What is the role of excretion of the daily acid load in the pathogenesis of metabolic acidosis?

Updated: Dec 08, 2020
  • Author: Christie P Thomas, MBBS, FRCP, FASN, FAHA; Chief Editor: Vecihi Batuman, MD, FASN  more...
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Excretion of the daily acid load (50-100 mEq of H+) occurs principally through H+ secretion by the apical H+/ATPase in α intercalated cells of the collecting duct.

HCO3- formed intracellularly is returned to the systemic circulation via the basolateral Cl-/HCO3- exchanger, AE1 (gene symbol SLC4A1), and H+ enters the tubular lumen via 1 of 2 apical proton pumps, H+/ATPase or H+ -K+/ATPase. The secretion of H+ in these segments is influenced by Na+ reabsorption in the adjacent principal cells of the collecting duct. The reabsorbed Na+ creates a relative lumen negativity, which decreases the amount of secreted H+ that back-diffuses from the lumen.

Hydrogen ions secreted by the kidneys can be excreted as free ions but, at the lowest achievable urine pH of 5.0 (equal to free H+ concentration of 10 µEq/L), would require excretion of 5000-10,000 L of urine a day. Urine pH cannot be lowered much below 5.0 because the gradient against which H+/ATPase has to pump protons (intracellular pH 7.5 to luminal pH 5) becomes too steep. A maximally acidified urine, even with a volume of 3 L, would thus contain a mere 30 µEq of free H+. Instead, more than 99.9% of the H+ load is excreted buffered by the weak bases NH3 or phosphate.

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