Anion gap vs non-AG metabolic acidosis?

[Daitong]

In AG metabolic acidosis, the bicarb forms with the H+, leaving the conjugate base, an anion free floating around, contributing to that unaccounted for ‘gap’.

However, in non-anion gap metabolic acidosis, we have a loss/waste of bicarb directly such as through diarrhea, but what replaces it so the AG does not rise? I’m assuming it must be the Cl- levels rising, but what is this due to? Greater NaCl retention, or the Cl shift, or another mechanism?


Please let me know and thanks in advance.

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[thehundredthone]

The former, i.e. mostly just Cl- retention because of HCO3- wasting since there is an HCO3-/Cl- exchange across the basolateral membrane in the renal tubules. No HCO3- to reabsorb means no Cl- to secrete. Note that this requires [Na] to be normal. (think about the formula for the anion gap)

 

[Jabbed]

Take a look at Na, K, HCO3 and Cl-. Na and K are right about what we expect (i.e., isosmolar reabsorption does not alter the net concentration. HCO3 decreases significantly because of the active reabsorption via the carbonic anhydrase mechanisms. Why oh why though does Cl concentration actually INCREASE in the tubular fluid of the PCT? Answer: to balance the electrochemical gradient produced by active HCO3 reabsorption?

Now to your point, what happens when there is less bicarbonate to reabsorb (i.e., non-anion gap acidosis)? There is no longer a need for the tubular [Cl] to be so high, so the relative concentration approximates closer to that of Na and K. Physiologically, this results in hyperchloremic metabolic acidosis.