In metabolic alkalosis, the renal threshold for bicarbonate reabsorption is normally exceeded. Which factor is most important in 'maintaining' metabolic alkalosis rather than allowing urinary bicarbonate excretion to correct it?
- A Volume depletion activating RAAS, which enhances proximal HCO3 reabsorption and distal H+ secretion ✓
- B Elevated aldosterone stimulating H+ secretion in the collecting duct
- C Hypokalemia shifting K+ out of cells and H+ into cells
- D Hypochloremia reducing Cl-dependent HCO3 secretion in the collecting duct
Explanation
Metabolic alkalosis is maintained primarily by volume depletion: low effective arterial volume activates the renin-angiotensin-aldosterone system and increases proximal tubular Na+ (and therefore HCO3) reabsorption, preventing the kidneys from excreting the excess bicarbonate. Chloride depletion (often the initiating cause, e.g., vomiting) also limits collecting duct HCO3 secretion via the pendrin Cl/HCO3 exchanger. Hypokalemia contributes by promoting H+ secretion but is secondary. The key clinical distinction is saline-responsive (volume-depleted) vs saline-resistant (mineralocorticoid excess) metabolic alkalosis.
Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.
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