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Hyperaldosteronism is a hormonal disorder characterised by the overproduction of aldosterone. This condition can lead to decreased potassium levels in the blood (hypokalaemia) and increased hydrogen ion excretion (alkalosis). Aldosterone is normally produced in the adrenal glands, and its excessive production can be categorised into primary and secondary hyperaldosteronism.

Aldosterone is a hormone produced by the adrenal glands, very important for maintaining blood pressure and electrolyte balance.

Signs and Symptoms

Hyperaldosteronism may be asymptomatic, but when symptoms are present, they can include:

  • Fatigue
  • Headache
  • High blood pressure
  • Hypokalaemia
  • Hypernatraemia
  • Hypomagnesaemia
  • Intermittent or temporary paralysis
  • Muscle spasms
  • Muscle weakness
  • Numbness
  • Polyuria (frequent urination)
  • Polydipsia (excessive thirst)
  • Tingling
  • Metabolic alkalosis


Primary Hyperaldosteronism

Primary aldosteronism, or hyporeninaemic hyperaldosteronism, is most often caused by bilateral idiopathic adrenal hyperplasia (nearly 70% of cases) and adrenal adenoma, also known as Conn's syndrome (about 30% of cases). These conditions result in the hyperplasia of aldosterone-producing cells in the adrenal cortex.

Two familial forms have been identified:

  • Type I: Dexamethasone suppressible
  • Type II: Linked to the 7p22 gene

Secondary Hyperaldosteronism

Secondary hyperaldosteronism, also known as hyperreninism or hyperreninaemic hyperaldosteronism, results from overactivity of the renin–angiotensin–aldosterone system (RAAS). Causes include:

  • Accessory renal veins
  • Fibromuscular dysplasia
  • Reninoma
  • Renal tubular acidosis
  • Nutcracker syndrome
  • Ectopic tumours
  • Massive ascites
  • Left ventricular failure
  • Cor pulmonale

These conditions either decrease circulating fluid volume or cardiac output, leading to increased renin release and subsequent secondary hyperaldosteronism. Genetic mutations causing sodium and potassium wasting in the kidneys can also lead to conditions like Bartter syndrome and Gitelman syndrome.


Pseudohyperaldosteronism mimics hyperaldosteronism without increasing aldosterone levels. It can be caused by excessive ingestion of licorice or plants from the Glycyrrhiza genus, which contain glycyrrhizin. This compound inhibits 11-beta-hydroxysteroid dehydrogenase type 2 (11-beta-HSD2), allowing cortisol to activate mineralocorticoid receptors in the kidney, leading to renal sodium reabsorption, expanded extracellular volume, increased peripheral resistance, and elevated arterial blood pressure.


Diagnosis involves blood tests where the aldosterone-to-renin ratio is abnormally increased in primary hyperaldosteronism and decreased or normal but with high renin in secondary hyperaldosteronism.


Treatment strategies depend on the underlying cause and may include:

  • Removing causative agents such as licorice
  • Dietary modifications: high-potassium, low-sodium diet for primary; high-sodium diet for secondary
  • Medications: Spironolactone and eplerenone, which are potassium-sparing diuretics that act as aldosterone antagonists
  • Surgery: Sometimes required for adrenal adenomas

Self-assessment MCQs (single best answer)

Which hormone is overproduced in hyperaldosteronism?

What electrolyte imbalance is commonly seen in hyperaldosteronism?

Which of the following is NOT a symptom of hyperaldosteronism?

What is the most common cause of primary hyperaldosteronism?

Which genetic mutation is associated with familial hyperaldosteronism type II?

Secondary hyperaldosteronism is often caused by overactivity of which system?

Pseudohyperaldosteronism can be caused by excessive ingestion of which compound?

Which diagnostic test is used to confirm hyperaldosteronism?

Which medication is commonly used to treat hyperaldosteronism by acting as an aldosterone antagonist?

In hyperaldosteronism, what dietary modification is recommended for primary hyperaldosteronism patients?


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