Secondary aldosteronism is a clinical syndrome caused by increased secretion of aldosterone by normal adrenal glands in response to changes in the electrolyte composition of the blood, and sometimes caused by insufficient inactivation of aldosterone in the liver.
Historical data. Increased excretion of aldosterone in the urine in a number of diseases was first reported in 1950-1955. Deming, Leucher, Axelrad and others.
Etiology. The cause of secondary aldosteronism can be diseases accompanied by severe renal ischemia (hypertonic disease, renal hypertension). Secondary aldosteronism can occur in heart failure, edematous forms of kidney disease (nephrotic syndrome, acute diffuse glomerulonephritis), liver disease (Botkin’s disease, chronic hepatitis, liver cirrhosis). Secondary aldosteronism occurs also in diseases accompanied by polyuria or natriuria (decompensated non-sugar and diabetes mellitus, nephritis with loss of sodium, etc.). The causes of secondary aldosteronism can be myocardial infarction, pneumonia, long-term therapy with diuretics, natriuretic properties, prolonged use of a diet, low-sodium chloride, etc.
Pathogenesis. The role of factors involved in the pathogenesis of secondary
aldosteronism is unequal and largely depends on the pathogenesis of the underlying disease. In hypertension and renal hypertension, renal-ischemic factor comes to the fore.
The resulting ischemia of the kidney leads to an increase in the activity of its juxtaglomerular apparatus with enhanced renin production and increased formation of angiotensin II. The latter stimulated the ^ -glossal zone of the adrenal cortex with an increased aldortra ^ ron secretion. In diseases accompanied by edema (heart failure, nephrotic syndrome, cirrhosis of the liver, etc.), the pathogenesis of secondary hyperalsonism is mainly due to hypovolemia, a decrease in oncotic pressure and hyponatremia.
Lowering oncotic pressure leads to the movement of intravascular sodium and water into the intercellular spaces. Due to hypovolemia and a decrease in the concentration of sodium in the bloodstream, baroreceptors are irritated (in the left ventricle, aorta, right atrium, and hollow veins). They reflex through the hypothalamic region cause a compensatory increase in aldosterone secretion. An increase in the secretion of aldosteroids in the context of the continued movement of intravascular sodium and water into the intercellular spaces further contributes to the retention of fluid and sodium in the body, and therefore edema develops.
The development of edema is also promoted by other factors that cause secondary aldosteronism: an increase in the activity of the renin – angiotensin system and a decrease in the inactivation of aldosterone in the liver. An increase in the level of anti-diuretic hormone in the blood leads to an increase in edema. On the one hand, this is due to an increase in the secretion of the hormone under the influence of aldosterone, and on the other hand
Goi – a decrease in its inactivation in the liver.
Increased edema also contributes to swelling.
capillary bridge as a result of increased activity of the enzyme hyaluronidase.
Pathological anatomy. Morphological and histological changes are due to the underlying disease.
Classification. Secondary aldosteronism is divided into forms with hypertensive syndrome, with edematous syndrome and forms without edema and hypertension.
Clinic. Clinic of secondary aldosteronism depends on the underlying disease. Most often secondary aldosteronism manifests itself as an edematous syndrome. Generalized edema, which develops for no apparent reason (without pathology of the heart, liver, check), is called idiopathic. In patients with idiopathic edema, along with normal arterial pressure, the absence of changes in the protein composition and the concentration of electrolytes in the blood, pronounced hyponatry and increased excretion of aldosterone in the urine are noted.
Forecast. The prognosis depends on the underlying disease.
Treatment. The treatment of the underlying disease and the elimination of factors contributing to increased aldosterone secretion are necessary. In secondary aldosteronism with edematous syndrome, along with ordinary diuretic drugs, aldosterone antagonis, spironolactone (aldactone, veroshpiron), is also used. To enhance the diuretic effect of spironolactone (aldactone), prednisone is used, which has natriuretic and diuretic effects, as well as capable of improving liver function and normalizing the protein composition of the blood.