Hypoaldosterosnism

Hypoaldosteronism is the disorder caused by a lack of the hormone aldosterone, which is manufactured by the adrenal glands.

How is it produced?

Aldosterone is a hormone that basically performs its function in the kidney where it retains sodium and eliminates potassium, while increasing the circulating volume of fluid in the blood (hypervolemia).

The kidney, in the face of stimuli such as a small amount of blood or a decrease in sodium in the blood, releases renin, which acts on a protein in the blood released by the liver, angiotensinogen. Due to the action of renin on angiotensinogen, angiotensin I is produced, which, due to the effect of ACE (a protein found in the pulmonary arteries), produces angiotensin II. Angiotensin II stimulates the production of aldosterone by the adrenal glands.

The causes of an aldosterone deficiency are varied. Some involve alterations of the adrenal glands themselves, which can be produced by a hereditary disorder that prevents the synthesis of aldosterone, or acquired in patients chronically treated with heparin or derivatives. Others are due to causes external to the adrenal glands; in this case, the most frequent form is usually secondary to kidney disorders such as kidney failure and diabetic neuropathy that cause hyporeninemic hypoaldosteronism (with decreased renin levels); They can also be seen in cases of removal of an adenoma of the adrenal glands.

Symptoms

Most of the symptoms are due to the effect that aldosterone deficiency has on the regulation of sodium and potassium levels. In general, the manifestation common to all of them is the inability of the patient to produce aldosterone adequately in response to salt restriction.

As normal levels of aldosterone produce sodium retention and loss of potassium in the kidney, in hypoaldosteronism the opposite effect will occur, causing an increase in potassium levels. This increase in potassium is also accentuated when the sodium ingested in the diet is reduced due to salt restriction. Hyperkalemia manifests as muscle and cardiac abnormalities: tingling and squatting, muscle weakness and even paralysis, respiratory arrest, and cardiac arrhythmias that can become severe and lead to cardiac arrest.

Diagnosis

Diagnosis begins by detecting abnormalities in the blood. The common manifestation of all forms of hypoaldosteronism is the inability to adequately increase aldosterone secretion in response to salt restriction. Most patients have low potassium that does not have a clear justification and that is accentuated by reducing sodium intake in the diet. In severe cases there is loss of sodium through the urine with normal salt intake, while in the milder forms there is only excessive loss of sodium through the urine during salt restriction.

In the more complex analytical determinations we find low aldosterone levels and renin variables, depending on the causes.

Treatment

Treatment consists of correcting the aldosterone deficiency and potassium disturbances.

In hypoaldosteronism with low renin, if the excess of potassium is slight and asymptomatic, treatment is usually not necessary. In severe forms, fludrocortisone is given. In congenital forms, salt and fludrocortisone supplements are given.

If the hyperkalemia is severe, diuretics such as hydrochlorothiazide and furosemide (which eliminate potassium in the urine) are recommended.

Precautionary measures

There are no measures to prevent these disorders. It will be suspected when in an individual there is an increase in potassium in the blood with no apparent cause of it.