Aldosterone normal, high and low values

What is aldosterone

L'aldosterone it's a hormone steroid produced at the level of the adrenal gland, the adrenal, from cholesterol. It is the main hormone produced in the first part of the serving cortical of the adrenal gland, called glomerular area.

What aldosterone is used for: metabolism and functions

Unlike most of the adrenal gland cortical tissue, it produces cortisol and which is controlled upstream by the axis hypothalamus-pituitary through the secretion of respectively CRH and of ACTH, aldosterone is synthesized on the basis of other secretory stimuli:

1) activation of the SRAA (acronym for Renin - Angiotensin - Aldosterone system), an effective blood pressure controller which, in case of low pressure or reduced renal perfusion, is stimulated to the cascade production of a series of factors, the last of which is aldosterone;

2) the increase in the concentration of potassium in the blood, which is "read" by specialized cells present inside the kidneys, which ultimately induce a greater synthesis of aldosterone;

3) a dense network of chemical modulators and hormones, but of secondary interest.

This hormone, belonging to the family of the so-called "mineralocorticoid" hormones, of which it is the main exponent, is in charge of controlling the electrolyte metabolism in the kidney, in particular in the collecting duct, allowing to conserve sodium, chlorine and water in facing an increase in potassium elimination. From a functional point of view, its antagonist is ANF (or Atrial Natriuretic Factor), produced by the distension of the muscle cells of the heart, which has functions exactly opposite to those of aldosterone.

Aldosterone and kidney-adrenal metabolism

SRAA or Renin Angiotensin Aldosterone system, the metabolic mechanism that, in the presence of low blood pressure, renal vasoconstriction, or hyperkalaemia, activates the production of aldosterone at the adrenal level.

Normal values of aldosterone

Normal aldosterone values are affected in particular by the position of the body at the time of blood sampling: there are substantial differences between a blood sampling from a patient lying on the couch (defined in medical jargon as "clinostatic position") and a sampling from a patient standing ("orthostatic position"). The reference values of aldosteronemia blood for both sexes are:

1) aldosterone in supine position: between 1.9 and 25.7 ng / dL;

2) aldosterone in standing position: between 2.4 and 40.3 ng / dL.

It is then possible to measure the production of aldosterone on the basis of the urinary excretion of this hormone in 24 hours. Urinary aldosterone levels should be evaluated after adequate sodium intake within 4 days prior to urine collection. The physiological excretion range of this hormone is between 2-16 pg / 24 h

High aldosterone

When aldosterone values exceed levels above the normal range (greater than 25.7 ng / dL in supine position and 40.3 ng / dL in standing position), a situation of overproduction of the hormone is entered. hyperaldosteronism. Knowing the location of the greatest production of aldosterone, we can differentiate the pathology into primary or secondary: in endocrinology, it is used "primary" to indicate an alteration present within the apparatus that produces the hormone in question (in our case therefore aautonomous hyper-production of aldosterone by the adrenal gland), while the term is used instead "secondary" to indicate the alteration of a physiological or metabolic pathway even at a distance from the site of hormone synthesis (in this case, an activation of the renin-angiotensin-aldosterone system, the ultimate result of which is an overproduction of aldosterone).

 Primary or primary hyperaldosteronism

Primary aldosteronism, also called Conn syndrome, is a disease in which the presence of elevated aldosterone levels derives from an internal adrenal problem. In this situation, the organ that normally produces the hormone in physiological quantities is instead synthesizing larger quantities autonomously and completely disconnected from the control mechanisms normally present in a healthy individual.

Conn syndrome is divided into two categories, type I and type II, based on the ability or inability of dexamethasone to suppress the condition of hyperaldosteronism resulting from the disease.

Causes of primary hyperladosteronism

The main causes of this condition can be:

  1. the presence of a adenoma, or a benign tumor with high cell proliferation in a precise and well-defined area of the adrenal cortex and therefore, at the same time, with high hormonal synthesis. This option is to be discarded in children as it is very rare in this age group;
  2. the presence of a malignant tumor of the adrenal cortex, usually a carcinoma;
  3. the presence of a hyperplasia of the same cells, ie a greater synthetic functionality of a group of cells scattered within the adrenal tissue. Statistically, currenal hyperplasia it is more typical of older men, who will suffer from a condition that affects both adrenal glands;
  4. congenital diseases due to genetic alterations of enzymes involved in the degradation of circulating aldosterone, leading to an accumulation of the hormone in the circulation. Much more frequent situations in infants and infancy, but overall much rarer than in previous cases.

Symptoms of primary aldosteronism

THE symptoms of high aldosterone depend on the state of electrochemical imbalance that the excess of aldosterone brings with it: due to the increased renal reabsorption of sodium and water, combined with an excessive excretion of potassium, the most frequent symptoms of this condition are the presence of paresthesias, tetany and transient paralysis, especially in the limbs. Others symptoms of hyperaldosteronism are the presence of tiredness and increased fatigue, high blood pressure and increased stress, weight gain and headache. From a clinical-laboratory point of view, in these patients it is possible to note the onset of high sodium or hypernatremia, low potassium or plasma hypokalaemia or hypokalaemia and increase in plasma volume.

Treatment of primary aldosteronism

There therapy it is based on a thorough knowledge of the underlying cause. In the case of a tumor, the therapy is of type surgical, whose invasiveness will depend on the benignity or malignancy of the lesion: the surgeon can opt for resections of the only diseased tissue by way laparoscopic, in order to preserve as much as possible the healthy part of the adrenal gland, with complete removal of the adrenal gland. In the case of cellular hyperplasia, a first therapy can be of a medical type through the constant intake of potassium-sparing diuretics, such as eplerenone, with greater specificity for the problem, and spironolactone; if this is not enough, the endocrinologist may decide to surgically remove both adrenal glands to avoid continued hormonal overproduction.

Secondary aldosteronism

As previously stated, thesecondary aldosteronism it is not a condition that directly affects the adrenal gland, but the mechanism for stimulating the production of the hormone. The main proponent of this stimulation is the Renin-Angiotensin-Aldosterone System (SRAA), a mechanism consisting of several hormonal factors able to regulate mainly the volume of circulating blood and arterial pressure in the kidney.

Causes of secondary aldosteronism

In this condition, the SRAA appears to be hyperactive due to a reduction in renal blood flow due to:

  1. edema conditions, such as cirrhosis liver with ascites, lo heart failure congestive type and the nephrotic syndrome, characterized by vasoconstriction of the renal arteries;
  2. a narrowing - stenosis - ofrenal artery. Among the main causes of this reduction in vascular caliber, we find atherosclerotic processes, the presence of a tumor of some cells specialized in the control of the ARS (called juxtaglomerular cells) inside the kidney, tumors external to the vessel and which lead to a compression of the same from the outside etc.

Symptoms of secondary aldosteronism

Symptomatically, there are many similarities with primary hyperaldosteronism: weakness, tiredness and increased fatigue, tingling mainly in the limbs, tetany, hypertension, peripheral edema.

Therapy of secondary aldosteronism

From a therapeutic point of view, as already seen with primary hyperaldosteronism, it is very important to know the triggering cause of this condition, in order to proceed with targeted remedies, of a medical or surgical type. For the treatment of high blood pressure, doctors generally recommend taking a particular category of potassium-sparing diuretics, including eplerenone, which effectively counteract the circulating aldosterone.

Low Aldosterone

On the other hand, when the values of aldosterone are lower than the minimum normal levels, we are faced with a diametrically opposite condition compared to those described above, called hypoaldosteronism.

Causes of hypoaldosteronism

What are the causes of low levels of aldosterone? This deficit can be a clinical form in its own right (isolated hypoaldosteronism), or it can be part of a condition of multi-level involvement of the adrenal cortex (called primary adrenal hypoadrenalism or Addison's disease)

In isolated hypoaldosteronism, the only hormone to be deficient is aldosterone, while all the other hormones produced in other areas of the adrenal cortex are found in physiological concentrations. The possible triggering causes can be divided into two categories:

  1. hyporeninemic hypoaldosteronism, in which the presence of low renin will determine a reduction in the stimulus to the secretion of aldosterone (through the SRAA). Among the possible causes, we find renal tubular acidosis associated with diabetic nephropathy, chronic therapy with heparin, NSAIDs, ketoconazole or cyclosporine; diseases of the nervous system; post-surgical excisional situation of aldosterone-secreting adrenal adenomas…;
  2. primary aldosterone deficiency. Much rarer condition than the previous one, which can be caused by deficiency of enzymes necessary for the synthesis of aldosterone, which give rise to the "familial" forms of hypoaldosteronism

On the other hand, in the case of primitive hypoadrenalism, all hormones are produced at the level of the adrenal cortex (among others, we recall cortisol) in deficient quantities compared to physiological values. Therefore, this condition will result from pathologies that indiscriminately affect all three levels of the adrenal gland cortex. In this case, however, we will find high renin values, as there is an attempt by the body to induce the synthesis of aldosterone by activating the SRAA to the maximum starting from an increase in renin plasma.

 Symptoms of hypoaldosteronism

What are the main ones symptoms of low aldosterone? The clinical picture of hypoaldosteronism is characterized by arterial hypotension, lipothymia or syncope, fatigue, increased fatigue, dizziness.

From a clinical-laboratory point of view, however, the most important signals that the disease provides us are the copious loss of sodium through the urine, which results in low plasma sodium, high potassium or hyperkalaemia or plasma hyperkalaemia and low levels of aldosterone. plasma.

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