Aldosterone (serum) | Laboratory research

Aldosterone Is a steroid hormone that is synthesized from cholesterol in the cells of the glomerular layer of the adrenal cortex. It is the main and most powerful mineralocorticoid. It is metabolized in the liver and kidneys, leading to increased reabsorption of sodium and chlorine in the renal tubules. As a result, sodium and chlorine retention is observed in the body, fluid excretion in the urine is reduced, and potassium excretion is increased in parallel. Aldosterone is involved in regulating electrolyte balance, maintaining blood volume, and maintaining blood pressure.

Normal aldosterone secretion depends on many factors - the action of the renin-angiotensin system, potassium content (stimulates hyperkalemia, and hypokalemia inhibits aldosterone production), ACTH (short-term increase in aldosterone secretion in physiological conditions, short-term increase in blood secretion).

Excess aldosterone causes hypokalemia, metabolic alkalosis, marked sodium retention, and increased urinary potassium excretion, which is clinically manifested in the form of arterial hypertension, muscle weakness, convulsions, and paresthesias and arrhythmias.

In primary hyperaldosteronism (Cone syndrome) there is an autonomic increase in aldosterone secretion, the most common cause of which is adenoma of the glomerular zone of the adrenal cortex (up to 62%).

Secondary hyperaldosteronism is associated with congestive heart failure, liver cirrhosis and ascites, certain kidney diseases, high-potassium and low-sodium diets, toxicosis in pregnant women, all cases of renal artery stenosis (2-3%).

Primary hyperaldosteronism is characterized by an increase in aldosterone levels, low plasma renin activity, for secondary hyperaldosteronism - an increase in aldosterone concentration, combined with high plasma renin activity.

Usually, hypoaldosteronism is accompanied by hyponatremia, hyperkalemia, decreased urinary potassium excretion and increased sodium excretion, metabolic acidosis, and hypotension. The most common cause of this condition is a decrease in renin due to kidney damage (hyporeninemic hypoaldosteronism), especially in diabetics.

Chronic adrenal insufficiency (Addison's disease), autoimmune pathology of the adrenal glands, amyloidosis are accompanied by a decrease in aldosterone levels and an increase in plasma renin.

Prior to testing for aldosterone, the patient should discontinue medications that act on the levels of this hormone.

When should we take an aldosterone test?

• Diagnosis of primary hyperaldosteronism caused by adrenal adenoma and adrenal hyperplasia;
• Arterial hypertension, including resistant forms;
• Orthostatic hypotension;
• Adrenal insufficiency.

How to prepare for the test?

In order to detect primary hyperaldosteronism, it is recommended:

1. Treatment with the drugs that affect the test should be stopped at least 4 weeks before the test: both potassium-sparing (spironolactone, amiloride, triamterene, elferonone) and potassium-sparing diuretics. As well as products derived from licorice root (licorice).
2. Normal intake of table salt in patients (approximately 3 g of sodium per day) is recommended.
3. If it is necessary to maintain control of blood pressure, it is advisable to take drugs with reduced impact on the test.
4. It is mandatory to specify the patient's posture when taking the sample. In the supine position it is advisable to do the test early in the morning. During orthostatic posture it is essential that the patient remain in this position for at least 30 minutes before receiving the sample.
5. It is advisable to know in advance the concentration of sodium and potassium in the blood and urine.
6. Taking radioactive isotopes 24 hours before should be avoided.

Research material

Venous blood

Possible interpretation of the results

Level increase:

• Cone syndrome (primary hyperaldosteronism);
• Aldosteroma;
• Adrenal hyperplasia.
• Secondary hyperaldosteronism:
• Heart failure;
• Cirrhosis of the liver with the formation of ascites;
• Nephrotic syndrome;
• Barter syndrome;
• Postoperative period in patients with bleeding caused by hypovolemia;
• Malignant hypertension of the kidney;
• Renal hemangioperitoma, which produces renin;
• Transudates;
• Periodic edema syndrome;
• Pseudo-hyperaldosteronism.

Level decrease:

• In the absence of hypertension:
• Addison's disease;
• Hypoaldosteronism.
• In the presence of hypertension:
• Excessive secretion of deoxycorticosterone, corticosterone;
• Turner syndrome (in 25% of cases);
• diabetes;
• Acute alcohol intoxication.
• Liddell Syndrome.
• Older age.