hypotension warrants adrenal function testing and consideration of hyporeninism (type IV renal tubular acidosis).

Note: Aldosterone must be interpreted with renin and clinical context — the ratio is a screening tool, not a diagnosis. False-positive ratios occur with renin suppression from any cause (age, chronic kidney disease, low-renin essential hypertension), so absolute aldosterone must be elevated for the screen to be positive. Posture, medications, potassium, and sodium all influence results; standardisation is essential, and guidelines recommend withdrawing interfering drugs when feasible. Confirmatory testing is mandatory before proceeding to imaging and invasive subtyping.

Frequently asked questions

Liquid chromatography–tandem mass spectrometry is more specific than immunoassay, with less cross-reactivity from structurally similar steroids. This improves diagnostic accuracy, particularly in borderline cases and in patients on medications that may interfere with antibody-based methods.

How to access the Aldosterone test

The Aldosterone reference page is free and open to all practitioners. Create a free practitioner account to see pricing, save tests to your list, and generate requisition forms. Verification takes 1–2 business days.

Create Free Account

About this page

Published: October 7, 2026

Last reviewed: October 7, 2026

References:

Funder JW, et al. The management of primary aldosteronism: case detection, diagnosis, and treatment — an Endocrine Society clinical practice guideline. J Clin Endocrinol Metab. (2016)
Rossi GP, et al. Primary aldosteronism: JACC state-of-the-art review. J Am Coll Cardiol. (2019)
Stowasser M, et al. Laboratory investigation of primary aldosteronism. Clin Biochem Rev. (2010)
Nanba K, et al. Confirmatory testing for primary aldosteronism. Best Pract Res Clin Endocrinol Metab. (2020)

This content is for licensed healthcare practitioners only and does not constitute medical advice. Clinical decisions should be based on the full clinical picture and not on any single test result.

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