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Hyperaldosteronism – Causes, Symptoms & Treatment

Hyperaldosteronism is a condition in which the adrenal glands produce too much aldosterone, leading to high blood pressure and low potassium levels.

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Things worth knowing about "Hyperaldosteronism"

Hyperaldosteronism is a condition in which the adrenal glands produce too much aldosterone, leading to high blood pressure and low potassium levels.

What is Hyperaldosteronism?

Hyperaldosteronism is a hormonal disorder in which the adrenal glands produce excess amounts of the hormone aldosterone. Aldosterone is a mineralocorticoid that plays a key role in regulating the body´s salt and water balance. When aldosterone levels are too high, the kidneys retain too much sodium and water while excreting too much potassium, resulting in high blood pressure (hypertension) and low potassium levels (hypokalemia).

Causes

There are two main forms of hyperaldosteronism:

  • Primary hyperaldosteronism (Conn syndrome): Excess aldosterone is produced directly by the adrenal glands, independent of the normal regulatory system. The most common causes are a unilateral adrenal adenoma (a benign tumor) or bilateral adrenal hyperplasia (enlargement of both adrenal glands).
  • Secondary hyperaldosteronism: Elevated aldosterone production is a response to increased activation of the renin-angiotensin-aldosterone system (RAAS), triggered by external factors such as renal artery stenosis, heart failure, liver cirrhosis, or kidney disease.

Symptoms

Many people with hyperaldosteronism have no symptoms initially, or only vague complaints. Common symptoms include:

  • Persistently elevated blood pressure that responds poorly to standard antihypertensive medications
  • Muscle weakness and cramps due to low potassium
  • Fatigue and general lack of energy
  • Frequent urination and increased thirst (polyuria and polydipsia)
  • Headaches
  • In severe cases: cardiac arrhythmias caused by hypokalemia

Diagnosis

The diagnosis of hyperaldosteronism involves several steps:

Laboratory Tests

The first step is measuring the aldosterone-to-renin ratio (ARR) in the blood. An elevated ratio strongly suggests primary hyperaldosteronism. Blood potassium and sodium levels are also assessed.

Confirmatory Tests

Confirmatory tests are performed to verify the diagnosis, such as the saline infusion test or the fludrocortisone suppression test, which assess whether aldosterone production can be suppressed.

Imaging

Once the diagnosis is confirmed biochemically, a CT scan of the adrenal glands is performed to identify an adenoma or hyperplasia. An adrenal vein sampling (AVS) procedure may also be used to precisely determine which adrenal gland is overproducing aldosterone.

Treatment

Treatment depends on the underlying cause of the hyperaldosteronism:

Surgical Treatment

When a unilateral adrenal adenoma is identified, surgical removal of the affected adrenal gland (laparoscopic adrenalectomy) is the preferred approach. In many cases, blood pressure and potassium levels normalize significantly or completely after the procedure.

Medical Treatment

For bilateral adrenal hyperplasia or when surgery is not feasible, mineralocorticoid receptor antagonists are used. Spironolactone is the first-line medication, with eplerenone as an alternative. These drugs block the effects of aldosterone on the kidneys, lowering blood pressure and normalizing potassium levels.

Lifestyle Measures

In addition to medical or surgical treatment, a low-sodium diet, regular physical activity, and management of other cardiovascular risk factors are strongly recommended.

References

  1. Funder JW et al. - The Management of Primary Aldosteronism: Case Detection, Diagnosis, and Treatment. Journal of Clinical Endocrinology and Metabolism, 101(5):1889-1916, 2016.
  2. Williams B et al. - ESC/ESH Guidelines for the management of arterial hypertension. European Heart Journal, 39(33):3021-3104, 2018.
  3. Mattsson C, Young WF Jr. - Primary aldosteronism: diagnostic and treatment strategies. Nature Clinical Practice Nephrology, 2(4):198-208, 2006.

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