- Start Date
- Expiration Date
- CPT Codes
- Reference Test
- Transport Info
Centrifuge and immediately transfer serum to separate plastic tube
- Fasting Required?
- Patient Instructions
Discontinue diuretics, antihypertensive drugs, cyclic progestogens, estrogens, and licorice for at least 2 weeks (preferred 4 weeks) prior to sample collection
Patients should be on normal salt diet: 3.0 grams of sodium a day for 2-4 weeks prior to sampling
Supine specimen: Draw before patient arises in morning
Upright specimen: Draw from patient who has been upright at least 2 hours
- Reference Range
Supine: 29.4-161.5 pg/mL
Upright: 38.1-313.3 pg/mL
Quantitative Radioimmunoassay (RIA)
Diagnosis and differential diagnosis of hyperaldosteronism in combination with the determination of renin and functional tests. Detection of mineralocorticoid deficiency.
Aldosterone (11ß, 21-Dihydroxy-3, 20-dioxo-4-pregnen-18-al), produced in the adrenal cortex, is the most potent mineralocorticoid in humans. As with other steroid hormones, aldosterone is synthesized from cholesterol through a series of enzyme-mediated steps. Aldosterone and cortisol differ only in that a hydroxyl modification occurs at the 18, rather than 17, position on the steroid molecule.
The first and rate-limiting step in steroidogenesis, conversion of cholesterol to pregnenolone, is stimulated by adrenocorticotropic hormone (ACTH). However, ACTH has only a minimal effect on aldosterone production. Aldosterone secretion appears to be stimulated primarily through the renin-angiotensin system: decreased plasma volume and renal perfusion (or decreased plasma sodium chloride concentration) leads to increased renin secretion and activation of angiotensin, with angiotensin II then stimulating aldosterone syntheses. Increased plasma potassium concentrations are also a strong independent stimulus for Aldosterone production, although this effect is partially countered by potassium inhibition of renin release.
The major defined action of Aldosterone is stimulation of renal tubular sodium and chloride reabsorption, primarily at the level of the collecting ducts. Other important renal actions include enhancement of urinary potassium and hydrogen (acid) excretion. Similar effects on transmembrane sodium and hydrogen transport have been observed in other tissues, including lymphocytes, brain and arterial smooth muscle.
Plasma Aldosterone levels normally vary with body position (upright greater than supine) and salt intake. Overall, plasma Aldosterone levels show a circadian rhythm that is similar to but less marked than cortisol, with peak levels in the early morning. Age-related levels tend to decline from fetal through adult life. Aldosterone concentrations in urine and saliva have also been characterized.
Abnormally high plasma Aldosterone concentrations can occur as either primary (e.g. adenomas, glucocorticoid-responsive hyperaldosteronism, idiopathic) or secondary conditions. In primary hyperaldosteronism, renin levels are low, blood pressure is elevated and the potassium level is decreased. Secondary hyperaldosteronism occurs because of elevated renin secretion, and is observed in renovascular hypertension, renin-secreting tumors, intravascular volume depletion (dehydration), hyponatremia, and in Bartter's syndrome. High Aldosterone and renin levels are also observed in pseudohypoaldosteronism, a condition caused by end-organ unresponsiveness to aldosterone leading to clinical features of aldosterone deficiency.
Abnormally low aldosterone secretion occurs in a number of conditions including salt-wasting forms of congenital adrenal hyperplasia, isolated 18-hydroxylase (carboxymethyl oxidase type ii) deficiency, renin deficiency (e.g. nephropathy), and type 4 renal tubular acidosis. Low aldosterone concentrations in the presence of clinical features of hyperaldosteronism can be observed in 11-hydroxylase (P450c11) deficiency, 11ß-hydroxysteroid dehydrogenase deficiency, and after ingestion of materials containing mineralocorticoid-like substances (e.g. licorice, glycyrrhizic acid).