Diagnosis of primary hyperaldosteronism

Diagnosis of primary hyperaldosteronism, differential diagnosis of its various forms and from other hypertensive conditions, mainly low-renin hypertension, is not simple and requires a series of sequential studies and functional tests.

In severe and typical clinical presentations, primary diagnosis is based on low plasma potassium and ARP levels and high aldosterone levels.

With normal sodium content in the diet (120 mEq/24 h), potassium excretion is about 30 mmol/l. Potassium load (up to 200 mEq/24 h) sharply increases potassium excretion and worsens the patient's well-being (severe muscle weakness, abnormal heart rhythm). Conducting the test requires great caution.

In case of aldosteronomas, stimulating tests: orthostatic load (4-hour walk), 3-day diet with low (less than 20 mEq/24 h) sodium content or intake of active saluretics do not stimulate ARP, and the aldosterone level may even decrease. Basal ARP is determined on an empty stomach after a night's rest in a supine position, with a diet containing 120 mEq/24 h sodium. Introduction of spironolactones at 600 mg/day for 3 days does not change the level of aldosterone secretion and does not stimulate ARP (spironolactone test). The captopril test has significant diagnostic value. In patients with aldosteronomas, both at rest and after a 4-hour walk, the circadian rhythm of aldosterone is preserved, coinciding with the rhythm of cortisol, which indicates dependence on ACTH. The absence of this rhythm indicates the presence of a malignant tumor, not an aldosterone-producing adenoma.

In idiopathic hyperaldosteronism, the intensity of metabolic disorders is lower than in aldosteroma, the level of aldosterone is lower and the content of 18-hydroxycorticosterone is significantly (many times) lower. ARP is also suppressed, but it increases, as does the content of aldosterone, under orthostatic load and injections of angiotensin II. However, the stimulation effect is significantly less than in healthy individuals. The introduction of spironolactones stimulates both ARP and the level of aldosterone secretion.

However, a saline test (2 liters of isotonic solution administered over 2 hours) does not suppress the level of aldosterone secretion in either aldosteromas or idiopathic primary hyperaldosteronism.

The DOXA test (10 mg, intramuscularly every 12 hours for 3 days) does not affect the plasma aldosterone content in patients with aldosteronoma and in most patients with idiopathic primary hyperaldosteronism. Suppression in the DOXA test is observed in unspecified primary hyperaldosteronism and in hypertension. Table 26 summarizes the main differential diagnostic tests for primary hyperaldosteronism.

In carcinoma, the level of aldosterone in both plasma and urine may be very high. There is no response to all stimulating and suppressing tests, including ACTH.

When conducting differential diagnostics with various hypertensive conditions, first of all, hypertension with unstimulated ARP should be excluded (in 10-20% of patients with hypertension, potassium and aldosterone levels remain within normal limits).

Primary hyperaldosteronism is differentiated from various diseases or conditions that cause secondary hyperaldosteronism.

1. Primary renal pathology, in which the ARP can be low, normal, or high.
2. Malignant variant of hypertension.
3. Pheochromocytoma.
4. Bartter syndrome (primary hyperreninism).
5. Hypertensive conditions associated with the use of contraceptives that stimulate the renin-angiotensin-aldosterone system.

In cases where primary hyperaldosteronism is complicated by acute and chronic renal pathology (infection, nephrosclerosis), differential diagnosis is complicated by a decrease in renal clearance, aldosterone and (mainly) potassium.

It should also be remembered that the widespread use of diuretics in the treatment of hypertension causes hypokalemia, but the ARP increases.

Patients with clinically and biochemically proven hyperaldosteronism undergo topical diagnostics, which allows localizing the pathological process. There are a number of methods for this purpose.

1. Computer tomography is the most modern examination with high resolution, allowing even small tumors with a diameter of 0.5-1 cm to be detected in 90% of patients.
2. Scanning of the adrenal glands with ¹³¹ 1-19-iodocholesterol or with ¹³¹ 1-6b-iodomethyl-19-norcholesterol. This study is best performed against the background of inhibition of glucocorticoid function with dexamethasone (0.5 mg every 6 hours for 4 days preceding the study). In the presence of a tumor, there is asymmetry (lateralization) of isotope accumulation in the adrenal glands.
3. Arterio- or venography after preliminary administration of ¹³¹ 1-19-iodocholesterol.
4. Catheterization of the adrenal veins with bilateral selective blood sampling and determination of aldosterone levels. The sensitivity and information content of this method increase after preliminary stimulation with synthetic ACTH, which sharply increases the aldosterone level on the tumor side.
5. Adrenal ultrasound.
6. Pneumoretroperitoneumsuprarenorentgenography, combined with intravenous urography or without it; a method that is formally obsolete, but has not lost its practical (diagnostic) value even today, for example in carcinomas, when, due to the large size of the tumor, radioisotope studies do not provide its visualization.

The most informative is computed tomography. Invasive angiographic studies are more complicated for both the patient and the doctor, and are also less reliable. However, none of the modern methods provides 100% visualization. In this regard, it is advisable to use 2-3 of them simultaneously.

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