Aldosterone, LC/MS

Serum or plasma

1.2 mL

1 mL (Note: This volume does not allow for repeat testing.)

Red-top tube, gel-barrier tube, or lavender-top (EDTA) tube

In order to facilitate interpretation of test results, the patient should be taken off medications for at least three weeks prior to sample collection. Dietary sodium levels during the period prior to testing can affect aldosterone levels. Reference intervals are based on the clinician's verification that the patient has been on a normal sodium diet.

Since patient posture prior to collection affects aldosterone levels, it is recommended that the patient be ambulatory for at least 30 minutes before blood collection. If inpatients are physically able, they should be asked to ambulate for 30 minutes before blood is drawn for aldosterone. Reference intervals are provided for patients who have ambulated for at least 30 minutes prior to collection (standing patients).

Evaluate patients with hypertension and possible hyperaldosteronism

Decreased perfusion of the kidneys leads to increased aldosterone and renin.

This test was developed and its performance characteristics determined by Labcorp. It has not been cleared or approved by the Food and Drug Administration.

Liquid chromatography/tandem mass spectrometry (LC/MS-MS)

• Premature infant:

− 26 to 28 weeks, day 4: 5.0−635.0 ng/dL

− 31 to 35 weeks, day 4: 19.0−141.0 ng/dL

• Full-term infant:

− 3 days: 7.0−184.0 ng/dL

− 7 days: 5.0−175.0 ng/dL

− 1 to 11 months: 5.0−90.0 ng/dL

− 1 year: 7.0−54.0 ng/dL

− 2 to 9 years: 5.0−80.0 ng/dL

− 10 to 14 years: 4.0−48.0 ng/dL

− >14 years: 0.0−30.0 ng/dL

The renin-angiotensin system and potassium ion are the major regulators of aldosterone secretion, whereas ACTH and other POMC peptides, sodium ion, vasopressin, dopamine, ANP, α-adrenergic agents, serotonin, and somatostatin are minor modulators.^1,2 Renin cleaves angiotensinogen, which is synthesized by the liver to produce angiotensin I. Angiotensin I is, in turn, rapidly cleaved by angiotensin-converting enzyme (ACE) in the lung and other tissues to form, angiotensin II. Angiotensin II stimulates aldosterone secretion and vasoconstriction. Factors that decrease renal blood flow, such as hemorrhage, dehydration, salt restriction, upright posture, and renal artery narrowing, increase renin levels which, in turn, raise aldosterone levels. In contrast, factors that increase blood pressure, such as high salt intake, peripheral vasoconstrictors, and supine posture, decrease renin and aldosterone levels.³ Aldosterone promotes active sodium transport and excretion of potassium.

Hypokalemia increases and hyperkalemia decreases renin release.¹ Potassium also directly increases aldosterone secretion by the adrenal cortex and aldosterone then lowers serum potassium by stimulating its excretion by the kidney. High dietary potassium intake increases plasma aldosterone and enhances the aldosterone response to a subsequent potassium or angiotensin II infusion.³

Aldosterone deficiency conditions typically present with electrolyte abnormalities, including a variable degree of hyponatremia, hyperkalemia, and metabolic acidosis.^1,2,4 Congenital aldosterone deficiency is characterized by poor growth in childhood and minimal symptoms in adults. Infants typically suffer recurrent dehydration, salt wasting, and failure to thrive. These symptoms are present generally within the first three months of life. A modest uremia with a normal creatinine level reflects dehydration in the presence of intrinsically normal renal function. Plasma renin activity is invariably elevated.

Hypoaldosteronism can occur in any condition that causes destruction or dysfunction of the adrenal gland.^1,2,4 These conditions include primary adrenal insufficiency, congenital adrenal hypoplasia, isolated mineralocorticoid deficiency, acquired secondary aldosterone deficiency (hyporeninemic hypoaldosteronism), and acquired primary aldosterone deficiency. Hyporeninemic hypoaldosteronism is the most common form of isolated hypoaldosteronism and is caused by impaired renin release from the kidney. Congenital hypoaldosteronism caused by inherited enzymatic defects in aldosterone biosynthesis are rare. Corticosterone methyloxidase I (CMO I) deficiency is associated with elevated serum levels of corticosterone and low levels of 18-hydroxy-corticosterone and aldosterone. Corticosterone methyloxidase II (CMO II) deficiency produces high levels of 18-hydroxy-corticosterone, the immediate precursor of aldosterone. Acquired primary hypoaldosteronism can be caused by the administration of heparin. Also, persistently hypotensive, critically ill patients with sepsis, pneumonia, peritonitis, cholangitis, and liver failure can have inappropriately low plasma aldosterone concentrations in relation to elevated plasma renin activity.

Primary hyperaldosteronism, also referred to as Conn syndrome, is caused by the overproduction of aldosterone by one or both of the adrenal glands.^1,2 Historically, primary aldosteronism was considered to be an uncommon cause of hypertension; however, recent studies indicate that 10% to 15% of cases are associated with primary hyperaldosteronism.⁵ Secondary hyperaldosteronism is relatively common and can occur as the result of any condition that decreases blood flow to the kidneys (ie, renal artery stenosis), decreases blood pressure, or lowers plasma sodium levels. Secondary hyperaldosteronism may also be seen with cirrhosis, congestive heart failure. and toxemia of pregnancy.

Hyperaldosteronism increases reabsorption of sodium and loss of potassium by the kidneys, resulting in an electrolyte imbalance.^1,6 The condition can be asymptomatic, although muscle weakness can occur if potassium levels are very low. Several studies have suggested that high-normal aldosterone levels predict development of high blood pressure in normotensive subjects⁷ and that increased aldosterone action contributes to hypertension, cardiovascular fibrosis, and cardiac hypertrophy.^6-8