Primary hyperaldosteronism: diagnosis, treatment, causes, symptoms, signs. Secondary hyperaldosteronism Primary hyperaldosteronism symptoms

Secondary hyperaldosteronism is a clinical syndrome caused by an increase in the level of aldosterone in the blood in response to activation. At the same time, the excess concentration of aldosterone is associated with the influence of pathological factors of extra-adrenal origin. Moreover, it is not inferior to that in primary hyperaldosteronism and is combined with an increase in the level of renin in the blood plasma.

The reasons

The causes of secondary hyperaldosteronism differ significantly from the causes of the primary, they include:

• damage to the renal parenchyma (with, of various origins);
• pathological process in the renal vessels (vascular anomalies, atherosclerosis, fibromuscular hyperplasia, tumor compression);
• hyperplasia of the juxtaglomerular apparatus in the kidneys ();
• liver disease;
• a tumor of the kidneys or other localization that produces renin;
• taking medications (oral contraceptives,);
• pregnancy.

Bartter's syndrome is a normotensive variant of hyperaldosteronism. It is a hereditary disorder characterized by hypokalemia and increased renin secretion with angiotensin II resistance and subsequent compensatory stimulation of the renin-angiotensin system.

Development mechanisms

In most cases, the mechanism of increasing the level of aldosterone in this pathology is based on a decrease in pressure in the afferent arterioles of the renal glomeruli. The consequence of this process is a decrease in renal blood flow and filtration pressure in the renal vessels. To maintain it at a sufficient level, the renin-angiotensin system is activated, which triggers a whole cascade of biochemical reactions. This increases the production of renin by the juxtaglomerular apparatus of the kidney. Renin has a stimulating effect on angiotensinogen, which is synthesized in the liver. This is how angiotensin 1 is formed, which transforms into a powerful pressor factor - angiotensin 2 under the action of a special enzyme (ACE). It is angiotensin 2 that increases blood pressure, the tone of the afferent arteriole and stimulates excess aldosterone synthesis, which in turn:

• retains sodium in the body, increasing its reabsorption in the kidneys;
• increases the volume of circulating blood;
• removes potassium.

In severe congestive heart failure, abnormal secretion of aldosterone is triggered by hypovolemia and low blood pressure. At the same time, there is a direct dependence of the degree of increase in the concentration of aldosterone in the blood on the severity of circulatory decompensation. The use of diuretics aggravates the course of secondary hyperaldosteronism by reducing the amount of blood circulating in the blood vessels.

Symptoms

The clinical picture of secondary hyperaldosteronism is determined by the disease that caused the increase in aldosterone in the body, and directly by the effects of the latter.

Patients are diagnosed, often resistant to treatment. In this regard, they are often disturbed by dizziness. The situation is aggravated by the fact that with this pathology in the blood there is a large amount of angiotensin 2, which has an independent vasopressor effect.

In addition, aldosterone has a negative effect on the heart, causing hypertrophy of the heart muscle (mainly the left ventricle) and pressure overload, so these individuals may experience discomfort in the heart area.

Often, signs of hypokalemia come to the fore:

• muscle weakness;
• paresthesia;
• convulsions;

With Bartter's syndrome, pathological symptoms appear from childhood. These include:

• delayed growth and development;
• myopathic syndrome;
• dehydration;
• violation of intestinal motility, etc.

Diagnostics

In the process of diagnosing secondary hyperaldosteronism, it is important to determine not only the very fact of an increased concentration of aldosterone in the blood, but also to identify the cause of the disease. This takes into account:

• patient complaints;
• history of his life and illness;
• data of examination and objective examination;
• results of laboratory and instrumental research.

To assess the condition of the kidneys and renal vessels, various instrumental diagnostic methods are used:

• ultrasound procedure;
• CT scan;

From laboratory tests it is important:

• determination of the concentration of aldosterone, renin, angiotensin 2;
• (liver, kidney tests, electrolytes);
• functional tests.

Among the latter, a test with ACE inhibitors or fludrocortisone can be used (leads to a decrease in the concentration of aldosterone).

It should be noted that tests designed to confirm the autonomous secretion of aldosterone are negative in secondary hyperaldosteronism.

The diagnosis of "Bartter's syndrome" is based on the identification of hyperplasia of the juxtaglomerular apparatus and the conclusion of a histological examination.

Treatment

The tactics of managing patients with secondary hyperaldosteronism is primarily determined by the underlying disease. If the cause of the high concentration of aldosterone is a renin-producing tumor, then it is removed. In other cases, treatment is conservative.

Such patients are prescribed lifelong drug therapy:

• aldosterone antagonists (spironolactone, eplerenone);
• ACE inhibitors (enalapril, ramipril);
• angiotensin II receptor blockers (losartan, valsartan, telmisartan);
• calcium antagonists (amlodipine).

It should be noted that with long-term use of drugs, which include spironolactone, its antiandrogenic effect is manifested. In males, sexual desire decreases, develops, ovarian dysfunction appears in women, and manifestations of premenstrual syndrome intensify.

Which doctor to contact

With secondary hyperaldosteronism, treatment by an endocrinologist is necessary. Additionally, the patient is observed by a nephrologist, a consultation with a cardiologist, ophthalmologist, neurologist, oncologist, vascular surgeon may be scheduled.

- a pathological condition caused by increased production of aldosterone - the main mineralocorticoid hormone of the adrenal cortex. With primary hyperaldosteronism, arterial hypertension, headaches, cardialgia and cardiac arrhythmia, blurred vision, muscle weakness, paresthesia, convulsions are observed. With secondary hyperaldosteronism, peripheral edema, chronic renal failure, changes in the fundus develop. Diagnosis of various types of hyperaldosteronism includes a biochemical analysis of blood and urine, functional stress tests, ultrasound, scintigraphy, MRI, selective venography, a study of the state of the heart, liver, kidneys and renal arteries. Treatment of hyperaldosteronism in aldosteroma, adrenal cancer, kidney reninoma is surgical, in other forms it is medication.

ICD-10

E26

General information

Hyperaldosteronism includes a whole complex of syndromes that are different in pathogenesis, but similar in clinical signs, occurring with excessive secretion of aldosterone. Hyperaldosteronism can be primary (due to the pathology of the adrenal glands themselves) and secondary (due to renin hypersecretion in other diseases). Primary hyperaldosteronism is diagnosed in 1-2% of patients with symptomatic arterial hypertension. In endocrinology, 60-70% of patients with primary hyperaldosteronism are women aged 30-50; described a few cases of detection of hyperaldosteronism among children.

Causes of hyperaldosteronism

Depending on the etiological factor, there are several forms of primary hyperaldosteronism, of which 60-70% of cases are Conn's syndrome, the cause of which is aldosteroma - an aldosterone-producing adenoma of the adrenal cortex. The presence of bilateral diffuse-nodular hyperplasia of the adrenal cortex leads to the development of idiopathic hyperaldosteronism.

There is a rare familial form of primary hyperaldosteronism with an autosomal dominant type of inheritance, caused by a defect in the 18-hydroxylase enzyme, which is out of control of the renin-angiotensin system and corrected by glucocorticoids (occurs in young patients with frequent cases of arterial hypertension in a family history). In rare cases, primary hyperaldosteronism can be caused by adrenal cancer that can produce aldosterone and deoxycorticosterone.

Secondary hyperaldosteronism occurs as a complication of a number of diseases of the cardiovascular system, pathology of the liver and kidneys. Secondary hyperaldosteronism is seen in heart failure, malignant arterial hypertension, cirrhosis of the liver, Bartter's syndrome, renal artery dysplasia and stenosis, nephrotic syndrome, renal reninoma, and renal failure.

To increase the secretion of renin and the development of secondary hyperaldosteronism leads to sodium loss (with diet, diarrhea), a decrease in circulating blood volume during blood loss and dehydration, excessive potassium intake, long-term use of certain drugs (diuretics, COCs, laxatives). Pseudohyperaldosteronism develops when the reaction of the distal renal tubules to aldosterone is disturbed, when, despite its high level in the blood serum, hyperkalemia is observed. Extra-adrenal hyperaldosteronism is noted quite rarely, for example, in the pathology of the ovaries, thyroid gland and intestines.

Pathogenesis

Primary hyperaldosteronism (low-reninated) is usually associated with a tumor or hyperplastic lesion of the adrenal cortex and is characterized by a combination of increased secretion of aldosterone with hypokalemia and arterial hypertension.

The basis of the pathogenesis of primary hyperaldosteronism is the effect of excess aldosterone on the water-electrolyte balance: an increase in the reabsorption of sodium and water ions in the renal tubules and an increased excretion of potassium ions in the urine, leading to fluid retention and hypervolemia, metabolic alkalosis, and a decrease in the production and activity of blood plasma renin. There is a violation of hemodynamics - an increase in the sensitivity of the vascular wall to the action of endogenous pressor factors and the resistance of peripheral vessels to blood flow. In primary hyperaldosteronism, a pronounced and prolonged hypokalemic syndrome leads to degenerative changes in the renal tubules (kaliepenic nephropathy) and muscles.

Secondary (high-renin) hyperaldosteronism occurs as a compensatory response to a decrease in renal blood flow in various diseases of the kidneys, liver, and heart. Secondary hyperaldosteronism develops due to the activation of the renin-angiotensin system and increased production of renin by the cells of the juxtaglomerular apparatus of the kidneys, which provide excessive stimulation of the adrenal cortex. The pronounced electrolyte disturbances characteristic of primary hyperaldosteronism do not occur in the secondary form.

Symptoms of hyperaldosteronism

The clinical picture of primary hyperaldosteronism reflects water and electrolyte imbalance caused by hypersecretion of aldosterone. Due to the retention of sodium and water in patients with primary hyperaldosteronism, severe or moderate arterial hypertension, headaches, aching pains in the region of the heart (cardialgia), cardiac arrhythmias, changes in the fundus of the eye with deterioration in visual function (hypertonic angiopathy, angiosclerosis, retinopathy) occur.

Potassium deficiency leads to fatigue, muscle weakness, paresthesia, seizures in various muscle groups, periodic pseudo-paralysis; in severe cases - to the development of myocardial dystrophy, kaliepenic nephropathy, nephrogenic diabetes insipidus. With primary hyperaldosteronism in the absence of heart failure, peripheral edema is not observed.

With secondary hyperaldosteronism, a high level of blood pressure is observed (with diastolic blood pressure> 120 mm Hg), gradually leading to damage to the vascular wall and tissue ischemia, deterioration of kidney function and the development of chronic renal failure, changes in the fundus (hemorrhages, neuroretinopathy). The most common sign of secondary hyperaldosteronism is edema, hypokalemia occurs in rare cases. Secondary hyperaldosteronism can occur without arterial hypertension (for example, with Bartter's syndrome and pseudohyperaldosteronism). Some patients have an asymptomatic course of hyperaldosteronism.

Diagnostics

Diagnosis involves the differentiation of various forms of hyperaldosteronism and the determination of their etiology. As part of the initial diagnosis, an analysis of the functional state of the renin-angiotensin-aldosterone system is carried out with the determination of aldosterone and renin in the blood and urine at rest and after stress tests, potassium-sodium balance and ACTH, which regulate aldosterone secretion.

Primary hyperaldosteronism is characterized by an increase in the level of aldosterone in the blood serum, a decrease in plasma renin activity (ARP), a high aldosterone / renin ratio, hypokalemia and hypernatremia, low relative density of urine, a significant increase in the daily excretion of potassium and aldosterone in the urine. The main diagnostic criterion for secondary hyperaldosteronism is an increased rate of ARP (with reninoma - more than 20-30 ng / ml / h).

In order to differentiate individual forms of hyperaldosteronism, a test with spironolactone, a test with a hypothiazide load, and a “marching” test are carried out. In order to identify the familial form of hyperaldosteronism, genomic typing is carried out by PCR. In case of hyperaldosteronism corrected by glucocorticoids, trial treatment with dexamethasone (prednisolone) is of diagnostic value, in which the manifestations of the disease are eliminated and blood pressure normalizes.

To determine the nature of the lesion (aldosteroma, diffuse nodular hyperplasia, cancer), topical diagnostic methods are used: ultrasound of the adrenal glands, scintigraphy, CT and MRI of the adrenal glands, selective venography with simultaneous determination of the levels of aldosterone and cortisol in the blood of the adrenal veins. It is also important to establish the disease that caused the development of secondary hyperaldosteronism using studies of the state of the heart, liver, kidneys and renal arteries (EchoCG, ECG, ultrasound of the liver, ultrasound of the kidneys, ultrasound and duplex scanning of the renal arteries, multispiral CT, MR angiography).

Treatment of hyperaldosteronism

The choice of method and tactics for the treatment of hyperaldosteronism depends on the cause of aldosterone hypersecretion. Examination of patients is carried out by an endocrinologist, cardiologist, nephrologist, ophthalmologist. Drug treatment with potassium-sparing diuretics (spirolactone) is carried out in various forms of hyporeninemic hyperaldosteronism (hyperplasia of the adrenal cortex, aldosterone) as a preparatory stage for surgery, which helps to normalize blood pressure and eliminate hypokalemia. A low-salt diet with an increased content of potassium-rich foods in the diet, as well as the introduction of potassium preparations, is shown.

Treatment of aldosteroma and adrenal cancer is surgical, it consists in removing the affected adrenal gland (adrenalectomy) with a preliminary restoration of water and electrolyte balance. Patients with bilateral adrenal hyperplasia are usually treated conservatively (spironolactone) in combination with ACE inhibitors, calcium channel antagonists (nifedipine). In hyperplastic forms of hyperaldosteronism, complete bilateral adrenalectomy and right-sided adrenalectomy in combination with subtotal resection of the left adrenal gland are ineffective. Hypokalemia disappears, but there is no desired hypotensive effect (BP normalizes only in 18% of cases) and there is a high risk of developing acute adrenal insufficiency.

With hyperaldosteronism, which can be corrected by glucocorticoid therapy, hydrocortisone or dexamethasone is prescribed to eliminate hormonal and metabolic disorders and normalize blood pressure. In secondary hyperaldosteronism, combined antihypertensive therapy is carried out against the background of pathogenetic treatment of the underlying disease under the mandatory control of ECG and potassium levels in blood plasma.

In the case of secondary hyperaldosteronism due to stenosis of the renal arteries, it is possible to perform percutaneous X-ray endovascular balloon dilatation, stenting of the affected renal artery, and open reconstructive surgery to normalize blood circulation and functioning of the kidney. When a kidney reninoma is detected, surgical treatment is indicated.

Forecast and prevention of hyperaldosteronism

The prognosis of hyperaldosteronism depends on the severity of the underlying disease, the degree of damage to the cardiovascular and urinary systems, timeliness and treatment. Radical surgical treatment or adequate drug therapy provide a high probability of recovery. The prognosis for adrenal cancer is poor.

In order to prevent hyperaldosteronism, constant dispensary observation of persons with arterial hypertension, diseases of the liver and kidneys is necessary; compliance with medical recommendations regarding the intake of medications and the nature of nutrition.

Hyperaldosteronism is a disorder of the adrenal glands caused by excessive secretion of aldosterone, one of the active mineralocorticoids. Its main symptom is an increase in blood pressure. The task of the adrenal glands is to produce a variety of hormones, including mineralocorticoids. With the help of the latter, the water-salt balance is regulated. Aldosterone plays a major role in this. Both excessive synthesis of the hormone and insufficient leads to disturbances in the functioning of the body. Hyperaldosteronism is a syndrome caused by excessive production of aldosterone.

Hyperaldosteronism

Aldosterone is the most active of the mineral corticoids and is produced in the zona glomeruli of the adrenal cortex. and release into the blood causes a low concentration of sodium and a high concentration of potassium in the blood. Also, ACTH and, of course, the renin-angiotensin system can act as a synthesis stimulator.

Aldosterone works by the following mechanism:

• the hormone binds to mineralocorticoid receptors in the renal tubules;
• at the same time, the synthesis of sodium ion transporter proteins is stimulated and the latter is excreted from the lumen of the tubule into the epithelial cell of the renal tubule;
• the production of potassium ion transporter proteins increases. Potassium is excreted from the cells of the renal tubule into the primary urine;
• the water-salt balance is restored.

The picture looks different when, for one reason or another, the secretion of aldosterone is unreasonably increased. The hormone promotes increased sodium reabsorption, which leads to an increase in the content of sodium ions in the blood. This stimulates the production of antidiuretic hormone and water retention. At the same time, hydrogen, magnesium, and, most importantly, potassium ions are excreted in the urine, which automatically leads to the development of hypernatremia and hypokalemia.

Both deviations contribute to a steady increase in blood pressure, in which an excess of mineralcorticoids causes direct damage to the myocardium, blood vessels and kidneys.

Hyperaldosteronism is a complex of symptoms resulting from excessive synthesis of aldosterone. At the same time, the synthesis is not caused by the action of conventional stimulants and practically does not depend on the renin-angiotensin system.

Etiology and pathogenesis

Primary hyperaldosteronism is the cause of elevated blood pressure in 10-15% of cases. Usually they suffer from middle-aged people - 30-50 years old, mostly women - up to 70%.

There are primary and secondary hyperaldosteronism. In the first case, the excessive production of aldosterone is due to disorders in the work of the adrenal cortex and does not depend on external factors. In the second case, the synthesis of the hormone is stimulated by an external factor - arterial hypertension, heart failure, cirrhosis of the liver.

The causes of the syndrome are very diverse.

Primary hyperaldosteronism is caused by:

• Kohn's syndrome - aldosterone-producing adrenal adenoma, accounts for more than 65% of cases;
• idiopathic hyperaldosteronism - is formed due to diffuse bilateral small-nodular hyperplasia of the adrenal cortex. It is the cause of 30-40% of cases of the disease. Its etiology remains unclear. But unlike other forms of the disease, the zona glomeruli remains sensitive to angiotensin II. ACTH regulates aldosterone synthesis;
• adrenal hyperplasia - unilateral and bilateral;
• glucocorticoid-dependent hyperaldosteronism - a hereditary disease caused by a gene defect;
• aldosterone-producing carcinoma is a very rare case, no more than 100 such patients have been described;
• pseudohyperaldosteronism - it is based on a congenital gene defect, which leads to inhibition of the production of angiotensin I and, ultimately, to a decrease in aldosterone;
• Itsenko-Cushing's syndrome - an excess of aldosterone is due to increased secretion of ACTH;
• congenital or drug-induced deficiency.

Causes of primary hyperaldosteronism

Secondary hyperaldosteronism is associated with the underlying pathology, which is the cause of its appearance:

• excessive activity of the renin-angiotensin-aldosterone system - pregnancy, excessive potassium intake, sodium loss associated with diet, diarrhea, medication, decrease in blood volume due to blood loss, and so on;
• organic secondary hyperaldosteronism - arterial stenosis, tumor;
• functional hyponatremia, hypovolemia and so on;
• violation of aldosterone metabolism in heart failure, kidney disease, and so on.

A characteristic difference between secondary hyperaldosteronism and primary hyperaldosteronism is that it does not cause disturbances in the electrolyte balance, as it is a natural reaction to excessive work of the renin-angiotensin-aldosterone system.

Causes of secondary hyperaldosteronism

Types and symptoms

Depending on the type of disease, the symptoms also differ. The decisive factor here is the method of regulating the synthesis and secretion of aldosterone. So, in primary hyperaldosteronism, the hormone is produced uncontrollably due to a violation in the adrenal cortex, while in the secondary form, the production is stimulated by the RAAS. Accordingly, in the first case, there is a violation of the water-salt balance, and in the second - no. The difference in the clinical picture is precisely this and explains.

Primary

Primary hyperaldosteronism is characterized by:

• - observed in 100% of patients, although recently they began to note the asymptomatic course of the disease. BP is constantly elevated, especially diastolic, which quickly leads to left ventricular hypertrophy, and, therefore, to changes in the ECG. At the same time, vascular lesions of the fundus are noted in 50% of patients, and visual impairment in 20%;
• hypokalemia - 100% of patients. Potassium deficiency leads to dysfunction of muscle and nervous tissue. This manifests itself as weakness and rapid muscle fatigue up to pseudo-paralytic states and convulsions;
• the analysis shows an increase in the level of aldosterone and a low level of renin in 100 cases out of 100. Moreover, the level of the hormone is not regulated;
• hypochloremic alkalosis is observed - an increase in the pH level in the blood due to the accumulation of alkaline metabolic products;
• and nocturnal polyuria - respectively, 85 and 72%, is caused by changes in the renal tubules caused by hypokalemia. The symptom is accompanied by a constant feeling of thirst;
• in 65% of cases, hypernatremia is observed - an increase in the concentration of sodium ions with a decrease in the concentration of potassium - a natural phenomenon. However, the sensitivity of the renal tubules to sodium retention caused by aldosterone can be markedly reduced. In the absence of hypernatremia, PHA is suspected by urinary potassium excretion greater than 40 mEq/day;
• in 51% of cases, AD causes persistent headache;
• water-electrolyte imbalance can also cause psycho-emotional disorders - hypochondria, asthenic syndrome, and so on.

All the described symptoms are most characteristic of Kohn's syndrome, the most common cause of RAH.

Other cases are much less common:

• idiopathic hyperaldosteronism with similar symptoms allows you to regulate the production of aldosterone, since the glomerular zone remains sensitive to the action of angiotensin II;
• bilateral hyperplasia is characterized by sensitivity to glucocorticosteroids: when taking GCS, potassium metabolism normalizes and blood pressure decreases;
• pseudohyperaldosteronism is accompanied by typical signs of PAH. However, there is no response to the drug.

Diagnosis of the disease is very difficult. Not only external symptoms are important, but the response to the introduction of certain drugs. Thus, the introduction of veroshpiron for 2 weeks normalizes potassium metabolism and reduces blood pressure. However, this effect is typical only for PHA. If it is absent, then the diagnosis was erroneous.

Symptoms and signs of primary hyperaldosteronism

Secondary

The clinical picture of HAV is strongly associated with the symptoms of the underlying disease. Secondary hyperaldosteronism is a kind of compensatory phenomenon and has no characteristic symptoms of its own. Its clear difference from PHA is the preservation of the water-salt balance, which means the absence of high blood pressure, hypernatremia or hypokalemia.

Often secondary hyperaldosteronism is associated with the appearance of edema. Fluid retention and sodium accumulation causes increased secretion of aldosterone. In fact, in HAV, aldosterone synthesis is driven by hypernatremia.

Diagnostics

The similarity of symptoms and their ambiguity makes the diagnosis of the disease very difficult and lengthy. Not only laboratory and instrumental studies are required, but also a number of functional tests of a different nature. Diagnostics is carried out in several stages.

Primary

It is carried out in order to exclude or confirm PHA. To do this, at least 2 times determine the level of potassium in the plasma in all patients with high blood pressure. Primary hyperaldosteronism is characterized by a stable low level of potassium in the blood - less than 2.7 mEq / l, regardless of the intake of antihypertensive drugs. With normokalemic hyperaldosteronism, the level of potassium against the background of an increased content of aldosterone is higher than 3.5 meq / l.

Diagnosis of PGA syndrome

At this stage, the level of hormones is examined in order to establish the true cause of the disease.

Primary PHA is characterized by:

• low renin activity is not an absolute indicator, since its insufficiency is, in principle, characteristic of 25% of hypertensive patients, especially the elderly;
• high concentration of aldosterone in the blood or increased urinary excretion of the breakdown products of the hormone. A symptom characteristic of 70% of patients. It should be borne in mind that the level of aldosterone decreases with hypervolemia, hypokalemia, and so on;
• a stimulation test with a sodium load may provide the desired response. The patient is injected with 2 liters of sodium chloride solution, which normally leads to a decrease in the concentration of aldosterone by 50%. With primary hyperaldosteronism, such a decrease does not occur, since the synthesis of the hormone is insensitive to external factors. The test requires great care, since the sodium load significantly worsens the patient's well-being - there is weakness, heart rhythm disturbances.

Differential diagnosis of hyperaldosteronism

Definition of nosological form

At this stage, functional tests and biochemical studies of blood and urine are carried out:

• An increase in the concentration of 18-hydroxycorticosterone is one of the most reliable signs of PHA. Again, with the exception of the idiomatic, where 18-hydroxycorticosterone remains normal or slightly elevated.
• High levels of cortisone breakdown products in the urine are also typical of PHA.
• Functional tests are based on the body's response to certain drugs and loads:
  • orthostatic load - 4 hours of walking, in combination with a 3-day low-salt diet does not stimulate the activity of renin in the blood - ARP, and the content of aldosterone may even decrease. The same response follows the reception of active saluretics. Basal ARP is measured on an empty stomach after a night's sleep on a diet containing no more than 120 mEq/day of sodium;
  • spironolactone test - 3-day administration of spironolactones (600 mg / day) does not stimulate renin activity and does not affect aldosterone production in any way;
  • test with captopril - with aldosterone, the circadian rhythm of aldosterone is maintained both after walking and at rest. The absence of a rhythm is an indicator of a malignant tumor;
  • test with DOXA - every 12 hours for 3 days, 10 mg of the drug is injected. With aldosterone and in most cases with idiopathic PHA, the drug does not affect the synthesis of aldosterone.
• Idiopathic PHA is more difficult to diagnose due to the preservation of the sensitivity of the renal tissue. With this disease, all signs are mild, but at the same time, stimulating tests are less effective than in healthy people: the level of aldosterone is lower, the concentration of 18-hydroxycorticosterone is much lower, renin activity is reduced, but increases after walking.
• With carcinoma, the reaction to the samples is completely absent.
• Glucocorticoid hyperaldosteronism is detected with the following signs: ineffectiveness of antihypertensive therapy, increased excretion of 18-oxocortisol and 18-hydroxycortisol against the background of a normal level of potassium in the blood, no change in the level of aldosterone during orthostatic exercise. Trial treatment with dexamethasone or prednisolone brings a quick and stable effect.
• Familial forms of PHA can only be established with the help of genetic diagnostics.

Instrumental Methods

If, according to the biochemical parameters, PHA can be considered proven, additional studies are prescribed to determine the localization of the pathology:

• - allows you to identify aldosterone-producing adenoma with an accuracy of 62%. In addition, the method allows to exclude tumors.
• CRT - the accuracy of adenoma detection is 100%.
• Ultrasound - sensitivity is 92%. This is one of the safest methods.
• Phlebography of the adrenal glands - here the concentration gradient of aldosterone and renin is studied at different levels. The method is accurate, but very complicated.
• adrenal glands - the most informative for small- and large-nodular hyperplasia, as well as tumors and adenomas. The test is carried out against the background of blockade of the thyroid gland.

On the video about the diagnosis of hyperaldosteronism:

Treatment

The main treatment for PHA is surgery, usually the removal of the affected adrenal gland. But in certain cases this method is unacceptable.

• So, with bilateral hyperplasia, surgery is indicated only with the complete failure of the drug treatment performed.
• In the idiopathic form of GPA, conservative treatment is prescribed.
• In the case of carcinoma, surgery is combined with chemotherapy.
• The glucocorticoid-dependent form does not require surgical intervention. The introduction of dexomethasone in 3-4 weeks completely normalizes blood pressure.
• Secondary hyperaldosteronism rarely requires self-treatment. Here it is necessary to eliminate the underlying disease.

Medical

With conservative treatment, the following drugs are used:

• aminoglutethimide - 2-3 times a day. Treatment is carried out against the background of control of blood pressure, the level of cortisol in the urine - at least 1 time per day, thyroid hormones, and so on;
• spironolactone - 2 times a day, 50 mg. Treatment can be combined with the use of potassium-sparing diuretins - this way side effects can be prevented;
• spironolactone - 1-2 times a day 25-50 mg with amyloid and triamterene. With severe hypokalemia, potassium preparations are added. After normalization of the concentration of potassium in plasma, the dose is reduced.

Pseudohyperaldosteronism, as well as the glucocorticoid-dependent form, is cured with small doses of dexamethasone.

Surgical intervention

The operation is quite complicated and requires a long preparation - at least 4 weeks. Its goal is to reduce ADL, restore the normal content of potassium in the blood and the function of the RAAS.

For this, appoint:

• aminoglutethimide - 250 mg 2-3 per day. The dose is increased if treatment is ineffective;
• spironolactone - 50-100 mg 2-4 times a day. A combination of spironolactone and amiloride is used. If blood pressure does not decrease, antihypertensive drugs may be administered.

Most often, a unilateral adrenalectomy is performed - the removal of the adrenal gland. The operation is performed through the entry into the abdominal cavity, without it and from the back. There are other methods - transarterial administration of alcohol, portalization of blood flow, but today they have not received distribution.

In the postoperative period, substitution therapy is carried out: every 4–6 hours for 2–3 days, 25–50 mg of hydrocortisone is administered. The dose is gradually reduced as signs of adrenal insufficiency decrease.

Clinical recommendations for this disease are only general. Treatment must be selected individually, taking into account the general condition of the patient and the characteristics of his body. Recommendations do not set standards because they do not guarantee results.

High blood pressure is a symptom of many diseases, which makes it extremely difficult to diagnose. Complaints of patients in this case are non-specific, so the question of referral to research remains open. The recommendations help to identify those groups of patients in whom PHA is more likely.

• arterial hypertension 1 and 2 stages;
• high blood pressure, insensitive to drug treatment;
• a combination of hypertension and hypokalemia, including drug-induced;
• a combination of hypertension and adrenal incidentaloma;
• family history of hypertension - prior development of hypertension, next of kin with PHA, and so on.

As a primary study of patients in these groups, the determination of the aldosterone-renin ratio is shown. To clarify PHA, it is recommended to conduct functional tests.

A CT scan is ordered to rule out cancer.

Patients with early development of the disease - up to 20 years old, and who have relatives with PHA, are assigned genetic testing in order to establish glucocorticoid-dependent PHA.

Forecasts

According to statistics, surgical intervention provides 50-60% of complete recovery, with adrenal adenoma. The prognosis for carcinoma is poor.

With a combination of adenoma with diffuse and diffuse-nodular hyperplasia, complete recovery cannot be achieved. To maintain remission, patients require continuous therapy with spironolactone or steroidogenesis inhibitors.

The same applies to patients with bilateral adrenal hyperplasia.

Hyperaldosteronism is a common name for a number of diseases that cause the same clinical picture. Secondary hyperaldosteronism, as a rule, disappears along with the underlying disease. The prognosis for a cure for PHA is not so good.