In primary adrenal insufficiency (Addison disease), hyponatremia with hyperkalemia and metabolic acidosis occur due to mineralocorticoid deficiency. The specific ion transport mechanism in the cortical collecting duct that is lost when aldosterone is absent is:

• A Aldosterone-induced Na+/K+-ATPase activation on the apical membrane of principal cells
• B Aldosterone-induced Cl-/HCO3- exchange on the luminal surface of intercalated cells
• C Aldosterone-induced ENaC upregulation and increased ROMK K+ secretion with H+ secretion via H+-ATPase ✓
• D Aldosterone-induced NKCC2 upregulation in the thick ascending limb

Explanation

Aldosterone acts on principal cells of the cortical collecting duct via mineralocorticoid receptors to increase transcription of ENaC (epithelial sodium channel) subunits and ROMK (K+ secretory channels), and to upregulate basolateral Na+/K+-ATPase (not apical). Na+ reabsorption via ENaC creates a lumen-negative potential that drives K+ secretion via ROMK and H+ secretion via H+-ATPase on alpha-intercalated cells. Loss of aldosterone therefore causes Na+ wasting (hyponatremia), K+ retention (hyperkalemia), and H+ retention (metabolic acidosis) — the classic electrolyte triad of Addison disease.

Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.