Hyperaldosteronism

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Overview

Hyperaldosteronism is characterised by excess levels of aldosterone and is the most common cause of curable secondary hypertension. It can be divided into two types:

  • Primary hyperaldosteronism:
    • Most commonly due to bilateral idiopathic adrenal hyperplasia
    • Secretion is independent of the renin-angiotensin-aldosterone system (RAAS)
  • Secondary hyperaldosteronism:

Conn’s syndrome is a form of primary hyperaldosteronism due to an adrenal adenoma. It was previously thought to be the most common cause, but recent studies demonstrate that bilateral idiopathic adrenal hyperplasia makes up most cases.

To help make sense of this chapter, it may be helpful to refer to Endocrine and Metabolic Physiology.

Renin-angiotensin-aldosterone system (RAAS)

The renin-angiotensin-aldosterone system (RAAS) system is a hormone system that regulates blood pressure, along with fluid and electrolytes. Reduced blood flow to the juxtaglomerular cells in the kidneys leads to the secretion of renin (an enzyme) into the circulation. The liver releases angiotensinogen, which is cleaved by renin to form angiotensin I. Angiotensin I is converted into angiotensin II by angiotensin-converting enzyme (ACE) predominantly in the lungs.

Angiotensin II leads to the following:

  • Vasoconstriction of vascular smooth muscle – increases blood pressure
  • Acts at the hypothalamus to stimulate ADH release and stimulates thirst
  • Acts on the renal tubules to increase Na+ and Cl- reabsorption, water retention, and K+ excretion
  • Acts on the adrenal gland cortex to release aldosterone

Aldosterone

Mineralocorticoids affect electrolyte and fluid balance, and aldosterone is the main endogenous mineralocorticoid. In summary, it retains sodium ions and increases the excretion of potassium ions. Since the sodium ions are retained, water follows, increasing the water content in the body. As there is a larger volume of fluid in the circulation, the blood pressure increases.

Epidemiology

  • Most common curable form of secondary hypertension
  • Around 70% of cases are due to idiopathic bilateral adrenal hyperplasia

Risk Factors

  • Family history

Presentation

Hyperaldosteronism should be considered in a patient with difficult-to-treat hypertension. Many patients may be asymptomatic. Features can be:

Differential Diagnoses

Primary hyperaldosteronism

  • Plasma aldosterone/renin ratio is elevated

Secondary hyperaldosteronism

  • Plasma aldosterone/renin ratio is reduced

Essential hypertension

  • Plasma aldosterone/renin ratio is normal if performed without medicines that may interfere with results (e.g. ACE inhibitors)

Investigations

  • Aldosterone/renin ratio:
    • If raised: primary hyperaldosteronism is the likely diagnosis (as there is more aldosterone than renin)
    • If reduced: secondary hyperaldosteronism is the likely diagnosis (e.g. due to renal artery stenosis as there is more renin than aldosterone)
  • U&Es:
    • May show hypokalaemia
  • Adrenal CT:
    • To look for any changes in adrenal gland structure (e.g. adenomas/hyperplasia)
  • Adrenal venous sampling (AVS):
    • Performed if the CT is normal. It can help to distinguish between bilateral idiopathic adrenal hyperplasia and an adrenal adenoma

Management

Primary hyperaldosteronism

  • If bilateral adrenal hyperplasia: aldosterone antagonist is 1st-line (e.g. spironolactone/eplerenone)
  • If an adrenal adenoma is present: consider surgery

Secondary hyperaldosteronism

  • 1st-line: manage underlying cause (e.g. renal artery stenosis)

Complications and Prognosis

Complications

Prognosis

  • The prognosis is generally good in patients with primary hyperaldosteronism that are receiving treatment. However, in many patients, they may need to continue treatment lifelong.

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