Aldosterone Unit Converter
Aldosterone Unit Converter
Convert plasma aldosterone between ng/dL, pg/mL and pmol/L, with the posture, sodium intake and drug-preparation rules that determine whether the result can be trusted.
Aldosterone converter
Mass ⇄ molarPlasma aldosterone 22 ng/dL, upright sample
Formula and conversion factor
ng/dL = pmol/L ÷ 27.7439
- 27.7439
- derived from the molecular weight of aldosterone, 360.45 Da
- pg/mL
- ng/dL × 10
- posture
- state on the request form whether the sample was drawn upright (after at least two hours out of bed) or supine — the two are not comparable
Worked example
Plasma aldosterone 22 ng/dL, upright sample
22 × 27.7439 = 610 pmol/L
= 220 pg/mL
Drug preparation before aldosterone and renin testing
| Drug class | Action | Washout |
|---|---|---|
| Mineralocorticoid receptor antagonists (spironolactone, eplerenone) | Stop | 4 – 6 weeks |
| Amiloride | Stop | 4 – 6 weeks |
| Beta-blockers, ACE inhibitors, ARBs, diuretics, NSAIDs, dihydropyridine calcium channel blockers | Stop or replace | 2 – 4 weeks where feasible |
| Verapamil (slow-release), doxazosin, hydralazine | Safe substitutes — continue blood pressure control during washout | — |
Why sampling conditions decide the result
Aldosterone secretion is posture-dependent: an upright, ambulant sample typically reads roughly twice a supine one, because standing activates the renin-angiotensin system. It is also suppressed by a high sodium intake and stimulated by a low one, so the sampling conditions have to be standardised — and stated on the request — before the number can be compared against a reference interval or used in a ratio.
The main practical obstacle is drug preparation. Mineralocorticoid receptor antagonists — spironolactone and eplerenone — and amiloride act directly on the pathway being tested and must be stopped for 4 to 6 weeks before sampling. Beta-blockers, ACE inhibitors, angiotensin receptor blockers, diuretics, NSAIDs and dihydropyridine calcium channel blockers all interfere with renin or aldosterone in ways that can push a result in either direction, and are ideally replaced during the washout period with agents that interfere far less: verapamil slow-release, doxazosin or hydralazine.
Hypokalaemia is the other confounder worth correcting first. Potassium is a direct secretagogue for aldosterone, so hypokalaemia suppresses secretion and can produce a falsely low or falsely normal aldosterone in a patient who genuinely has primary aldosteronism. Correcting potassium before testing, rather than testing around it, avoids a result that has to be repeated.
Frequently asked questions
How do I convert aldosterone from ng/dL to pmol/L?
Multiply by 27.7. An aldosterone of 22 ng/dL is 610 pmol/L. Divide by 27.7 to go the other way.
Why does posture affect aldosterone?
Standing activates the renin-angiotensin system, so an upright sample typically reads about twice a supine one. State which posture was used, since the two are not directly comparable.
Which drugs must be stopped before aldosterone testing?
Spironolactone, eplerenone and amiloride for 4 to 6 weeks, since they act directly on the pathway. Beta-blockers, ACE inhibitors, ARBs, diuretics, NSAIDs and dihydropyridine calcium channel blockers also interfere and are usually replaced with verapamil, doxazosin or hydralazine during washout.
Why does hypokalaemia matter before testing aldosterone?
Potassium directly stimulates aldosterone secretion, so hypokalaemia suppresses it and can produce a falsely low or normal result even in genuine primary aldosteronism. Correct potassium before, not instead of, testing.
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References
- Funder JW et al. The management of primary aldosteronism: case detection, diagnosis, and treatment. Endocrine Society clinical practice guideline. J Clin Endocrinol Metab. 2016;101(5):1889–916.
- Young WF Jr. Primary aldosteronism: renaissance of a syndrome. Clin Endocrinol. 2007;66(5):607–18.