Aldosterone in the blood

The reference concentration (norm) of aldosterone in the blood plasma of newborns is 1060-5480 pmol/l (38-200 ng/dl); in children under 6 months - 500-4450 pmol/l (18-160 ng/dl); in adults (when taking blood in the supine 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. It is the most potent mineralocorticoid, 30 times more active than deoxycorticosterone. 0.05-0.23 g of aldosterone is synthesized in the adrenal glands per day. The synthesis and release of aldosterone into the blood is regulated by angiotensin II. Aldosterone leads to an increase in the sodium content in the kidneys, which is accompanied by increased excretion 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 affects the excretion of sodium in the intestine and the distribution of electrolytes in the body.

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

Primary hyperaldosteronism (Conn's syndrome) is a rather rare disease, most often caused by an adenoma synthesizing 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 (with a combination of arterial 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 renin activity is sharply reduced (down to zero). Conn's syndrome is the only form of arterial hypertension in which the levels of renin and aldosterone in the blood are in inverse proportions (if such a pattern is detected, the diagnosis of primary hyperaldosteronism can be considered proven).

Secondary hyperaldosteronism is a consequence of disturbances in the regulation of the renin-angiotensin-aldosterone system. Unlike Cohn's syndrome, in this case renin activity and angiotensin concentration in the blood also increase. Secondary hyperaldosteronism usually accompanies diseases characterized by the formation of edema and Na ⁺ retention ( liver cirrhosis with ascites, nephrotic syndrome, heart failure ). Aldosterone secretion also increases when renin secretion increases due to impaired renal blood flow, for example, in renal artery stenosis. Sometimes renin is secreted by Williams tumor or tumors from juxtaglomerular cells (reninomas), which can also cause secondary hyperaldosteronism (characterized by very high renin activity in the blood).

Bartter syndrome is characterized by hyperreninemia against the background of hyperplasia of juxtaglomerular cells, hyperaldosteronemia, potassium deficiency, metabolic alkalosis, and vascular resistance to angiotensin. The syndrome is associated with a hereditary decrease in vascular sensitivity to the pressor effect of angiotensin II. Primary renal defect causing loss of potassium by the kidneys is also possible. Clinically, this disease is characterized by adynamia, polyuria, polydipsia, and headache.

The diseases in the pathogenesis of which secondary hyperaldosteronism plays an important role include periodic edema syndrome. This is a common disease that occurs in women aged 30-55 years and is rarely observed in men. The pathogenesis of periodic edema syndrome is due to a number of neurogenic, hemodynamic and hormonal disorders. Clinically, this syndrome is characterized by the development of edema, a decrease in urination to 300-600 ml per day, thirst, rapid weight gain, imbalance of sex hormones (low progesterone levels and hyperprolactinemia) and an increased level of aldosterone in the blood.

In pseudohyperaldosteronism, the increased aldosterone concentration is associated with a defect in mineralocorticoid receptors in tissues, which leads to activation of the renin-aldosterone system. Increased renin activity in the blood plasma indicates that hyperaldosteronism is secondary to hyperactivity of the renin-angiotensin system. In addition to the distal renal tubules, the defect can manifest itself in the salivary and sweat glands, as well as in the cells of the colon mucosa. In pseudohyperaldosteronism, against the background of a high concentration of aldosterone and renin activity in the blood plasma, hyponatremia (less than 110 mmol / l) and hyperkalemia are detected.

Hypoaldosteronism results in decreased sodium and chloride concentrations in blood plasma, hyperkalemia, and metabolic acidosis. Plasma aldosterone concentrations are sharply reduced, and renin activity is significantly increased. The ACTH aldosterone stimulation test is used to assess potential aldosterone reserves in the adrenal cortex. In severe aldosterone deficiency, especially in congenital defects of its synthesis, the test is negative, i.e. the blood aldosterone concentration remains low after ACTH administration.

When studying aldosterone in the blood, it is necessary to take into account that its release into the blood is subject to a daily rhythm, similar to the rhythm of cortisol release. The peak concentration of the hormone is noted in the morning hours, the lowest concentration - approximately at midnight. The concentration of aldosterone increases in the luteal phase of the ovulatory cycle and during pregnancy.

Liddle syndrome is a rare familial kidney disease that must be differentiated from hyperaldosteronism, as it is accompanied by arterial hypertension and hypokalemic metabolic alkalosis, but in most patients, renin activity and aldosterone concentrations in the blood are reduced.

Diseases and conditions that may alter plasma aldosterone activity

Aldosterone is reduced

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

Aldosterone is elevated

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

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