Symptoms of primary hyperaldosteronism

The clinical features of primary hyperaldosteronism are composed of severe electrolyte balance disorders, renal dysfunction and arterial hypertension. Along with general and muscular weakness, often the first reason to call a doctor, patients are concerned about headaches, thirst and increased, mostly night, urination. The change in the levels of potassium and magnesium increases neuromuscular excitability and causes periodic seizures of seizures of varying intensity. Characteristic of paresthesia in various muscle groups, twitching of the face muscles, positive symptoms of Khvostek and Tissaur.

The exchange of calcium, as a rule, does not suffer. There are periodic attacks of severe muscle weakness, up to the complete immobility of the lower extremities (pseudoparachic) lasting from several hours to several days. One of the indirect symptoms that are of diagnostic importance is a significant increase in electrical potential in the large intestine. Most of the symptoms of hyperaldosteronism (excluding hypertension) are nonspecific and are determined by hypokalemia and alkalosis.

The table summarizes the main symptoms of hyperaldosteronism (E. Glaz, based on the work of Conn, 1971). Attention is drawn to the asymptomatic course of the disease in 6% of patients and hypokalemia in 100%. At the same time, at present, normocalic forms of primary hyperaldosteronism are known. It is reported and about casuistic normotensive options of the disease, which retains all the other features of a typical primary hyperaldosteronism. The most important, and in the early stages often the only symptom is hypertension. Dominant in the clinical picture for many years, it can mask the signs of hyperaldosteronism. The existence of low-grade hypertensive disease (10-20% of all patients with hypertensive disease) makes it especially difficult to recognize primary hyperaldosteronism. Hypertension can be stable or combined with paroxysms. Its level rises with the duration and severity of the disease, but malignant course is noted infrequently. Hypertension does not respond to ortho-static stress, and in the Valsalva trial its level does not increase with primary hyperaldosteronism, unlike hypertension of another etiology. The introduction of spironolactones (veroshpiron, aldactone) in a daily dose of 400 mg for 10-15 days reduces hypertension simultaneously with the normalization of the potassium level. The latter occurs only in patients with primary hyperaldosteronism. The absence of this effect casts doubt on the diagnosis of primary hyperaldosteronism, excluding those patients who have severe atherosclerosis. In half of the patients, retinopathy is noted , but its course is benign, usually without signs of proliferation, degeneration and hemorrhage. Hypertension of the left ventricle and signs of its congestion on the ECG are noted in most cases. However, cardiovascular failure is not characteristic of primary hyperaldosteronism. Serious vascular changes occur only with a long-term unidentified diagnosis. Although hypokalemia and hypokalemic alkalosis are the basis of many symptoms of primary hyperaldosteronism, the level of potassium in the blood may fluctuate, so it is necessary to do a second analysis. Its content increases and even normalizes with a long low-salt diet and taking spironolactones. Hypernatremia is much less characteristic than hypokalemia, although sodium exchange and its content in cells is increased.

Symptoms of primary hyperaldosteronism (Connes syndrome)

Symptoms	Frequency,%	Symptoms	Frequency,%
Hypertension	100	Hypernatremia	65
Hypokalemia	100	Decreased glucose tolerance	60
Hypochloremic alkalosis	100
Increased levels of aldosterone	100	Headache	51
Low level of renin	100	Retinopathy	50
Proteinuria	85	Thirst	46
Hyposthenia, resistant to vasopressin	80	Paresthesia	24
		Periodic Pallas	21
Disruption of urine oxidation	80	Tetany	21
ECG changes	80	General weakness	19
Elevated levels of potassium in the urine	75	Pain in the muscles	10
Muscle weakness	73	Asymptomatic forms	6th
Night polyuria	72	Edema	3

Absence of pronounced and stable hypernatremia is associated with a decrease in the sensitivity of the renal tubules to the sodium-blocking effect of aldosterone with increased secretion and excretion of potassium.

However, this refractoriness does not apply to the cation exchange mechanism of the salivary, sweat glands and intestinal mucosa. The release of potassium is mainly carried out by the kidneys and to a lesser extent through sweat, saliva, and the gastrointestinal tract. This loss (70% of intracellular stores) reduces the level of potassium not only in plasma, but also in red blood cells, in cells of smooth and striated muscle. His urinary excretion, exceeding 40 meq / 24 h, raises suspicion of primary hyperaldosteronism. It should be noted that patients are not able to keep potassium in the body, taking it is ineffective, and a diet rich in sodium, boosts the release of potassium and aggravates clinical symptoms. On the contrary, sodium-depleted diet limits the excretion of potassium, its level in the blood increases markedly. Hypokalemic damage to the epithelium of the renal tubules against the background of general hypokalemic alkalosis disrupts a number of renal functions and mainly the mechanisms of urine oxidation and concentration. "Kaliopenic kidney" is insensitive to endogenous (and exogenous) vasopressin, whose level is compensatory and, in connection with high plasma osmolality, increases. Patients experience mild, periodic proteinuria, polyuria, nocturia, hypoisostenuria with a relative density of individual portions of urine of 1008-1012.

Refractory to the introduction of vasopressin. The reaction of urine is more often alkaline. At the initial stages of the disease, kidney disorders can be minor. Polydipsia with complex genesis is characteristic: compensatory - in response to polyuria, central - as a result of the influence of low potassium level on the center of thirst and reflex - in response to sodium retention in cells. Edema is not characteristic of primary hyperaldosteronism, since polyuria and the accumulation of sodium inside cells, and not in interstitium, do not contribute to fluid retention in the intercellular spaces. Along with this, for primary hyperaldosteronism, there is a specific increase in intravascular volume and its invariance when introducing a salt isotonic solution and even albumin. Stable hypervolemia in combination with high plasma osmolarity suppresses ARP. Histochemical studies reveal the disappearance of renin granulations in secretory cells of vas efferens, a decrease in renin activity in renal homogenates, and renal biopsy in patients. Low, non-stimulated ARP is the cardinal symptom of primary hyperaldosteronism in aldoste rum. The levels of secretion and excretion of aldosterone vary considerably in patients with primary hyperaldosteronism, but in most cases they are elevated, and the content of glucocorticoids and androgens is normal. The level of aldosterone and its immediate precursor is 18-hydroxycorticosterone higher for aldosteromas and lower for hyperplastic variants of primary hyperaldosteronism.

Long-term hypokalemia can cause a gradual decrease in the secretion of aldosterone. Unlike healthy people, its level falls paradoxically with orthostatic load (4-hour walking) and spironolactone therapy. The latter block the synthesis of aldosterone in the tumor. In the postoperative study, in patients who received long-term verospheron, the remote aldosterone-producing tissue does not respond to the addition of angiotensin II and ACTH. There are cases of an aldosterium producing non-aldosterone, and 18-oxycorticosterone. The possibility of development of primary hyperaldosteronism in connection with increased production of other mineralocorticoids: corticosterone, MLC, 18-oxycorticosterone or unknown yet steroids is not rejected. The severity of primary hyperaldosteronism is determined by the intensity of metabolic disorders, their prescription and the development of vascular complications. In general, the disease is characterized by a relative good flow.

[1], [2], [3], [4], [5]