Physiology · Renal Physiology (GFR, Tubular Function, Acid-Base, Concentration)

A patient with pyloric stenosis from peptic ulcer disease presents with vomiting of 3 weeks' duration. ABG shows pH 7.55, PaCO2 50 mmHg, HCO3- 42 mEq/L. The paradoxical aciduria in this setting results from:

  • A Hypokalaemia causing K+ to exit cells in exchange for H+ entry, acidifying urine
  • B Hypovolaemia activating aldosterone, driving H+ secretion in the collecting duct despite alkalosis
  • C Metabolic alkalosis directly stimulating H+ secretion by the proximal tubule
  • D Compensatory respiratory acidosis causing renal H+ excretion
Correct answer: B. Hypovolaemia activating aldosterone, driving H+ secretion in the collecting duct despite alkalosis

Explanation

Loss of HCl from repeated vomiting causes hypochloraemic, hypokalaemic metabolic alkalosis. Hypovolaemia strongly activates the renin-angiotensin-aldosterone system. Aldosterone stimulates H+ secretion by alpha-intercalated cells and Na+/H+ exchange in collecting ducts; despite systemic alkalosis, the kidney excretes an acid urine ('paradoxical aciduria') because volume conservation takes precedence over pH correction. Hypokalaemia contributes by shifting K+/H+ exchanges but volume depletion is the primary driver.

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

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