demographics

• 5–12% of hypertensive patients
• Adrenal adenoma: female  > male (2:1)
• Adrenal hyperplasia: male  > female (4:1)

aetiology

• primary (Conn syndrome): Overproduction of aldosterone in the zona glomerulosa of the adrenals.

  • Most commonly due to:
    • Bilateral idiopathic hyperplasia of the adrenal glands (60%)
    • Adrenal adenoma or aldosteronoma (30%)
  • Less common causes :
    • Unilateral hyperplasia of one adrenal gland
    • Aldosterone-secreting carcinomas of the adrenal cortex
    • Familial hyperaldosteronism (FH-I)

• Secondary: Excessive activation of the renin angiotensin aldosterone system due to:

  • Renal artery stenosis
  • Renin-secreting tumor
  • Chronic kidney disease
  • Advanced CHF
  • Fibromuscular dysplasia
  • Liver cirrhosis
  • Diuretics, Laxative abuse

pathophysiology

increased aldosterone → increased ENaC in CD → increased Na+ reabsorption / retention → increased H2O retention → hypertension (suppresses RAAS)

Aldosterone Escape: evasion of Na+ retaining effects of inappropriately elevated aldosterone in conditions such as primary hyperaldosteronism and CHF.

• Na+/H2O retention → volume expansion → ANP secretion and pressure natriuresis → compensatory diuresis → “escape” from oedema formation and hypernatremia

Hypokalaemia / Metabolic Alkalosis: increased Na+ reabsorption → electronegative lumen → electrical gradient through open K+ channels → K+ excretion → hypokalaemia

• Hypokalaemia → metabolic alkalosis via efflux of K+ from intracellular space to extracellular space in exchange for H+ ions → more H+ intracellularly → increased pH

• Also H+ excretion from kidney in order to enable K+ reabsorption via H+/K+ antiporter

• Diabetes Insipidus – hypokalaemia → desensitisation of renal tubules to ADH → polyuria / polydipsia