Type of test Blood; urine (24-hour)

 Normal findings

Blood

 Supine: 3-10 ng/dL or 0.08-0.30 nmol/L (SI units)

 Upright:

 Female: 5-30 ng/dL or 0.14-0.80 nmol/L (SI units)

Male: 6-22 ng/dL or 0.17-0.61 nmol/L (SI units)

 Child/adolescent:

 Newborn: 5-60 ng/dL 1 week-1 year: 1-160 ng/dL; 1-3 years: 5-60 ng/dL;

 3-5 years: 5-80 ng/dL; 5-7 years: 5-50 ng/dL 7-11 years: 5-70 ng/dL

11-15 years: 5-50 ng/Dl

Urine (24-hour)

 2-26 mcg/24hr or 6-72 nmol/24hr (SI units)

Test explanation and related physiology

 This test is used to diagnose hyperaldosteronism. Production of aldosterone, a hormone produced by the adrenal cortex, is regulated primarily by the renin-angiotensin system. Secondarily, aldosterone is stimulated by ACTH, low serum sodium levels, and high serum potassium levels. Aldosterone in turn stimulates the renal tubules to absorb sodium (water follows) and to secrete potassium into the urine. In this way, aldosterone regulates serum sodium and potassium levels. Because water follows sodium transport, aldosterone also partially regulates water absorption (and plasma volume).

 Increased aldosterone levels are associated with primary aldosteronism, in which a tumor (usually an adenoma) of the adrenal cortex (Conn syndrome) or bilateral adrenal nodular hyperplasia causes increased production of aldosterone. Patients with primary aldosteronism characteristically have hypertension, weakness, polyuria, and hypokalemia. Increased aldosterone levels also occur with secondary aldosteronism caused by nonadrenal conditions. These include:

 • Renal vascular stenosis or occlusion

• Hyponatremia (from diuretic or laxative abuse) or low salt intake

 • Hypovolemia

• Pregnancy or use of estrogens

 • Malignant hypertension

 • Potassium loading

Edematous states (e.g., congestive heart failure, cirrhosis, nephrotic syndrome)

The aldosterone assay can be done on a 24-hour urine specimen or a plasma blood sample. The advantage of the 24-hour urine sample is that short-term fluctuations are eliminated. Plasma values are more convenient to sample, but they are affected by the short-term fluctuations.

Primary aldosteronism can be diagnosed by demonstrating very little to no rise in serum renin levels after an aldosterone stimulation test (using salt restriction as the stimulant). This is because aldosterone is already maximally secreted by the pathologic adrenal gland. Failure to suppress aldosterone with saline infusion (1.5-2 L of NSS infused between 8 pm and 10 am) or oral salt loading is the aldosterone suppression test. The stimulation and suppression tests confirm primary aldosteronism. Aldosterone can also be measured in blood obtained from adrenal venous sampling.

The aldosterone-to-renin ratio (ARR)—that is, the ratio of plasma aldosterone (expressed in ng/dL) to plasma renin activity (PRA, expressed in ng/mL/h)—is the most sensitive means of differentiating primary from secondary causes of hyperaldosteronism. It can be obtained under random conditions of sodium intake. The principle behind this test is that as aldosterone secretion rises, PRA should fall because of sodium retention. Persistent relatively high levels of aldosterone above 30 ng/dL per ng/mL/hour indicate primary aldosteronism. APR is used to screen patients with stage 2 or 3 hypertension, drug-resistant hypertension, or a strong family history of hypertension. One should also be aware that a Captopril Challenge Test  can also act as a confirmatory test for primary aldosteronism.

Interfering factors

 • Strenuous exercise and stress can stimulate adrenocortical secretions and increase aldosterone levels.

• Excessive licorice ingestion can cause decreased levels because it produces an aldosterone-like effect.

 • Values are influenced by posture, position, diet, diurnal variation, and pregnancy. • If the test is performed using radioimmunoassay, recently administered radioactive medications will affect test results.

* Drugs that may cause increased levels include diazoxide, diuretics, hydralazine, laxatives, nitroprusside, potassium, and spironolactone.

* Drugs that may cause decreased levels include angiotensin converting inhibitors (e.g., captopril), fludrocortisone, and propranolol, as well as licorice.

Procedure and patient care

 • See inside front cover for Routine Blood Testing.

 • Fasting: no

• Blood tube commonly used: serum separator

* Note that the patient is asked to be in the upright position (at least sitting) for at least 2 hours before the blood is drawn.

* Explain the procedure for collecting a 24-hour urine sample if urinary aldosterone is ordered. (See inside front cover for Routine Urine Testing.)

* Give the patient verbal and written instructions regarding dietary and medication restrictions.

* Instruct the patient to maintain a normal sodium diet (~3 g/day) for at least 2 weeks before the blood or urine collection.

* Have the patient ask the physician whether drugs that alter sodium, potassium, and fluid balance (e.g., diuretics, antihypertensives, steroids, oral contraceptives) should be withheld. Test results will be more accurate if these are suspended at least 2 weeks before either the blood or the urine test.

* Inform the patient that renin inhibitors (e.g., propranolol) should not be taken 1 week before the test.

* Tell the patient to avoid licorice for at least 2 weeks before the test because of its aldosterone-like effect.

During

 • Occasionally, for hospitalized patients, draw the sample with the patient in the supine position before he or she rises.

 • Obtain the specimen in the morning.

 • Note that sometimes a second specimen (upright sample) is collected 4 hours later, after the patient has been up and moving.

After

• Indicate on the laboratory slip if the patient was supine or standing during the venipuncture.

 • Handle the blood specimen gently. Rough handling may cause hemolysis and alter the test results.

• Transport the specimen on ice to the laboratory.

Abnormal findings

 Increased levels

 Primary aldosteronism

- Aldosterone-producing adrenal adenoma (Conn syndrome)

- Adrenal cortical nodular hyperplasia Bartter syndrome

Secondary aldosteronism

- Hyponatremia

- Hyperkalemia

- Diuretic ingestion resulting in hypovolemia and hyponatremia

- Laxative abuse

-Stress

-Malignant hypertension

- Generalized edema

- Renal arterial stenosis

-Pregnancy

- Oral contraceptives

- Hypovolemia or hemorrhage

- Cushing syndrome

Decreased levels

- Aldosterone deficiency

-Renin deficiency

-Steroid therapy

-Addison disease

-Patients on a high sodium diet

-Hypernatremia

-Hypokalemia

-Toxemia of pregnancy

- Antihypertensive therapy

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beta-hydroxybutyrate (Beta-hydroxybutyric acid)

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Biological Variation

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