Aldosterone

Aldosterone is a hormone formed in the glomerular zone of the adrenal cortex, whose function is to maintain water–salt balance in the body. The hormone is part of the renin-angiotensin-aldosterone system (RAAS).

The principle of operation of the RAAS: in humans, for some reason, the volume of circulating blood, blood pressure or sodium concentration (necessary for water retention in the body) in blood vessels decreases - this may be blood loss or kidney disease, in which a large amount of fluid and trace elements are lost. The kidneys detect such changes in the water-salt balance and produce the hormone renin. Renin activates a substance previously found in the blood in an inactive form, angiotensin. Angiotensin narrows blood vessels (to raise blood pressure) and stimulates the adrenal glands to produce aldosterone. Under the influence of aldosterone, the kidneys stop excreting sodium and chlorine in the urine (instead of potassium). Sodium retains water to increase the volume of circulating blood. The level of potassium in the body also affects the production of aldosterone: an increase in the amount of potassium (hyperkalemia) increases the synthesis of aldosterone, a decrease in potassium (hypokalemia) reduces it.

There are a number of diseases in which an inadequately high aldosterone content is observed (hyperaldosteronism). Such diseases manifest themselves as follows:

Clinically:

• High blood pressure;
• Muscle weakness and fatigue, a feeling of "goosebumps" on the skin;
• Convulsions;
• Swellings;
• Cardiac arrhythmia;

Laboratory:

• Increased aldosterone concentration;
• Increased sodium in the blood;
• Decreased potassium in the blood, increased urine;
• Blood alkalinization (metabolic alkalosis).

There are three types of hyperaldosteronism: primary, secondary, and pseudo-hyperaldosteronism. In the primary case, the essence of the disease lies in the autonomous, independent hyperproduction of aldosterone. An example is Cohn's disease, in which a tumor forms in the kidneys that produces large amounts of this hormone. If the blood shows increase in aldosterone and decrease in renin, the diagnosis of Cohn's disease can be considered proven.

Secondary hyperaldosteronism is a consequence of a malfunction in the work of the RAAS (see above). The pathology is caused by excessive production of renin, which directly increases the concentration of aldosterone. The cause may be a Williams tumor (juxtaglomerular apparatus) or stenosis (narrowing) of the renal artery, leading to activation of the RAAS.

Pseudohyperaldosteronism - the increase in aldosterone levels is due to a defect in the receptors for aldosterone. The normal level of the hormone becomes unable to perform its function, as a result of which its production increases.