Synonym/Acronym
N/A
Rationale
To assist in the evaluation of hypertension and diagnosis of primary hyperaldosteronism disorders such as Conn syndrome and Addison disease.
Patient Preparation
There are no fluid restrictions unless by medical direction. The required position, supine/lying down or upright/sitting up, must be maintained for 2 hr before specimen collection. The patient may be prescribed a normal-sodium diet (1 to 2 g of sodium per day) 2 to 4 wk before the test. Under medical direction, the patient should avoid diuretics, antihypertensive drugs and herbals, and cyclic progestogens and estrogens for 2 to 4 wk before the test. The patient should also be advised to avoid consuming any products derived from or that contain licorice root for 2 wk before the test. Protocols may vary among facilities.
Normal Findings
Method: Chemiluminescent Immunoassay.
| Age | Conventional Units | SI Units (Conventional Units × 0.0277) |
|---|
| Newborn | 5–102 ng/dL | 0.14–2.82 nmol/L | | 1–3 wks | 6–180 ng/dL | 0.17–5 nmol/L | | 1 mo–2 yr | 7–99 ng/dL | 0.19–2.7 nmol/L | | 3–14 yr | 4–30 ng/dL | 0.11–0.83 nmol/L | | 15 yr–adult | 31 ng/dL or less | 0.86 nmol/L or less | | Supine | 3–16 ng/dL | 0.08–0.44 nmol/L | | Upright (sitting for at least 2 hr) | 4–30 ng/dL | 0.11–0.83 nmol/L | | Older adult | Levels decline with age | |
These values reflect a normal sodium diet. Values for a low-sodium diet are three to five times higher. Blood levels fluctuate with dehydration and fluid overload. |
Study type: Blood collected in a gold-, red-, red/gray-, green- [heparin], or lavender-top [EDTA] tube; related body system: Endocrine and Urinary systems.
Aldosterone is a mineralocorticoid secreted by the zona glomerulosa of the adrenal cortex and is regulated by the renin-angiotensin system. Changes in renal blood flow trigger or suppress release of renin from the glomeruli. The presence of circulating renin stimulates the liver to produce angiotensin I. Angiotensin I is converted by the lungs and kidneys into angiotensin II, a potent trigger for the release of aldosterone. Aldosterone and the renin-angiotensin system work together to regulate sodium and potassium levels. Aldosterone acts to increase sodium reabsorption in the renal tubules. This results in excretion of potassium, increased water retention, increased blood volume, and increased blood pressure.
A variety of factors influence serum aldosterone levels, including sodium intake, certain medications, and activity. Secretion of aldosterone is also affected by adrenocorticotropic hormone (ACTH), a pituitary hormone that primarily stimulates secretion of glucocorticoids and minimally affects secretion of mineralocorticosteroids. Patients with serum K+ less than 3.6 mEq/L and 24-hr urine K+ greater than 40 mEq/L fit the general criteria to test for aldosteronism. Plasma renin activity and aldosterone levels should be measured simultaneously to differentiate primary and secondary aldosteronism (see study titled “Renin”). Renin activity, measured in ng/mL/hr, is low in primary aldosteronism and high in secondary aldosteronism.
CT can miss adrenal adenomas; therefore, measurement of the aldosterone/renin ratio (ARR) from an adrenal venous sampling technique is the gold standard to distinguish between adrenal cortex adenoma (a benign unilateral hyperplasia that can be surgically corrected) and bilateral hyperplasia (treated medically with aldosterone antagonists). Specimens are obtained by an experienced health-care provider (HCP), customarily a radiologist, using an imaging-guided catheter inserted into the adrenal veins to collect blood for analysis. Specimen labels must include time of collection, patient position (upright or supine), and exact source of specimen (left versus right) in addition to the corresponding patient demographics and date. A normal ARR is less than 25.
Ratios greater than 20 obtained after a screening test may indicate the need for further evaluation with a challenge study such as a sodium-loading protocol. A captopril protocol can be substituted for patients who may not tolerate the sodium-loading protocol. An ARR between 25 and 40 is suggestive of primary hyperaldosteronism, a condition most commonly identified in patients ages 30 to 50 years; some criteria require both an elevated ratio and an aldosterone level that exceeds 15 ng/dL. An ARR greater than 50 is significant. The ratio is markedly increased in both unilateral and bilateral hyperaldosteronism. Unilateral hyperplasia is associated with an increase in the ARR from samples obtained on the side of the tumor relative to the values measured from the other side; there is little difference between the ratios obtained from both sides in patients with bilateral hyperplasia.
Factors That May Alter the Results of the Study
- Drugs and other substances that may increase aldosterone levels include amiloride, angiotensin, angiotensin II, dobutamine, dopamine, endralazine, fenoldopam, hydralazine, hydrochlorothiazide, laxatives (misuse), metoclopramide, nifedipine, opiates, potassium, and spironolactone.
- Drugs and other substances that may decrease aldosterone levels include atenolol, captopril, carvedilol, cilazapril, enalapril, indomethacin, lisinopril, NSAIDs, perindopril, and ranitidine. Prolonged heparin therapy also decreases aldosterone levels.
- Diet can significantly affect results. A low-sodium diet can increase serum aldosterone, whereas a high-sodium diet can decrease levels. Decreased serum sodium and elevated serum potassium increase aldosterone secretion. Elevated serum sodium and decreased serum potassium suppress aldosterone secretion.
- Upright body posture, stress, strenuous exercise, and late pregnancy can lead to increased levels.
- Ingestion of large amounts of licorice can result in symptoms also associated with hyperaldosteronism; most candy contains very little real licorice. Licorice inhibits short-chain dehydrogenase/reductase enzymes. These enzymes normally prevent cortisol from binding to aldosterone receptor sites in the kidney. In the absence of these enzymes, cortisol acts on the kidney and triggers the same effects as aldosterone, which include increased potassium excretion, sodium retention, and water retention. Aldosterone levels are not affected by licorice ingestion, but the simultaneous measurements of electrolytes may provide misleading results.
Increased In
Increased With Decreased Renin Levels
Primary hyperaldosteronism (evidenced by overproduction related to abnormal adrenal gland function)
- Adenomas (Conn syndrome)
- Bilateral hyperplasia of the aldosterone-secreting zona glomerulosa cells
Increased With Increased Renin Levels
Secondary hyperaldosteronism (related to conditions that increase renin levels, which then stimulate aldosterone secretion)
- Bartter syndrome(related to excessive loss of potassium by the kidneys, leading to release of renin and subsequent release of aldosterone)
- Chronic obstructive pulmonary disease
- Cirrhosis with ascites formation (related to diluted concentration of sodium by increased blood volume)
- Diuretic misuse (related to direct stimulation of aldosterone secretion)
- Heart failure (related to diluted concentration of sodium by increased blood volume)
- Hypovolemia(secondary to hemorrhage and transudation)
- Laxative misuse(related to direct stimulation of aldosterone secretion)
- Nephrotic syndrome(related to excessive renal protein loss, development of decreased oncotic pressure, fluid retention, and diluted concentration of sodium)
- Starvation (after 10 days) (related to diluted concentration of sodium by development of edema)
- Thermal stress (related to direct stimulation of aldosterone secretion)
- Toxemia of pregnancy (related to diluted concentration of sodium by increased blood volume evidenced by edema; placental corticotropin-releasing hormone stimulates production of maternal adrenal hormones that can also contribute to edema)
Decreased In
Without Hypertension
With Hypertension
- Acute alcohol intoxication (related to toxic effects of alcohol on adrenal gland function and therefore secretion of aldosterone)
- Diabetes (related to impaired conversion of prorenin to renin by damaged kidneys, resulting in decreased aldosterone)
- Excess secretion of deoxycorticosterone (related to suppression of ACTH production by cortisol, which in turn affects aldosterone secretion)
- Turner syndrome (25% of cases) (related to congenital adrenal hyperplasia resulting in underproduction of aldosterone and overproduction of androgens)
Potential Nursing Problems: Assessment & Nursing Diagnosis
| Problems | Signs and Symptoms |
|---|
| Electrolytes: (related to increased aldosterone, evidenced by hypokalemia, hypernautremia secondary to hyperaldosteronism) | Hypokalemia—weakness, fatigue, drowsiness, muscle cramps, cognitive changes; Hypernatremia—confusion, agitation, muscle twitching, seizures, tremors | | Fluid volume: (excess—related to increased aldosterone, evidenced by hypervolemia associated with excessive production of aldosterone, hypernatremia, and excessive water reabsorption) | Shortness of breath, peripheral edema, increased work of breathing, weight gain, hypertension, hypertension, tachycardia, jugular vein distention, crackles in lungs, abnormal blood gas results, hypokalemia, hypernatremia | | Mobility: (related to decreased aldosterone, evidenced by dizziness, fatigue, weakness secondary to adrenal insufficiency, and decreased cortisol levels) | Weakness, wasting, pain in muscles and joints, decreased endurance, activity intolerance, difficult purposeful movement, reluctance to attempt to engage in activity | | Tissue perfusion: (inadequate—related to decreased aldosterone, evidenced by inadequate fluid volume, decreased cortisol levels) | Hypotension, dizziness, cool extremities, pallor, capillary refill greater than 3 sec in fingers and toes, weak pedal pulses, altered level of consciousness, altered sensation, urinary output less than 30 mL/hr |
|
Before the Study: Planning and Implementation
Teaching the Patient What to Expect
- Discuss how this test evaluates dehydration and can assist in identification of the causes of muscle weakness or high blood pressure.
- Explain that a blood sample is needed for the test.
- Explain that multiple specimens may be required.
- As appropriate, explain that blood specimens may be collected directly from the left and right adrenal veins by a radiologist via catheterization and takes approximately 1 hr.
- Explain that the required positions, supine/lying down or upright/sitting up, must be maintained for 2 hr before specimen collection.
- Specimens collected on an inpatient should be collected early in the morning before rising.
Potential Nursing Actions
Electrolytes
- Monitor and trend potassium and sodium levels.
- Administer medications as ordered to treat electrolyte excess or deficit.
- Discuss reportable symptoms of electrolyte alterations with the patient.
Fluid Volume
- Facilitate management of fluid volume excess.
- Trend laboratory values that reflect alterations in fluid status related to fluid volume excess: K+, BUN, Ca, Cr, Hgb and Hct, and Na+.
- Manage underlying cause of fluid alteration.
- Collaborate with HCP to adjust oral and IV fluids to provide optimal hydration status.
Tissue Perfusion
- Facilitate management of inadequate tissue perfusion.
- Monitor blood pressure for orthostatic changes related to inadequate tissue perfusion.
- Monitor and trend Hgb and Hct.
- Use pulse oximetry to monitor oxygen saturation titrating ordered oxygen delivery to meet patient needs.
- Administer ordered parenteral fluids.
- Place in a high Fowlers position to improve gas exchange.
- Administer ordered medications based on causal factors (antiplatelets, anticoagulants, peripheral vasodilators, antihypertensives, inotropes).
After the Study: Implementation & Evaluation Potential Nursing Actions
Avoiding Complications
- Monitor blood pressure; assess for dizziness; assess extremities for skin temperature, color, warmth; assess capillary refill; assess pedal pulses; monitor for numbness, tingling, hyperesthesia, hypoesthesia; monitor for deep venous thrombosis; carefully use heat and cold on affected areas; use foot cradle to keep pressure off of affected body parts.
- Administer ordered aldosterone.
Treatment Considerations
- Collaborate with HCP to administer ordered electrolyte replacement therapy and trend associated laboratory results.
- Monitor for ongoing symptoms of electrolyte disturbance (hypokalemia, hypernatremia).
- Monitor and trend serum cortisol level and results of ACTH stimulation test.
Safety Considerations
- Discuss how muscle atrophy can make safe mobility a concern.
- Provide assistance with mobility and teach the safe use of assistive devices; allow sufficient time to perform tasks without being rushed.
- Monitor weakness and fatigue pacing activities to meet patient abilities.
Nutritional Considerations
- Discuss how aldosterone levels are involved in the regulation of body fluid volume.
- Discuss the importance of proper water balance.
- Advise that some water-softening systems replace minerals (e.g., calcium, magnesium, iron) with sodium; if a low-sodium diet is prescribed, consideration should be given to the type of water softener being used in the home.
- Discuss how aldosterone levels affect sodium levels possibly requiring adjustments to dietary sodium.
- Explain to patients with low sodium levels that the major source of dietary sodium is table salt.
- Discuss how foods such as milk and other dairy products are good sources of dietary sodium.
- Explain that consumption of processed foods is a good source of dietary sodium; baking mixes (pancakes, muffins), sauces (barbecue), butter, canned soups and sauces, dry soup mixes, frozen or microwave meals, ketchup, pickles, and snack foods (potato chips, pretzels).
- Advise those following a low-sodium diet to avoid beverages containing sodium such as colas, ginger ale, lemon-lime sodas, root beer, and sports drinks.
- Request consultation from the HCP or a registered dietitian before considering the use of salt substitutes.
- Discuss how some over-the-counter medications, including antacids, laxatives, analgesics, sedatives, and antitussives, contain significant amounts of sodium.
- Emphasize the importance of reading all food, beverage, and medicine labels.
- Explain that potassium is present in all plant and animal cells, making dietary replacement simple.
- Recommend a diet with foods rich in potassium such as fruits, vegetables, and meats (e.g., artichokes, avocados, bananas, beef, cantaloupe, chicken, dried fruits, fish, kiwi, mango, milk, dried beans, nuts, oranges, peaches, pears, pomegranate, potatoes, prunes, pumpkin, seafood, spinach, sunflower seeds, Swiss chard, tomatoes, and winter squash).
Clinical Judgement
- Consider how to support electrolyte homeostasis by recommending foods that are most likely to appeal to the individual patient.
Follow-Up and Desired Outcomes
- Demonstrates self-care techniques as taught by occupational therapy.
- Acknowledges the detrimental effect of emotional stress on adrenal insufficiency and agrees to stress management therapy.
- Accepts the necessity of using assistive devices to maintain independence and prevent injury.
- Performs a self evaluation to identify limitations with the ability to engage in activities of daily living (e.g., difficulty fastening clothing, performing personal hygiene; inability to maintain appropriate appearance).
- Agrees to notify the HCP of any signs and symptoms of dehydration or fluid overload related to elevated aldosterone levels or compromised sodium regulatory mechanisms.
- Understands the importance of adhering to the medication regime with the understanding that sudden cessation can be dangerous.