Hyperaldosteronism (Conn's syndrome)

Introduction

Hyperaldosteronism is a condition characterized by excessive production of aldosterone, a mineralocorticoid hormone produced by the zona glomerulosa of the adrenal cortex. Aldosterone plays a key role in the regulation of sodium, potassium and water balance.

Conn's syndrome refers specifically to primary hyperaldosteronism caused by autonomous secretion of aldosterone, most commonly due to an adrenal adenoma.

Excess aldosterone leads to sodium retention, potassium loss, metabolic alkalosis and hypertension.

Physiology of aldosterone

Adrenal gland

Aldosterone acts mainly on the distal tubules and collecting ducts of the kidney.

Its main effects are:

  • increased sodium reabsorption
  • increased water retention
  • increased potassium excretion
  • increased hydrogen ion excretion

Regulation of aldosterone secretion:

  • renin–angiotensin–aldosterone system (RAAS)
  • plasma potassium levels
  • adrenocorticotropic hormone (minor role)

Types of hyperaldosteronism

Primary hyperaldosteronism (Conn's syndrome)

Cause: autonomous secretion of aldosterone independent of RAAS.

Common causes:

  • adrenal adenoma (Conn's syndrome)
  • bilateral adrenal hyperplasia
  • rarely adrenal carcinoma

Hormonal profile:

  • ↑ aldosterone
  • ↓ renin

Secondary hyperaldosteronism

Cause: activation of RAAS due to decreased renal perfusion.

Common causes:

  • renal artery stenosis
  • heart failure
  • liver cirrhosis
  • nephrotic syndrome

Hormonal profile:

  • ↑ aldosterone
  • ↑ renin

Pathophysiology

Excess aldosterone leads to several key changes:

Sodium and water retention

Aldosterone increases sodium reabsorption in the kidneys. Water follows sodium, leading to:

  • expansion of extracellular fluid volume
  • increased blood volume
  • hypertension

Despite sodium retention, edema is usually mild due to a phenomenon called "aldosterone escape".

Potassium loss (hypokalemia)

RAAS

Increased potassium excretion leads to hypokalemia.

Consequences:

  • muscle weakness
  • fatigue
  • arrhythmias
  • impaired neuromuscular function

Metabolic alkalosis

Aldosterone increases hydrogen ion secretion in the distal nephron.

This leads to:

  • increased bicarbonate concentration
  • metabolic alkalosis

Hypertension

The combination of sodium retention and increased blood volume leads to persistent hypertension, which is often resistant to treatment.

Conn's syndrome

Conn's syndrome is a form of primary hyperaldosteronism caused by an aldosterone-producing adrenal adenoma.

Characteristics:

  • autonomous aldosterone secretion
  • suppressed renin levels
  • hypertension
  • hypokalemia
  • metabolic alkalosis

Patients often present with resistant hypertension and symptoms related to low potassium.

Clinical manifestations

  • hypertension (often resistant)
  • hypokalemia
  • muscle weakness
  • fatigue
  • polyuria and polydipsia
  • headaches
  • arrhythmias

In mild cases, hypokalemia may be absent.

Summary

Hyperaldosteronism is characterized by excessive aldosterone production leading to sodium retention, potassium loss and metabolic alkalosis. Primary hyperaldosteronism (Conn's syndrome) is caused by autonomous adrenal secretion, while secondary hyperaldosteronism results from increased RAAS activation. The main clinical features include hypertension, hypokalemia and metabolic alkalosis.

References

  1. Kumar V, Abbas AK, Aster JC. Robbins and Cotran Pathologic Basis of Disease.
  2. Hall JE. Guyton and Hall Textbook of Medical Physiology.
  3. AMBOSS. Hyperaldosteronism.
  4. Guyton and Hall: Renal regulation of electrolytes.