Alternative Names: Aldosterone, S, ALD
Includes: Aldosterone (1763-2)
Sample Type: Serum or Plasma
Preferred Container: Serum Separator Tube (SST)
Alternate Container: EDTA (Lavender Top) Tube or K2 EDTA (pink Top) Tube
Sample Volume: 1.0 mL
Minimum Volume: 0.5 mL (does not allow for repeat testing)
Handling Instructions: Sample should be collected mid-morning after the patient has been active for at least two hours. Collect specimen per tube manufacturer’s instructions. Centrifuge sample and separate serum from cells ASAP. Aliquot and freeze.
Transport Temperature: Frozen
Specimen Stability: Ambient: 8 hours, Refrigerated: 5 days; Frozen: 1 month
Testing Frequency: Monday- Saturday
Expected Turn Around Time: 2-3 days
CPT Codes: 82088
Note: Mineralocorticoids regulate salt homeostasis and fluid volume by binding to mineralocorticoid receptors in the colon, salivary glands, and nephron of the kidney to promote sodium reabsorption and potassium and hydrogen ion excretion. Synthesized in the adrenal cortex, aldosterone is the most potent naturally occurring mineralocorticoid. Its production and secretion are primarily regulated by the renin-angiotensin system in response to renal perfusion and sodium concentration in the distal convoluted tubule. This system ultimately leads to the production of angiotensin II which stimulates aldosterone synthesis. The synergy of aldosterone and other physiological downstream effects of angiotensin II work to regulate blood volume and pressure.
Evaluation of aldosterone is intended for the diagnosis and treatment of primary hyperaldosteronism, hypertension caused by primary hyperaldosteronism, hypoaldosteronism, edematous states and other conditions of electrolyte imbalance. Primary hyperaldosteronism is characterized by excessive secretion of aldosterone in the presence of low renin concentrations or activity levels. This disorder leads to cardiovascular damage, suppression of plasma renin, hypertension, sodium retention and potassium excretion that may lead to hypokalemia if prolonged and severe. The major causes of hyperaldosteronism are adrenal adenoma and adrenal hyperplasia. Secondary hyperaldosteronism is caused by inappropriate activation of the renin-angiotensin-aldosterone axis resulting in excessive production of aldosterone. This condition may be found in renovascular disease, salt depletion, potassium loading, cardiac failure with ascites, pregnancy, and Bartter syndrome. Hypoaldosteronism is a rare condition where low concentrations of aldosterone are found in the presence of high concentrations of plasma renin, often due to adrenal failure.