how does acetazolamide cause hyperchloremia?

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axeon123

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I'm trying to figure out why (mechanism). Acidosis makes sense, and so does hypokalemia. Thanks.

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I think it's because carbonic anhydrase inhibitors prevent HCO3 reabsorption, so more sodium is being excreted as NaHCO3 instead of NaCl.
 
It causes a non-anion gap metabolic acidosis. As the negative bicarb is ridded by the kidney, another anion needs to fill its place in the serum, and this is done by Cl.
 
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What makes sense to me, but I could be totally wrong is:

Acidosis stimulates the release of aldosterone -> increase in activity of NaCl Cotransporter in early DCT-> Hyperchloremia
 
Lol, sorry to pick on you, but you couldn't be more wrong. I don't think there's one correct statement in there.

Technically, acidosis could INDIRECTLY stimulate Aldo via increased K+. But yeah, that response was certainly not correct (no offense to the poster).
 
every non-anion gap acidosis has hyperchloremia. it's inevitable, and unimportant

It causes a non-anion gap metabolic acidosis. As the negative bicarb is ridded by the kidney, another anion needs to fill its place in the serum, and this is done by Cl.

Thanks - these make the most sense. :)
 
Lol, sorry to pick on you, but you couldn't be more wrong. I don't think there's one correct statement in there.


Not even the part where I state "I could be totally wrong"?

Thanks for your input though, you're very helpful. :thumbup:
 
Recovered bicarb is transported into the blood across the basolateral membrane by HCO3/Cl exchanger. Decrease recovered bicarb and you decrease Cl exchange and thus secretion.
 
It may be due to the b intercalated cells at the collecting ducts that take in cl- and excrete hco3-. More hco3- in the tubule, less hco3 from intracellular side wants to go into the lumen of the tubule, and hence less cl- being excreted out.
 
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