Primary aldosteronism (Conn's syndrome) is aldosteronism caused by the autonomous production of aldosterone by the adrenal cortex (due to hyperplasia, adenoma or carcinoma). Symptoms and signs include occasional weakness, increased blood pressure, and hypokalemia. Diagnosis includes determination of plasma aldosterone levels and plasma renin activity. Treatment depends on the cause. The tumor is removed if possible; in case of hyperplasia, spironolactone or related drugs can normalize blood pressure and cause the disappearance of other clinical manifestations.

Aldosterone is the most potent mineralocorticoid produced by the adrenal glands. It regulates sodium retention and potassium loss. In the kidneys, aldosterone causes the transfer of sodium from the lumen of the distal tubules into the tubular cells in exchange for potassium and hydrogen. The same effect is observed in the salivary and sweat glands, intestinal mucosal cells, and the exchange between intracellular and extracellular fluid.

Aldosterone secretion is regulated by the renin-angiotensin system and, to a lesser extent, by ACTH. Renin, a proteolytic enzyme, accumulates in the juxtaglomerular cells of the kidneys. A decrease in the volume and velocity of blood flow in the afferent renal arterioles induces the secretion of renin. Renin converts liver angiotensinogen to angiotensin I, which is converted to angiotensin II by angiotensin-converting enzyme. Angiotensin II causes the secretion of aldosterone and, to a lesser extent, the secretion of cortisol and deoxycorticosterone, which also have pressor activity. Sodium and water retention caused by increased secretion of aldosterone increases circulating blood volume and reduces renin secretion.

The syndrome of primary hyperaldosteronism was described by J. Conn (1955) in connection with an aldosterone-producing adenoma of the adrenal cortex (aldosteroma), the removal of which led to a complete recovery of the patient. Currently, the collective concept of primary hyperaldosteronism unites a number of diseases that are similar in clinical and biochemical characteristics, but different in pathogenesis, which are based on excessive and independent (or partially dependent) on the renin-angiotensin system production of aldosterone by the adrenal cortex.

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ICD-10 code

E26.0 Primary hyperaldosteronism

What causes primary aldosteronism?

Primary aldosteronism may be caused by an adenoma, usually unilateral, of the glomerular layer of the adrenal cortex or, less commonly, by carcinoma or adrenal hyperplasia. In adrenal hyperplasia, which is more often observed in older men, both adrenal glands are overactive and there is no adenoma. The clinical picture can also be observed in congenital adrenal hyperplasia due to 11-hydroxylase deficiency and in dominantly inherited dexamethasone-suppressed hyperaldosteronism.

Symptoms of primary aldosteronism

Clinical case of primary hyperaldosteronism

Patient M., a 43-year-old woman, was admitted to the endocrinology department of the Kazan Republican Clinical Hospital on January 31, 2012 with complaints of headaches, dizziness when blood pressure rose to a maximum of 200/100 mm Hg. Art. (with a comfortable blood pressure of 150/90 mm Hg), generalized muscle weakness, leg cramps, general weakness, fatigue.

History of the disease. The disease developed gradually. For five years, the patient has noted an increase in blood pressure, for which she was observed by a therapist at her place of residence and received antihypertensive therapy (enalapril). About 3 years ago, I began to experience periodic leg pain, cramps, and muscle weakness that occurred without visible provoking factors and went away on their own within 2-3 weeks. Since 2009, she received inpatient treatment 6 times in the neurological departments of various medical institutions with a diagnosis of Chronic demyelinating polyneuropathy, subacutely developing generalized muscle weakness. One of the episodes involved neck muscle weakness and head drooping.

With the infusion of prednisolone and a polarizing mixture, improvement occurred within several days. According to blood tests, potassium is 2.15 mmol/l.

From 12/26/11 to 01/25/12 she was hospitalized at the Republican Clinical Hospital, where she was admitted with complaints of generalized muscle weakness and periodic leg cramps. An examination was carried out, which revealed: blood test on December 27, 2011: ALT - 29 U/L, AST - 14 U/L, creatinine - 53 µmol/L, potassium 2.8 mmol/L, urea - 4.3 mmol/L, total Protein 60 g/l, bilirubin total. - 14.7 µmol/l, CPK - 44.5, LDH - 194, phosphorus 1.27 mmol/l, Calcium - 2.28 mmol/l.

Urinalysis dated 12/27/11; specific weight - 1002, protein - traces, leukocytes - 9-10 per cell, epit. pl - 20-22 in p/z.

Hormones in the blood: T3sv - 4.8, T4sv - 13.8, TSH - 1.1 μmE/l, cortisol - 362.2 (normal 230-750 nmol/l).

Ultrasound: Left kidneys: 97x46 mm, parenchyma 15 mm, increased echogenicity, FLS - 20 mm. Echogenicity is increased. The cavity is not expanded. Right 98x40 mm. The parenchyma is 16 mm, the echogenicity is increased, the CL is 17 mm. Echogenicity is increased. The cavity is not expanded. A hyperechoic rim is visualized around the pyramids on both sides. Based on the physical examination and laboratory data, further examination was recommended to exclude endocrine pathology of adrenal origin.

Ultrasound of the adrenal glands: in the projection of the left adrenal gland an isoechoic round formation of 23x19 mm is visualized. In the projection of the right adrenal gland, pathological formations are not reliably visualized.

Urine for catecholamines: Diuresis - 2.2 l, adrenaline - 43.1 nmol/day (normal 30-80 nmol/day), norepinephrine - 127.6 nmol/l (normal 20-240 nmol/day). These results excluded the presence of pheochromocytoma as a possible cause of uncontrolled hypertension. Renin from 01/13/12-1.2 µIU/ml (N vertical - 4.4-46.1; horizontal 2.8-39.9), aldosterone 1102 pg/ml (normal: lying 8-172, sitting 30 -355).

RCT dated 01/18/12: RCT signs of a formation in the left adrenal gland (in the medial peduncle of the left adrenal gland an oval-shaped isodense formation with dimensions of 25*22*18 mm, homogeneous, with a density of 47 NU is determined.

Based on the anamnesis, clinical picture, data from laboratory and instrumental research methods, a clinical diagnosis was established: Primary hyperaldosteronism (aldosteroma of the left adrenal gland), first identified in the form of hypokalemic syndrome, neurological symptoms, and sinus tachycardia. Hypokalemic periodic convulsions with generalized muscle weakness. Hypertension, stage 3, stage 1. CHF 0. Sinus tachycardia. Urinary tract infection is in the resolution stage.

Hyperaldosteronism syndrome occurs with clinical manifestations caused by three main symptom complexes: arterial hypertension, which can have either a crisis course (up to 50%) or persistent; impairment of neuromuscular conduction and excitability, which is associated with hypokalemia (in 35-75% of cases); impaired renal tubular function (50-70% of cases).

The patient was recommended surgical treatment to remove a hormone-producing tumor of the adrenal gland - laparoscopic adrenalectomy on the left. An operation was performed - laparoscopic adrenalectomy on the left in the abdominal surgery department of the RCH. The postoperative period was uneventful. On the 4th day after surgery (02/11/12), the blood potassium level was 4.5 mmol/l. Blood pressure 130/80 mm Hg. Art.

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Secondary aldosteronism

Secondary aldosteronism is increased production of aldosterone by the adrenal glands in response to non-pituitary, extra-adrenal stimuli, including renal artery stenosis and hypovolemia. Symptoms are similar to those of primary aldosteronism. Treatment includes correction of the underlying cause.

Secondary aldosteronism is caused by a decrease in renal blood flow, which stimulates the renin-angiotensin mechanism with resulting hypersecretion of aldosterone. Causes of decreased renal blood flow include obstructive diseases of the renal artery (for example, atheroma, stenosis), renal vasoconstriction (with malignant hypertension), diseases accompanied by edema (for example, heart failure, cirrhosis with ascites, nephrotic syndrome). Secretion may be normal in heart failure, but hepatic blood flow and aldosterone metabolism are reduced, so circulating levels of the hormone are high.

Diagnosis of primary aldosteronism

The diagnosis is suspected in patients with hypertension and hypokalemia. Laboratory testing consists of determining plasma aldosterone levels and plasma renin activity (PRA). Tests should be performed when the patient is off medications that affect the renin-angiotensin system (eg, thiazide diuretics, ACE inhibitors, angiotensin antagonists, blockers) for 4-6 weeks. ARP is usually measured in the morning with the patient lying down. Typically, patients with primary aldosteronism have plasma aldosterone levels greater than 15 ng/dL (>0.42 nmol/L) and low levels of ARP, with a ratio of plasma aldosterone (in nanograms/dL) to ARP [in nanograms/(mLh)] greater than 20 .

Definition of the concept

In 1955, Cohn described a syndrome characterized by arterial hypertension and decreased serum potassium levels, the development of which is associated with aldosteroma (adenoma of the adrenal cortex that secretes aldosterone).

Primary hyperaldosteronism is more common in adults, affecting women more often (ratio 3:1) aged 30-40 years. Among children, the incidence of the disease is the same in girls and boys.

Causes of the disease

1. Aldosteromas (Conn syndrome)

2. Bilateral adrenal hyperplasia or multiple adenomatosis of the adrenal cortex (15%):

a) idiopathic hyperaldosteronism (hyperproduction of aldosterone is not suppressed);

3. Aldosterone-producing adenoma is completely suppressed by glucocorticoids.

4. Carcinoma of the adrenal cortex.

5. Extra-adrenal hyperaldosteronism

Mechanisms of occurrence and development of the disease (pathogenesis)

1. Aldosteromas (Conn syndrome)- aldosterone-producing adrenal tumor (70% of cases of primary hyperaldosteronism). Aldosterone-producing adenoma of the adrenal cortex is usually unilateral, no more than 4 cm in size. Multiple and bilateral adenomas are extremely rare. Adrenal cancer as a cause of aldosteronism is also uncommon - 0.7-1.2%. In the presence of an adenoma, aldosterone biosynthesis does not depend on ACTH secretion.

2. Bilateral adrenal hyperplasia(30% of cases) or multiple adenomatosis of the adrenal cortex (15%):

a) idiopathic hyperaldosteronism (overproduction of aldosterone, not suppressed);

b) undefined hyperaldosteronism (overproduction of aldosterone, selectively suppressed);

c) hyperaldosteronism, completely suppressed by glucocorticoids.

3. Aldosterone-producing adenoma, is completely suppressed by glucocorticoids.

4. Carcinoma of the adrenal cortex.

A relatively rare cause of primary aldosteronism is a malignant tumor of the adrenal cortex.

5. Extra-adrenal hyperaldosteronism (tumor of the ovaries, intestines, thyroid gland).

Malignant tumors account for 2-6% of all cases.

Clinical picture of the disease (symptoms and syndromes)

1. Arterial hypertension. Persistent hypertension is sometimes accompanied by severe headaches in the forehead. Hypertension is stable, but paroxysms are also possible. Malignant hypertension is very rare.

Hypertension does not respond to orthostatic load (renin-dependent reaction), resistant to the Valsalva maneuver (during the test, blood pressure does not increase, unlike other types of hypertension).

Blood pressure is corrected with spironolactone (400 mg/day for 10-15 days), as is hypokalemia.

2. "Kalipenic kidney"

In almost all cases, primary aldosteronism is accompanied by hypokalemia due to excessive renal potassium loss under the influence of aldosterone. Potassium deficiency causes the formation of a “kaliopenic kidney.” The epithelium of the distal renal tubules is affected, in combination with general hypokalemic alkalosis, leading to disruption of the mechanisms of oxidation and concentration of urine.

In the initial stages of the disease, renal impairment may be minor.

1) Polyuria, mainly nocturnal, reaches 4 liters per day, nocturia (70% of patients). Polyuria in primary hyperaldosteronism is not suppressed by vasopressin drugs and does not decrease with fluid intake restriction.

2) Characteristic hypoisosthenuria - 1008-1012.

3) Transient, moderate proteinuria is possible.

4) The urine reaction is often alkaline, which increases the frequency of concomitant pyelitis and pyelonephritis.

Thirst and compensatory polydipsia develop as a reaction to polyuria. Polydipsia and polyuria at night, along with neuromuscular manifestations (weakness, paresthesia, myoplegic attacks) are mandatory components of the hypokalemic syndrome. Polydipsia has a central genesis (hypokalemia stimulates the thirst center) and reflex genesis (due to the accumulation of sodium in the cells).

Edema is not typical - only in 3% of patients with concomitant kidney damage or circulatory failure. Polyuria and sodium accumulation in cells do not contribute to fluid retention in the interstitial space.

3. Muscle damage. Muscle weakness, pseudoparalysis, periodic attacks of convulsions of varying intensity, tetany, obvious or latent, is observed. Possible twitching of facial muscles, positive Chvostek and Trousseau symptoms. Increased electrical potential in the rectum. Characteristic paresthesias in various muscle groups.

4. Changes in the central and peripheral nervous system

General weakness occurs in 20% of patients. Headaches are observed in 50% of patients and are intense - caused by increased blood pressure and hyperhydration of the brain.

5. Disturbance of carbohydrate metabolism.

Hypokalemia suppresses insulin secretion and contributes to the development of reduced tolerance to carbohydrates (60% of patients).

Diagnosis of the disease

1. Hypokalemia

Increased urinary potassium excretion (normal 30 mmol/l).

2. Hypernatremia

3. Hyperosmolarity

Specific stable hypervolemia and high plasma osmolarity. The 20% to 75% increase in intravascular volume is unaffected by saline or albumin administration.

Alkalosis is present in 50% of patients - blood pH reaches 7.60. Increased blood bicarbonate content up to 30-50 mmol/l. Alkalosis is combined with a compensatory decrease in the level of chlorine in the blood. The changes are enhanced by salt intake and are eliminated by spironolactone.

4. Hormonal imbalance

The level of aldosterone in the blood is often elevated from a norm of 2-16 ng/100 ml to 50 ng/100 ml. Blood sampling should be carried out with the patient in a horizontal position. Increased levels of aldosterone metabolites in the blood. Changes in the daily profile of aldosterone secretion: determination of the level of aldosterone in the blood serum at 8 a.m. and at 12 p.m. With aldosterome, the content of aldosterone in the blood at 12 o'clock in the afternoon is lower than at 8 o'clock in the morning, while with small or large nodular hyperplasia, the concentration of aldosterone during these periods remains almost unchanged or is slightly higher at 8 o'clock in the morning.

Increased urinary excretion of aldosterone.

Reduced unstimulated plasma renin activity is a cardinal symptom of primary hyperaldosteronism. Renin secretion is suppressed by hypervolemia and hyperosmolarity. In healthy people, the renin content in the blood in a horizontal position is 0.2-2.7 ng/ml/hour.

The criterion for the diagnosis of primary hyperaldosteronism syndrome is a combination of reduced plasma renin activity with hyperaldosteronemia. Differential diagnostic criterion from secondary hyperaldosteronism in renovascular hypertension, chronic renal failure, renin-forming kidney tumor, malignant arterial hypertension, when both renin and aldosterone levels are elevated.

5. Functional tests

1. Sodium load 10 g/day for 3-5 days. In practically healthy individuals with normal regulation of aldosterone secretion, the serum potassium level will remain unchanged. With primary aldosteronism, the potassium content in the blood serum decreases to 3-3.5 mmol/l, the excretion of potassium in the urine increases sharply, and the patient’s condition worsens (severe muscle weakness, cardiac arrhythmia).

2. 3-day low (20 mEq/day) sodium diet - renin levels remain unchanged, aldosterone levels may even decrease.

3. Test with furosemide (Lasix). Before the test, the patient should be on a diet with a normal sodium chloride content (about 6 g per day), not receive any antihypertensive drugs for a week and not take diuretics for 3 weeks. During the test, the patient takes 80 mg of furosemide orally and remains in an upright position (walks) for 3 hours. After 3 hours, blood is drawn to determine renin and aldosterone levels. With primary aldosteronism, there is a significant increase in aldosterone levels and a decrease in the concentration of renin in the blood plasma.

4. Test with capoten (captopril). In the morning, blood is taken from the patient to determine the content of aldosterone and renin in the plasma. Then the patient takes 25 mg of capoten orally and remains in a sitting position for 2 hours, after which his blood is taken again to determine the content of aldosterone and renin. In patients with essential hypertension, as well as in healthy people, there is a decrease in aldosterone levels due to inhibition of the conversion of angiotensin I to angiotensin II. In patients with primary aldosteronism, the concentration of aldosterone is increased, the ratio of aldosterone/renin activity is more than 50.

5. Spironolactone test. The patient is on a diet with a normal sodium chloride content (6 g per day) and receives the aldosterone antagonist aldactone (veroshpiron) 100 mg 4 times a day for 3 days. On the 4th day, the potassium content in the blood serum is determined, and an increase in its blood level by more than 1 mmol / l compared to the initial level confirms the development of hypokalemia due to excess aldosterone. The level of aldosterone and renin in the blood remains unchanged. Arterial hypertension is eliminated.

6. Test with non-aldosterone mineralocorticoids. The patient takes 400 mcg of fluorocortisol acetate for 3 days or 10 mg of deoxycorticosterone acetate for 12 hours. The level of aldosterone in the blood serum and the excretion of its metabolites in the urine do not change with primary aldosteronism, whereas with secondary hyperaldosteronism it decreases significantly. In some cases, there is a slight decrease in the level of aldosterone in the blood, also with aldosterome.

7. Test with DOX. Prescribe DOXA 10-20 mg/day for 3 days. In patients with secondary hyperaldosteronism, the level of aldosterone decreases, but in Cohn syndrome - not. Levels of glucocorticosteroids and androgens are normal.

8. Orthostatic test (walking for 4 hours). Unlike healthy people, aldosterone levels paradoxically decrease.

9. Topical diagnosis of adrenal lesions. Aldosteroma adenomas are small in size, less than 3 cm in diameter in 80% of patients, and are often located in the left adrenal gland.

10. Computed tomography is the most informative study with high sensitivity. In 90% of patients, tumors with a diameter of 5-10 mm are detected.

11. Scanning of the adrenal glands with I-131-iodine-cholesterol against the background of inhibition of glucocorticoid function by dexamethasone (0.5 mg every 4 hours for 4 days). Asymmetry of the adrenal glands is characteristic. Sensitivity - 85%.

12. Catheterization of the adrenal veins with bilateral selective blood sampling and determination of aldosterone levels in them. The sensitivity of the study increases after preliminary stimulation of the adenoma with synthetic ACTH - the production of aldosterone on the tumor side increases sharply. The sensitivity of the study is 90%.

13. X-ray contrast venography of the adrenal glands - the sensitivity of the method is 60%: the vascularization of the tumor is insignificant, the size is small.

14. Echography of the adrenal glands.

15. Suprarenorography under conditions of pneumoretroperitonium, combined with or without intravenous urography. The method is informative only for large tumors and more often gives false negative results. The small size of the aldosteres, located inside, rarely change the contours of the adrenal glands.

Differential diagnosis

1. Secondary aldosteronism (hyperreninemic hyperaldosteronism) - conditions in which increased formation of aldosterone is associated with long-term stimulation of its secretion by angiotensin II. Secondary aldosteronism is characterized by increased levels of renin, angiotensin and aldosterone in the blood plasma. Activation of the renin-angiotensin system occurs due to a decrease in effective blood volume while simultaneously increasing the negative balance of sodium chloride. Develops with nephrotic syndrome, liver cirrhosis in combination with ascites, idiopathic edema, which often occurs in premenopausal women, congestive heart failure, and renal tubular acidosis.

2. Barter syndrome: hyperplasia and hypertrophy of the juxtaglomerular apparatus of the kidneys with hyperaldosteronism. Excessive potassium loss in this syndrome is associated with changes in the ascending tubules and a primary defect in chloride transport. Characterized by dwarfism, mental retardation, and the presence of hypokalemic alkalosis with normal blood pressure.

3. Tumors that produce renin (primary reninism), including Wilms tumors (nephroblastoma) - secondary aldosteronism occurs with arterial hypertension. Malignant hypertension with damage to the vessels of the kidneys and retina is often combined with increased secretion of renin and secondary aldosteronism. Increased renin formation is associated with the development of necrotizing renal arteriolitis. After nephrectomy, both hyperaldosteronism and hypertension disappear.

4. Long-term use of thiazide diuretics for arterial hypertension causes secondary aldosteronism. Therefore, determination of the level of renin and aldosterone in the blood plasma should be carried out only 3 weeks or later after discontinuation of diuretics.

5. Long-term use of contraceptives containing estrogen leads to the development of arterial hypertension, an increase in the level of renin in the blood plasma and secondary aldosteronism. The increase in renin formation is associated with the direct effect of estrogens on the liver parenchyma and an increase in the synthesis of the protein substrate - angiotensinogen.

6. Pseudomineralocorticoid hypertensive syndrome is accompanied by arterial hypertension, a decrease in the content of renin and aldosterone in the blood plasma. It develops with excessive consumption of glycyrrlisic acid preparations (glycyram, sodium glycyrinate), contained in the rhizomes of Ural licorice or licorice glabra.

7. Liddle syndrome is a hereditary disease accompanied by increased sodium reabsorption in the renal tubules with the subsequent development of arterial hypertension, a decrease in the content of potassium, renin and aldosterone in the blood.

8. Ingestion or excess production of deoxycorticosterone in the body leads to sodium retention, excess potassium excretion and hypertension. With a congenital disorder of cortisol biosynthesis distal to 21-hydroxylase, namely with deficiency of 17a-hydroxylase and 11b-hydroxylase, excessive formation of deoxycorticosterone occurs with the development of the corresponding clinical picture.

9. Hypertension with a low content of renin in the blood plasma (low-renin arterial hypertension) accounts for 20-25% of all patients suffering from this disease. The use of steroidogenesis inhibitors in hypertensive patients with low renin levels led to normalization of blood pressure, whereas in hypertensive patients with normal renin levels such treatment was ineffective. Normalization of blood pressure was observed in such patients after bilateral total adrenalectomy. It is possible that low-renin hypertension is a hypertensive syndrome that develops due to excess secretion of as yet unidentified mineralocorticoids.

Increased aldosterone levels (hyperaldosteronism) are one of the causes of increased blood pressure, cardiovascular complications, decreased kidney function and changes in electrolyte ratios. Primary and secondary hyperaldosteronism are classified, based on different etiological factors and pathogenetic mechanisms. The most common cause of the development of the primary type of pathology is Conn's syndrome.

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Conn's syndrome

Conn's syndrome– a disease that occurs due to increased production of aldosterone by a tumor of the adrenal cortex. In the structure of primary aldosteronism (PGA), the incidence of this pathology reaches 70% of cases, so some people combine these concepts. According to the latest data, among patients with arterial hypertension that is difficult to treat with medication, Conn's syndrome occurs in 5-10% of cases. Women get sick 2 times more often, while the onset of the pathology is gradual, symptoms appear after 30-40 years.

The concept and causes of primary and secondary hyperaldosteronism:

	Primary hyperaldosteronism	Secondary hyperaldosteronism
Definition	A syndrome that develops as a result of excessive production of aldosterone by the adrenal cortex (rarely an aldosterone-producing tumor of extra-adrenal localization), the level of which is relatively independent of the renin-angiotensin-aldosterone system (RAAS) and is not suppressed by sodium load	A syndrome resulting from a decrease in colloid osmotic blood pressure and stimulation of the RAAS (as a complication of a number of diseases)
Causes	The disease is associated with pathology of the adrenal glands: aldosterone-producing adenoma (Conn's syndrome) – 70%; bilateral hyperplasia of the zona glomerulosa of the adrenal cortex (idiopathic hyperaldosteronism) – up to 30%; rare diseases (aldosterone-producing carcinoma, unilateral hyperplasia of the zona glomerulosa of the adrenal cortex, familial hyperaldosteronism types I, II, III, MEN – I).	Associated with pathology of other organs and systems: kidney diseases (nephrotic syndrome, renal artery stenosis, kidney tumors, etc.); heart disease (congestive heart failure); other causes (hypersecretion of ACTH, taking diuretics, liver cirrhosis, fasting)

Etiology

The most common location of aldosterone-producing adenoma is the left adrenal gland. The tumor is solitary, does not reach large sizes (up to 3 cm), and is benign in nature (malignant aldosteromas occur extremely rarely).



CT scan of the abdomen. Adrenal adenoma



Pathogenesis

Aldosterone is a mineralocorticoid hormone produced by the adrenal cortex. Its synthesis occurs in the zona glomerulosa. Aldosterone plays a leading role in regulating water and electrolyte balance in the body. Its secretion is controlled mainly by the PAA system.

Excess aldosterone plays a major role in the pathogenesis of Conn's syndrome. It promotes increased excretion of potassium by the kidneys (hypokalemia) and sodium reabsorption (hypernatremia), leading to alkalization of the blood (alkalosis). Sodium ions accumulate fluid in the body, increasing the circulating blood volume (CBV), which entails an increase in blood pressure. High blood volume suppresses renin synthesis by the kidney. Long-term loss of potassium ions subsequently leads to nephron dystrophy (potassium-penic kidney), arrhythmias, myocardial hypertrophy, and muscle weakness. It is noted that the risk of sudden death from cardiovascular accidents increases sharply in patients (on average 10–12 times).






Clinic

Symptoms of primary hyperaldosteronism develop gradually. Patients with Conn's syndrome are diagnosed with:

• persistent increase in blood pressure, resistant to drug treatment in the medical history;
• headache;
• heart rhythm disturbances due to potassium deficiency, bradycardia, the appearance of a U wave on the ECG;
• neuromuscular symptoms: weakness (especially in the calf muscles), cramps and paresthesia in the legs, tetany may occur;
• renal dysfunction (hypokalemic nephrogenic diabetes insipidus): increased urine volume per day (polyuria), predominance of nighttime diuresis over daytime (nocturia);
• thirst (polydipsia).

Secondary aldosteronism is expressed in manifestations of the underlying disease; arterial hypertension and hypokalemia may not be present; the presence of edema is characteristic.

Diagnostics

Diagnosis of Conn's syndrome is recommended in persons with arterial hypertension that is not amenable to drug therapy, with a combination of increased blood pressure and hypokalemia (identified by clinical symptoms or blood test results), with the onset of hypertension before 40 years of age, with a family history of cardiovascular diseases , as well as if relatives have a confirmed diagnosis of PHA. Laboratory diagnosis is quite difficult and requires confirmation using functional tests and instrumental research methods.

Laboratory research

After forming a risk group, patients are determined:

• blood plasma aldosterone level (increased by 70%);
• blood potassium (decrease in 37-50% of patients);
• plasma renin activity (PRA) or its direct concentration (PCR) (decrease in most patients);
• Aldosterone-renin ratio (ARR) is a mandatory screening method.

Obtaining reliable results of the APC level depends on the preparation of the patient before the analysis and compliance with the blood sampling conditions according to the protocol. The patient should eliminate Veroshpiron and other diuretics, licorice medications at least a month in advance, and other medications that affect the level of aldosterone and renin about 2 weeks in advance: beta-blockers, ACE inhibitors, AR I blockers, central a-adrenergic agonists, NSAIDs, inhibitors renin, dihydropyridines. Hypertension control should be carried out using drugs with minimal effect on aldosterone levels (Verapamil, Hydralazine, Prazosin hydrochloride, Doxazosin, Terazosin). If a patient has a malignant course of hypertension and the withdrawal of antihypertensive drugs can lead to serious consequences, ARS is determined against the background of their use, taking into account the error.

Medicines that affect the results of ARS:

In addition to taking various medications, there are other factors that affect the interpretation of results :

• age > 65 years (renin levels decrease, leading to overestimation of APC values);
• time of day (the study is carried out in the morning);
• the amount of salt consumed (usually not limited);
• dependence on body position (when waking up and moving to a vertical position, the level of aldosterone increases by a third);
• marked decrease in kidney function (ARS increases);
• in women: the phase of the menstrual cycle (the study is carried out in the follicular phase, since physiological hyperaldosteronemia occurs in the luteal phase), taking contraceptives (decreased plasma renin), pregnancy (decreased APC).

If APC is positive, one of the functional tests is recommended. If a patient has spontaneous hypokalemia, renin is not detected, and the aldosterone concentration is above 550 pmol/l (20 ng/dl), the diagnosis of PHA does not need to be confirmed by stress testing.

Functional tests to determine aldosterone levels:

Functional tests	Methodology	Interpretation of test results
Sodium load test	Within three days, salt intake increases to 6 g per day. It is necessary to control daily sodium excretion and normalize potassium levels with the help of medications. Daily aldosterone excretion (DAE) is determined on the third day of the study in the morning	PGA is unlikely – SEA< 10 мг или 27,7 нмоль (исключить ХПН); PHA is highly probable – SEA >12 mg (>33.3 nmol)
Test with 0.9% sodium chloride solution	In the morning, administer an intravenous infusion of 2 liters of 0.9% solution over 4 hours (provided you are in a supine position one hour before). Blood test for aldosterone, renin, cortisone, potassium at the beginning of the test and after 4 hours. Monitor blood pressure and pulse rate. Option 2: the patient takes a sitting position 30 minutes before and during the infusion	PHA is unlikely with post-infusion aldosterone levels< 5 нг/дл; Doubtful - from 5 to 10 ng/dl; PGA is probable at levels > 10 ng/dL (sitting > 6 ng/dL)
Captopril test	Captopril at a dose of 25-50 mg one hour after waking up. Aldosterone, ARP and cortisol are determined before taking Captopril and after 1-2 hours (all this time the patient must be in a sitting position)	The norm is a decrease in aldosterone levels by more than a third from the initial value. PHA - aldosterone remains elevated with low ARP
Suppression test with fludrocortisone	Taking 0.1 mg fludrocortisone 4 times a day for 4 days, potassium supplements 4 times a day (target level 4.0 mmol/l) with unlimited salt intake. On the 4th day at 7.00 am, cortisol is determined, at 10.00 - aldosterone and ARP while sitting, cortisol is repeated	For PHA – aldosterone > 170 pmol/l, ARP< 1 нг/мл/ч; Cortisol at 10:00 is not lower than at 7:00 (excluding the influence of cortisol)

Instrumental studies

Carry out to all patients after receiving the results of laboratory tests:

• Ultrasound of the adrenal glands - detection of tumors more than 1.0 cm in diameter.
• CT scan of the adrenal glands - with an accuracy of 95% determines the size of the tumor, shape, topical location, differentiates benign neoplasms and cancer.
• Scintigraphy - with aldosteroma there is a unilateral accumulation of 131 I-cholesterol, with adrenal hyperplasia - accumulation in the tissue of both adrenal glands.
• Catheterization of the adrenal veins and comparative selective venous blood sampling (CVBS) - allows you to clarify the type of primary aldosteronism, is the preferred method for the differential diagnosis of unilateral aldosterone secretion in adenoma. Based on the ratio of aldosterone and cortisol levels on both sides, the lateralization gradient is calculated. The indication for this is to clarify the diagnosis before surgical treatment.
Differential diagnosis

Differential diagnosis of Conn's syndrome is carried out with idiopathic hyperplasia of the adrenal cortex, with secondary hyperaldosteronism, essential hypertension, endocrine diseases accompanied by increased blood pressure (Itsenko-Cushing syndrome, pheochromocytoma), with a hormonally inactive neoplasm and cancer. A malignant aldosterone-producing tumor on CT can reach large sizes and is characterized by high density, inhomogeneity, and blurred contours.

Differential diagnosis:

	Conn's syndrome (aldosterone-producing adenoma)	Idiopathic hyperaldosteronism	Secondary hyperaldosteronelowness
Laboratory indicators		aldosterone, ↓↓renin, ARS, ↓potassium	aldosterone, renin, - APC, ↓potassium
Orthostatic (march) test - study of aldosterone levels upon awakening in a horizontal position, repeated study after being in a vertical position (walking) for 3 hours	High aldosterone levels initially, some decrease with repeated testing, or at the same level	Increased aldosterone levels (maintained sensitivity to AT-II)	Increased aldosterone levels
CT	small mass formation of one of the adrenal glands	the adrenal glands are not changed, or there are small nodular formations on both sides	The adrenal glands are not enlarged, the size of the kidneys may be reduced
Catheterization of adrenal veins with selective blood sampling	Lateralization	-	-

Treatment

For aldosteroma, laparoscopic adrenalectomy is performed (after 4 weeks of preoperative preparation on an outpatient basis). Drug treatment is carried out for contraindications to surgery or for other forms of hyperaldosteronism:

• The main pathogenetic treatment is aldosterone antagonists - Veroshpiron 50 mg 2 times a day with an increase in dose after 7 days to 200 - 400 mg / day in 3-4 doses (maximum up to 600 mg / day);
• To lower blood pressure levels - Dihydropyridines 30–90 mg/day;
• Correction of hypokalemia - potassium supplements.



Spironolactone is used to treat idiopathic HA. To reduce blood pressure, it is necessary to add saluretics, calcium antagonists, ACE inhibitors and angiotensin II antagonists. If differential diagnosis reveals glucocorticoid-suppressed hyperaldosteronism, dexamethasone is prescribed.

– 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 heart rhythm disturbances, blurred vision, muscle weakness, paresthesia, and convulsions are observed. With secondary hyperaldosteronism, peripheral edema, chronic renal failure, and fundus changes develop. Diagnosis of various types of hyperaldosteronism includes biochemical analysis of blood and urine, functional stress tests, ultrasound, scintigraphy, MRI, selective venography, examination of the heart, liver, kidneys and renal arteries. Treatment of hyperaldosteronism in aldosteroma, adrenal cancer, and renal reninoma is surgical; in other forms, it is medicinal.

ICD-10

E26

General information

Hyperaldosteronism includes a whole complex of syndromes, different in pathogenesis, but similar in clinical signs, occurring with excessive secretion of aldosterone. Hyperaldosteronism can be primary (caused by pathology of the adrenal glands themselves) and secondary (caused by hypersecretion of renin 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 years; A few cases of hyperaldosteronism among children have been described.

Causes of hyperaldosteronism

Depending on the etiological factor, several forms of primary hyperaldosteronism are distinguished, 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 beyond the control of the renin-angiotensin system and corrected by glucocorticoids (occurs in young patients with frequent cases of arterial hypertension in the family history). In rare cases, primary hyperaldosteronism may be caused by adrenal cancer, which can produce aldosterone and deoxycorticosterone.

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

Increased renin secretion and the development of secondary hyperaldosteronism are caused by sodium loss (due to diet, diarrhea), a decrease in circulating blood volume due to blood loss and dehydration, excessive potassium consumption, and long-term use of certain medications (diuretics, COCs, laxatives). Pseudohyperaldosteronism develops when the response of the distal renal tubules to aldosterone is impaired, when, despite its high level in the blood serum, hyperkalemia is observed. Extra-adrenal hyperaldosteronism is observed quite rarely, for example, in pathologies of the ovaries, thyroid gland and intestines.

Pathogenesis

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

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

Secondary (high aldosteronism) hyperaldosteronism occurs compensatory, in response to a decrease in the volume of renal blood flow in various diseases of the kidneys, liver, and heart. Secondary hyperaldosteronism develops due to 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. Severe electrolyte disturbances characteristic of primary hyperaldosteronism do not occur in the secondary form.

Symptoms of hyperaldosteronism

The clinical picture of primary hyperaldosteronism reflects disturbances in water and electrolyte balance caused by hypersecretion of aldosterone. Due to sodium and water retention, patients with primary hyperaldosteronism experience severe or moderate arterial hypertension, headaches, aching pain in the heart (cardialgia), heart rhythm disturbances, changes in the fundus of the eye with deterioration of visual function (hypertensive angiopathy, angiosclerosis, retinopathy).

Potassium deficiency leads to rapid fatigue, muscle weakness, paresthesia, seizures in various muscle groups, periodic pseudoparalysis; in severe cases - to the development of myocardial dystrophy, kalipenic nephropathy, nephrogenic diabetes insipidus. In 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 Barter syndrome and pseudohyperaldosteronism). Some patients experience asymptomatic hyperaldosteronism.

Diagnostics

Diagnosis involves differentiating various forms of hyperaldosteronism and determining 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 the secretion of aldosterone.

Primary hyperaldosteronism is characterized by an increase in the level of aldosterone in the blood serum, a decrease in plasma renin activity (PRA), 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 level of ARP (for 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 performed. In order to identify the familial form of hyperaldosteronism, genomic typing is performed using PCR. In hyperaldosteronism corrected by glucocorticoids, trial treatment with dexamethasone (prednisolone) is of diagnostic value, which eliminates the manifestations of the disease and normalizes blood pressure.

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 through studies of the condition of the heart, liver, kidneys and renal arteries (EchoCG, ECG, liver ultrasound, kidney ultrasound, Doppler ultrasound and duplex scanning of the renal arteries, multislice CT, MR angiography).

Treatment of hyperaldosteronism

The choice of method and tactics for treating hyperaldosteronism depends on the cause of aldosterone hypersecretion. Patients are examined by an endocrinologist, cardiologist, nephrologist, and ophthalmologist. Drug treatment with potassium-sparing diuretics (spirolactone) is carried out for various forms of hyporeninemic hyperaldosteronism (adrenal hyperplasia, aldosteroma) as a preparatory stage for surgery, which helps 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 administration of potassium supplements, is indicated.

Treatment of aldosteroma and adrenal cancer is surgical and consists of removing the affected adrenal gland (adrenalectomy) with 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 adrenalectomy in combination with subtotal resection of the left adrenal gland are ineffective. Hypokalemia disappears, but the desired hypotensive effect is absent (BP is normalized only in 18% of cases) and there is a high risk of developing acute adrenal insufficiency.

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

In the case of secondary hyperaldosteronism due to renal artery stenosis, to normalize blood circulation and kidney function, percutaneous x-ray endovascular balloon dilation, stenting of the affected renal artery, or open reconstructive surgery are possible. If renal 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 provides a high probability of recovery. Adrenal cancer has a poor prognosis.

In order to prevent hyperaldosteronism, constant clinical monitoring of persons with arterial hypertension, liver and kidney diseases is necessary; compliance with medical recommendations regarding medication and diet.

Primary hyperaldosteronism (Conn's syndrome)

What is primary hyperaldosteronism (Conn's syndrome) -

In 1955, Conn described a syndrome accompanied by arterial hypertension and a decrease in potassium levels in the blood, the development of which is associated with a tumor (adenoma) of the adrenal cortex that produces the hormone aldosterone. This pathology is called Conn's syndrome.

Primary hyperaldosteronism (Conn's syndrome)- a disease characterized by an increase in the secretion of aldosterone by the adrenal glands, manifested in a decrease in the activity of a specific substance - renin in the blood plasma - which plays an important role in regulating the functioning of the body, arterial hypertension and a decrease in potassium content in the blood. Later, many other cases of hyperplasia (excessive tissue growth and changes) of the adrenal cortex with increased aldosterone secretion were described, and now the term “primary hyperaldosteronism” is used both to describe Conn’s syndrome itself and other pathologies accompanied by hypersecretion of aldosterone, for example, cortical hyperplasia adrenal glands Currently, primary hyperaldosteronism (PHA), and in particular Conn's syndrome, is the most common cause of secondary arterial hypertension.

What provokes / Causes of primary hyperaldosteronism (Conn's syndrome):

Currently, two main causes of PHA, accompanied by an increase in aldosterone secretion, have been identified:

• unilateral aldosterone-producing tumor - adenoma or Conn's syndrome (50-60% of cases);
• bilateral adrenal hyperplasia or idiopathic hyperaldosteronism (40-50% of cases).

There are rare types of diseases and tumors that have similar symptoms, including hereditary diseases, accompanied by an increase in aldosterone concentrations.

Even less common are aldosterone-secreting adrenal cancers or ovarian tumors.

The most common cause of PHA is Conn's syndrome, and the adenoma usually does not exceed 3 cm in diameter, is unilateral and renin-independent. This means that aldosterone secretion is not affected by changes in body position. Less commonly, an adenoma may be renin-dependent (that is, aldosterone levels increase in an upright position). Conn's syndrome occurs in 50-60% of cases.

The remaining 40-50% of cases are due to bilateral adrenal hyperplasia, when aldosterone levels increase in an upright position. Less common is primary adrenal hyperplasia, in which aldosterone levels do not depend on body position, as in renin-independent adenoma.

Aldosterone can be secreted by tumors of extra-adrenal localization - in the kidneys or ovaries.

Symptoms of primary hyperaldosteronism (Conn's syndrome):

Complaints of patients with severe hypokalemia: fatigue, muscle weakness, muscle cramps, headaches and palpitations. Such patients may also experience increased thirst: as a result, they drink a lot, and polyuria (excreting a lot of urine) due to the so-called diabetes insipidus, which developed as a result of hypokalemia and corresponding changes in the kidneys due to the influence of aldosterone on them.

Relative hypocalcemia (decreased calcium levels in the blood) develops with the development of a feeling of numbness in the extremities and around the mouth, muscle spasms in the hands and feet and, to an extreme extent, spasm of the larynx with a feeling of suffocation and cramps. In this case, calcium supplements are not prescribed, since the total calcium content in the blood is normal, but due to hormonal imbalance, the balance of calcium in the body changes.

Long-term hypertension can lead to complications from the cardiovascular and nervous systems with all the accompanying symptoms.

Diagnosis of primary hyperaldosteronism (Conn's syndrome):

There are no specific manifestations of Conn's syndrome.

When patients develop heart failure, stroke, or intracranial hemorrhage due to increased blood pressure, corresponding symptoms appear.

Laboratory research

• Studies of sodium, potassium and calcium in the blood plasma (biochemical analysis) may show an increase in sodium in the blood, the presence of hypokalemia and “alkalinization” of the blood, which is a consequence of the effect of aldosterone on the kidneys. A relative decrease in calcium levels in the blood can also be easily detected. In almost 20% of patients, carbohydrate metabolism disorders (increased blood glucose levels) can be detected, although diabetes rarely develops. It should be noted that normal potassium levels in the blood do not exclude PHA. Studies show that 7 to 38% of patients with PHA have normal serum potassium levels. Hypokalemia develops when eating a significant amount of sodium.
• There is a characteristic decrease in the level of renin in the blood plasma in patients with PHA, and this figure does not rise above certain values ​​when diuretics are administered or when moving to an upright position (which usually occurs normally). Some experts suggest that an analysis of the level of renin in blood plasma should be considered a special test for detecting PHA. However, according to some data, low renin levels occur in 30% of patients with hypertension. Therefore, low plasma renin levels should not be considered a specific test for PHA.
• Determining the ratio of plasma aldosterone activity (AAP) to plasma renin activity (PRA) should be considered a sufficiently sensitive test for PGA. Possible drug interactions should be taken into account when performing the test.
• If the AAP/ARP ratio test is positive, additional tests are performed: determining the level of aldosterone in a daily urine sample, adjusted for the level of potassium in the blood serum (since these indicators influence each other).

Instrumental examination

• Computed tomography (CT) of the abdominal cavity. It is a mandatory examination method in the case of PGA. When a diagnosis of PHA is established, the purpose of CT is to determine the type of pathology and the possibility of its surgical treatment (adrenal adenoma or bilateral hyperplasia). CT scan determines the extent of the operation.
• Scintigraphy with 131-I-iodocholesterol is used to detect a unilateral functional (hormone-secreting) adrenal mass. However, this procedure is not widely used due to the need for careful preparation of the patient, high cost, and the fact that the method rarely detects formations larger than 1.5 cm in diameter.
• Magnetic resonance imaging (MRI). It is not more sensitive than CT.

Other diagnostic methods

Postural test (transition from a horizontal body position to a vertical one). Can be used in the clinic for the primary diagnosis of renin-dependent adrenal adenoma. Currently rarely used.

Due to the difficulty of differentiating the diagnosis between adrenal hyperplasia and adenoma, after a CT examination, a procedure for taking analysis directly from the adrenal vein can be performed. This involves inserting a catheter into the adrenal vein through a vein in the thigh. Blood tests are taken from both adrenal veins, as well as from the inferior vena cava. The level of aldosterone is determined after maximum ACTH stimulation.

Treatment of primary hyperaldosteronism (Conn's syndrome):

The main goal is to prevent complications due to hypokalemia and hypertension.

If in Conn's syndrome hypertension is corrected with unilateral adrenalectomy, then bilateral lesions are most often treated conservatively, since the effectiveness of unilateral or bilateral adrenalectomy is only 19%. In the case of adenoma, drug therapy is also carried out to control blood pressure and correct hypokalemia, which reduces the risk of subsequent surgery.

Main components of therapy:

• Sodium-restricted diet (< 2 г натрия в день), поддержание оптимальной массы тела, регулярные аэробные физические нагрузки.
• Treatment of hypokalemia and hypertension consists of potassium-sparing drugs such as spironolactone. Moreover, if hypokalemia disappears almost immediately, then reducing blood pressure may require 4-8 weeks of therapy. Additional administration of potassium supplements is not required. If, despite treatment, elevated blood pressure remains, second-line drugs are added to therapy.
• Second-line drugs are: diuretics, blood pressure-lowering drugs.

Surgery

Surgery is the main treatment method for Conn's syndrome. If possible, laparoscopic adrenalectomy is performed (see below).

In patients with Conn's syndrome, the effectiveness of future unilateral adrenalectomy in relation to arterial hypertension is indicated by a decrease in blood pressure in response to spironolactone in the preoperative period. Spironolactone is prescribed for at least 1-2 weeks (preferably 6 weeks) before surgery to reduce the risk of surgery, correct hypokalemia, and control blood pressure.

Please note that hypertension usually does not disappear immediately after surgery. Blood pressure gradually decreases over 3-6 months. Almost all patients note a decrease in blood pressure numbers after surgery. A long-term therapeutic effect is observed after unilateral adrenalectomy for Conn's syndrome in an average of 69% of patients.

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