Secondary Hyperaldosteronism

What is secondary hyperaldosteronism?

Secondary hyperaldosteronism is an increase in the level of aldosterone, which develops as a result of activation of the renin-angiotensin-aldosterone system in various disorders of water-electrolyte metabolism, due to an increase in renin production.

Causes of Secondary Hyperaldosteronism

Secondary hyper aldosteronism occurs when:

  • heart failure
  • cirrhosis of the liver,
  • chronic nephritis (contributes to the development of edema).

The rate of aldosterone production in patients with secondary aldosteronism is often higher than during primary aldosteronism.

Secondary aldosteronism is usually combined with the rapid development of hypertension or occurs due to edematous conditions. In pregnancy, secondary aldosteronism is a normal physiological response to an estrogen-induced increase in the level of renin substrate in the blood and plasma renin activity.

In hypertensive states, secondary aldosteronism develops as a result of primary hyperproduction of renin (primary reninism) or on the basis of such hyperproduction, which is caused by a decrease in renal blood flow or renal perfusion pressure. Secondary renin hypersecretion is a consequence of narrowing of one or both major renal arteries caused by an atherosclerotic plaque or fibro muscular hyperplasia.

Renin hyperproduction with both kidneys occurs in severe arteriolar nephrosclerosis (malignant hypertension) or due to narrowing of the deep renal vessels (phase of acceleration of hypertension).

Pathogenesis during Secondary Hyperaldosteronism

Secondary aldosteronism is characterized by hypokalemic alkalosis, increased plasma renin activity and increased aldosterone levels.

Secondary aldosteronism with hypertension also occurs with rare renin-producing tumors. In these patients, there is a vascular hypertension, the primary violation is the secretion of renin by a tumor originating from juxtaglomerular cells. The diagnosis is made on the basis of the absence of changes in the renal vessels or during the radiological detection of a volumetric process in the kidney and a unilateral increase in the activity of renin in the blood from the renal vein.

Secondary aldosteronism accompanies many types of edema. The increase in aldosterone secretion under conditions of intravascular sodium and water movement into the intercellular spaces further contributes to fluid retention and sodium in the body, due to which edemas develop. Lowering oncotic pressure leads to the movement of intravascular sodium and water into the intercellular spaces. Due to hypovolemia and a decrease in sodium concentration in the bloodstream, baroreceptors are irritated (in the left ventricle, aorta, right atrium, and hollow veins). In a reflex way through the hypothalamic region, they cause a compensatory increase in aldosterone secretion. Other factors causing secondary hyperaldosteronism also contribute to the development of edema: an increase in the activity of the renin-angiotensin system and a reduction in the inactivation of aldosterone in the liver. An increase in the content of antidiuretic 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, a decrease in its inactivation in the liver. Increased edema also contributes to the increase in capillary permeability as a result of increased activity of the enzyme hyaluronidase. In patients with edema on the basis of liver cirrhosis or nephrotic syndrome, an increase in the rate of aldosterone secretion is observed.

In diseases involving edema (heart failure, nephrotic syndrome, liver cirrhosis, etc.), the pathogenesis of secondary hyperaldosteronism is mainly due to hypovolemia, decreased oncotic pressure and hyponatremia.

In case of congestive heart failure, the degree of increase in aldosterone secretion depends on the severity of circulatory decompensation, the cause is arterial hypovolemia or a decrease in blood pressure.

Reception of diuretics enhances secondary aldesteronism, hypokalemia and alkalosis appear to the fore.

Secondary hyper aldosteronism sometimes occurs in the absence of edema or hypertension (Barter syndrome). This syndrome is characterized by signs of severe hyperaldosteronism (hypokalemic alkalosis) with moderate or increased renin activity, but normal arterial pressure and the absence of edema. Biopsy of the kidney reveals hyperplasia of the juxtaglomerular complex. Pathogenetic role is played by impaired ability of the kidneys to retain sodium or chloride. The loss of sodium through the kidneys stimulates the secretion of renin and then the production of aldosterone.

The role of factors involved in the pathogenesis of secondary hyperaldosteronism depends largely on the pathogenesis of the underlying disease. In hypertension and renal hypertension, renal-ischemic factor plays a major role. The resulting renal ischemia leads to an increase in the activity of its juxtaglomerular apparatus with enhanced renin production and increased formation of angiotensin II. The latter stimulates the glomerular zone of the adrenal cortex with enhanced secretion of aldosterone.

Symptoms of Secondary Hyperaldosteronism

Secondary hyperaldosteronism has no specific clinical manifestations, since it is a compensatory phenomenon in many diseases and conditions, and electrolyte changes characteristic of primary hyperaldosteronism never develop.

Diagnosis of Secondary Hyperaldosteronism

The diagnosis of hyper aldosteronism is based on the results of biochemical analyzes (increased excretion of aldosterone in the urine during normal elimination of 17-oxycorticosteroids, low plasma levels of potassium ions, increased excretion of potassium in the urine, alkalosis).

Treatment of Secondary Hyperaldosteronism

In case of secondary hyperaldosteronism, symptomatic therapy is aimed at increasing sodium excretion in the urine (veroshpiron, etc.), as well as treating the underlying disease that caused hyperaldosteronism.

In secondary hyper aldosteronism, the prognosis depends on the severity of the underlying disease and the success of its treatment.

Prevention of Secondary Hyperaldosteronism

Prevention of hyper aldosteronism consists in regular follow-up of patients with arterial hypertension, liver and kidney diseases, compliance with the doctor’s recommendations regarding the nature of the diet and diuretic and laxative drugs.