Aldosterone
The aldosterone test measures serum concentration of the adrenal mineralocorticoid governing sodium retention and blood pressure. It is interpreted with simultaneously measured renin to calculate the aldosterone-to-renin ratio, the screening test for primary aldosteronism in resistant hypertension and hypokalaemia, and to distinguish primary from secondary aldosteronism and diagnose…
1
Biomarkers
Blood (serum)
Sample
3–5 business days
Turnaround
No
Fasting
What is the Aldosterone test?
The Aldosterone test measures the serum concentration of the principal mineralocorticoid hormone, which governs sodium retention, potassium excretion, and blood pressure. It is ordered almost exclusively to investigate suspected disorders of the renin-angiotensin-aldosterone axis, most commonly primary aldosteronism in patients with resistant hypertension, hypokalaemia, or an incidental adrenal mass. Aldosterone is rarely ordered alone; it forms one half of the aldosterone-to-renin ratio, the first-line screening test for autonomous aldosterone excess. Because both hormones are profoundly influenced by posture, sodium intake, and interfering medications, collection conditions must be standardised and interpreted by practitioners familiar with the nuances of these assays. The ratio and absolute aldosterone then guide decisions about confirmatory suppression testing — oral sodium loading, saline infusion, or fludrocortisone suppression — to prove or exclude primary aldosteronism before cross-sectional adrenal imaging and, in confirmed cases, adrenal vein sampling.
What does the Aldosterone test measure?
Aldosterone is a mineralocorticoid synthesised in the zona glomerulosa of the adrenal cortex under the control of the renin-angiotensin system, serum potassium, and to a lesser degree ACTH. It binds to mineralocorticoid receptors in the distal nephron to promote sodium reabsorption and potassium and hydrogen secretion, thereby regulating extracellular volume, blood pressure, and electrolyte balance. Aldosterone secretion is exquisitely sensitive to posture and dietary sodium — upright posture and sodium restriction both stimulate renin release and drive aldosterone higher, whereas supine rest and sodium loading suppress it.
Aldosterone measurement is central to diagnosing disorders of the renin-angiotensin-aldosterone axis. Autonomous overproduction (primary aldosteronism) is the most common curable cause of hypertension and must be distinguished from appropriate secondary aldosteronism driven by renal or renovascular disease. Aldosterone is never interpreted in isolation — the aldosterone-to-renin ratio (ARR) is the screening test, followed by confirmatory suppression studies. Low aldosterone with low renin suggests hyporeninaemic hypoaldosteronism (type 4 renal tubular acidosis), while low aldosterone with high renin points to primary adrenal insufficiency or aldosterone synthase defects.
Why is the Aldosterone test ordered?
- Screening for primary aldosteronism in patients with sustained hypertension and spontaneous or diuretic-induced hypokalaemia
- Evaluation of resistant hypertension (blood pressure uncontrolled on three drugs including a diuretic) in which primary aldosteronism prevalence is high
- Work-up of hypertension in patients with an incidental adrenal adenoma discovered on cross-sectional imaging
- Investigation of unexplained hypokalaemia with inappropriate urinary potassium wasting
- Assessment of hyporeninaemic hypoaldosteronism (type 4 renal tubular acidosis) in patients with hyperkalaemia, low renin, and low aldosterone
- Evaluation of suspected primary adrenal insufficiency when paired with cortisol and renin to distinguish adrenal from secondary causes
- Follow-up after adrenalectomy or initiation of mineralocorticoid receptor antagonist therapy for primary aldosteronism
- Rare investigation of familial hyperaldosteronism syndromes or aldosterone synthase deficiency in selected paediatric or familial cases
Sample collection and turnaround
Sample type
Blood (serum)
Fasting required
No
Collection method
Venipuncture at patient service centre
Turnaround
3–5 business days
Collection notes
Phlebotomy required. Standardised collection conditions are critical: many protocols specify morning sampling (0800–1000 hours) after the patient has been upright (seated or ambulatory) for at least two hours, or alternatively after overnight supine rest if a supine protocol is used; the chosen posture must be documented and replicated for serial testing. Potassium should be repleted to above 4.0 mmol/L before the draw. Ideally, interfering antihypertensive drugs are withdrawn two to four weeks beforehand under specialist guidance, substituting non-interfering agents; if withdrawal is unsafe, results are interpreted with caution. Dietary sodium should be unrestricted or standardised (liberal intake) for screening; confirmatory suppression tests may specify high sodium loading. Record time of day, posture, medications, and recent sodium intake on the requisition.
Specimen requirements
Minimum 1 mL serum, separated promptly and frozen if not assayed within a few hours; aldosterone is relatively stable but freezing is preferred for batched or send-out testing. Note the performing laboratory and assay platform for serial comparability, as reference intervals and ARR cut-offs are method-specific.
What can affect Aldosterone results?
Upright posture for at least two hours activates the renin-angiotensin system and raises aldosterone by 50–100 per cent; standardised collection (morning, seated after rest or after ambulation) is essential for serial comparability.
High sodium intake and volume expansion suppress renin and aldosterone, while sodium restriction and hypovolaemia stimulate both; uncontrolled diet invalidates ratio interpretation, so some protocols specify sodium loading or liberal intake before screening.
Renin-angiotensin-system blockers raise renin and lower the ARR (false-negative); diuretics raise both renin and aldosterone but affect renin more, also lowering the ratio; beta-blockers suppress renin, raising the ratio; many centres require withdrawal of interfering drugs for two to four weeks before screening, substituting non-interfering agents such as verapamil or doxazosin.
Hypokalaemia directly suppresses aldosterone secretion even in primary aldosteronism, potentially masking the diagnosis; potassium must be repleted to above 4.0 mmol/L before testing to avoid false-negative results.
Oestrogen raises angiotensinogen and can modestly increase aldosterone; the luteal phase may show higher values, though the clinical significance for ARR screening is debated and routine cycle timing is not mandated by most guidelines.
What do Aldosterone results mean?
Elevated
Primary aldosteronism (unilateral adenoma, bilateral adrenal hyperplasia, rarely carcinoma or familial forms) when paired with suppressed or inappropriately normal renin, yielding a high ARR. Less commonly, secondary aldosteronism in response to high renin (renal artery stenosis, renin-secreting tumour, severe heart failure, cirrhosis with ascites, or diuretic use) — here aldosterone is elevated but appropriate. The ARR distinguishes the two: high in primary, normal or low in secondary aldosteronism.
Normal
A normal aldosterone in the face of suppressed renin may still represent early or mild primary aldosteronism if the ARR is elevated; conversely, normal aldosterone with high renin is appropriate secondary aldosteronism or excluded primary aldosteronism. Interpretation hinges on the ratio and clinical context, never the absolute aldosterone alone.
Reduced
Hyporeninaemic hypoaldosteronism (diabetic nephropathy, chronic interstitial nephritis, NSAIDs, calcineurin inhibitors) when paired with low or low-normal renin; primary adrenal insufficiency (Addison disease, adrenal haemorrhage or infarction, congenital adrenal hyperplasia) when paired with high renin and low cortisol; aldosterone synthase deficiency (rare genetic defect); or suppression by exogenous mineralocorticoid, liquorice, or Liddle syndrome (though the latter is a renal tubular defect with low renin and aldosterone).
Note: Aldosterone must be interpreted with simultaneously measured renin (mass or activity) to calculate the ARR. Reference intervals and ARR cut-offs are assay-dependent and differ between laboratories and between renin activity and direct renin concentration units; a high ARR is a screening test, not a diagnosis — positive screens require confirmatory suppression testing. Interfering medications, posture, sodium intake, and potassium status profoundly affect results, so collection conditions must be recorded and interpreted by endocrinology or hypertension specialists.
Frequently asked questions
Aldosterone and renin are interpreted together to calculate the aldosterone-to-renin ratio, the screening test for primary aldosteronism. A high ratio (autonomous aldosterone with suppressed renin) suggests primary aldosteronism, while a normal or low ratio with high renin indicates appropriate secondary aldosteronism.
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.
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Published: October 7, 2026
Last reviewed: October 7, 2026
- 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)
- Young WF. Diagnosis and treatment of primary aldosteronism: practical clinical perspectives. J Intern Med. (2019)
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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