Aldosterone in the blood

The reference concentration (norm) of aldosterone in blood plasma in newborns is 1060-5480 pmol / l (38-200 ng / dL); in children up to 6 months - 500-4450 pmol / l (18-160 ng / dL); in adults (when taking blood in the lying position) - 100-400 pmol / l (4-15 ng / dL).

Mineralocorticoids - aldosterone and deoxycorticosterone - are formed in the adrenal cortex. Aldosterone is synthesized from cholesterol in the cells of the glomerular layer of the adrenal cortex. This is the most potent mineralocorticoid, its activity is 30 times greater than deoxycorticosterone. For a day, 0.05-0.23 g of aldosterone is synthesized in the adrenal glands. Synthesis and release of aldosterone into the blood regulates angiotensin II. Aldosterone leads to an increase in the sodium content in the kidneys, which is accompanied by an increased release of K ⁺ and H ⁺. The concentration of sodium in the urine is low, if there is a lot of aldosterone in the bloodstream. In addition to the cells of the renal tubules, aldosterone has an effect on the excretion of sodium in the intestine and the distribution of electrolytes in the body.

Normal secretion of aldosterone depends on many factors, including the activity of the renin-angiotensin system, the potassium content, ACTH, magnesium and sodium in the blood.

Primary hyperaldosteronism (Cohn syndrome) is a rather rare disease, most often caused by an adenoma that synthesizes aldosterone. This disease is characterized by a high degree of sodium retention in the body (hypernatremia) and increased excretion of K ⁺ in the urine, which leads to hypokalemia (in the combination of hypertension and hypokalemia, the probability of primary hyperaldosteronism is 50%). The concentration of aldosterone in the blood plasma is usually increased (in 72% of patients), and the activity of renin is sharply reduced (down to zero). In Kon syndrome, the only form of arterial hypertension develops, in which the levels of renin and aldosterone in the blood are in inverse ratios (in the detection of this pattern, the diagnosis of primary hyperaldosteronism can be considered proven).

Secondary hyperaldosteronism is a consequence of disorders in the regulation of the renin-angiotensin-aldosterone system. In contrast to the syndrome of Cohn in this case, the activity of renin and the concentration of angiotensin in the blood also increase. Secondary hyperaldosteronism usually accompanies diseases characterized by edema formation and delayed Na ⁺ (cirrhosis of the liver with ascites, nephrotic syndrome, heart failure). The secretion of aldosterone also increases when, due to renal blood flow disorders, renin secretion is enhanced, for example, with renal artery stenosis. Sometimes renin secrete Williams tumor or tumors from juxtaglomerular cells (reninoma), which can also cause secondary hyperaldosteronism (a very high renin activity in the blood is characteristic).

Bartter's syndrome is characterized by hyper-reninemia in the background of hyperplasia of juxtaglomerular cells, hyperaldosteronemia, potassium deficiency, metabolic alkalosis, and angiotensin-resistant vessels. The syndrome is associated with a hereditary conditioned decrease in vascular sensitivity to the pressor effect of angiotensin II. It is not excluded and the primary renal defect causing loss of potassium by the kidneys. Clinically, this disease is characterized by adynamia, polyuria, polydipsia, headache.

To diseases in the pathogenesis of which an important role is played by secondary hyperaldosteronism, the syndrome of periodic edema also applies. It is a common disease that occurs in women aged 30-55 years and is rarely seen in men. The pathogenesis of the syndrome of periodic edema is due to a number of neurogenic, hemodynamic and hormonal disorders. Clinically, this syndrome is characterized by the development of edema, a decrease in urine output to 300-600 ml per day, thirst, rapid increase in body weight, imbalance of sex hormones (low levels of progesterone and hyperprolactinemia) and elevated levels of aldosterone in the blood.

In pseudohydaldosteronism, an increase in aldosterone concentration is associated with a defect in the mineralocorticoid receptors in the tissues, which leads to the activation of the renin-aldosterone system. The increased activity of renin in the blood plasma testifies to the secondary nature of hyperal-dosteronism in relation to the hyperactivity of the renin-angiotensin system. In addition to the distal tubules of the kidneys, the defect can be manifested in the salivary and sweat glands, as well as in the cells of the mucous membrane of the colon. In pseudohydaldosteronism against a background of high aldosterone concentration and renin activity in the blood plasma, hyponatremia (less than 110 mmol / l) and hyperkalemia are revealed.

Hypoaldosteronism leads to a decrease in the concentration of sodium and chlorides in the blood plasma, hyperkalemia and metabolic acidosis. The concentration of aldosterone in blood plasma is sharply reduced, and the activity of renin is significantly increased. To assess the potential reserves of aldosterone in the adrenal cortex, the stimulation test of aldosterone ACTH is used. With severe aldosterone deficiency, especially congenital defects in its synthesis, the test is negative, that is, the concentration of aldosterone in the blood after the introduction of ACTH remains low.

In the study of aldosterone in the blood, it must be taken into account that its release into the blood is subordinated to the daily rhythm, similar to the rhythm of cortisol release. The peak of the hormone concentration is noted in the morning hours, the lowest concentration is at about midnight. The concentration of aldosterone increases in the luteal phase of the ovulatory cycle and during pregnancy.

Liddle syndrome is a rare family kidney disease that needs to be differentiated with hyperaldosteronism, as it is accompanied by hypertension and hypokalemic metabolic alkalosis, but in most patients renin activity and aldosterone concentration in the blood are reduced.

Diseases and conditions in which the activity of aldosterone in the blood plasma can change

Aldosterone is lowered

• In the absence of arterial hypertension:
  • Addison's disease; hypoaldosteronism
• In the presence of arterial hypertension:
  • excessive secretion of deoxy corticosterone, corticosterone;
  • Turner syndrome (in 25% of cases);
  • diabetes;
  • acute alcohol intoxication
• Liddle Syndrome

Aldosterone elevated

• Cohn's syndrome (primary hyperaldosteronism):
  • aldosterome;
  • adrenal hyperplasia
• Secondary hyperaldosteronism:
  • heart failure
  • cirrhosis of the liver with ascites
  • nephrotic syndrome
  • Bartter's syndrome
  • postoperative period
  • in patients with hemovolemia caused by bleeding
  • malignant renal hypertension
  • kidney hemangiocypericotoma producing renin
  • transudates

[1], [2]