Acetzaolamide Questions

[ray656712]

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FA says that CAI's are a cause of Type 2 RTA, in which the urine pH is <5.5. By inhibiting bicarb reabsorption in the PCT, CAI's alkalinize the urine....they are used clinically for this.

From what I understand, in type 2 RTA, as bicarb levels are depleted, the CD eventually starts pumping out H+ (hence the lower pH of the urine).

Is this what happens with CAI's as well? And if so, is it accurate to say that you only get a type 2 RTA with CHRONIC CAI use?

 

[slz1900]

I don't think it would have to be chronic CAI use. Acetazolamide works very fast. With most forms of proximal RTA there is still the ability to reabsorb bicarbonate, just at lower levels. Thus, initially the bicarb overwhelms the ability to CD ability to properly acidify urine, so there may be transient elevation in urine pH, however there is still a reabsorption threshold that is not that low (just to make up numbers, maybe you normally reabsorb all bicarb up to 26, and with proximal RTA that number is 15). The CD acification will happen normally, since there is no change in electrical gradient (normally you pee out chloride and retain bicarb, but in RTA 2 you pee out bicarb and retain chloride). Once you have peed your bicarb level down to 15, the acidification process will be normal. As for why I think acidosis would develop quickly, the answer is the chloride. You will increase passive reabsorption immediately, and the net effect of elevated chloride with no change in Na+ is an acidosis due to strong ion difference. Anyway, I may be wrong, but acetazolamide is used in icu setting sometimes and I don't believe it has a delayed onset with acid base changes.