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).

Gold serum separator (SST) tube

Immediatley following collection, mix sample by gently inverting 5 times

1. Allow sample to clot for a minimum of 30 minutes
2. Spin

Gold serum separator (SST) tube

Red serum vial/tube, 5 mL

Lavender (EDTA), 4mL

Red:

1. Allow sample to clot
2. Spin
3. Transfer serum to a Transfer vial/tube with cap - 12mL (LabCorp) labelled as "serum"

Lavender:

1. Spin
2. Transfer plasma to a Transfer vial/tube with cap - 12mL (LabCorp) labelled as "EDTA plasma"

Transfer vial/tube with cap - 12mL (LabCorp)

Refrigerated (preferred) - 14 days

Ambient - 3 days

Frozen - 14 days

Freeze/thaw cycles - stable x 3

• Gross hemolysis
• Gross lipemia

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

0 - 2 years:      See report
2 - 9 years:      5.0−80.0 ng/dL
10 - 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. 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. Aldosterone promotes active sodium transport and excretion of potassium.

Hypokalemia increases and hyperkalemia decreases renin release. 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.

Primary hyperaldosteronism, also referred to as Conn syndrome, is caused by the overproduction of aldosterone by one or both of the adrenal glands. 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. 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. The condition can be asymptomatic, although muscle weakness can occur if potassium levels are very low. A number of studies have suggested that high-normal aldosterone levels predict development of high blood pressure in normotensive subjects6 and that increased aldosterone action contributes to hypertension, cardiovascular fibrosis, and cardiac hypertrophy.