How does RTA 1 and RTA 4 cause an increase in Chloride ions? they both cause an increase in H+, but by which mechanism is CL- increased?
@13Cyko38
5 жыл бұрын
and 1 more question: With intracellular buffering the pH is low. When renal compensation kicks in, is the pH going to be corrected towards normal? Or is it just closer to normal, but still below 7.35?
@PathophyswithMac
5 жыл бұрын
Good question! In RTA-4 (low aldost. And hypovol.) The trick in proximal tubule works more in order to reabsorb Na (for volume) so u might end up with more Cl coming along Na. As for RTA-1 (it's not clear why) but it seems TO ME that in the hypokalemic type there will be increased Aldost. (Hypokalemia increases aldost. And Hyper-K decreases Aldost.) So as Na is reabsorbed Cl tags along. 😉
@PathophyswithMac
5 жыл бұрын
2. Actually, it depends on the extent of the acidosis. If it's mild then it goes back to normal, if not or it persists for too long then it only comes close to 7.35 initially then drops down again.
@13Cyko38
5 жыл бұрын
Thanks for the reply. Lets say we have chronic respiratory acidosis, and the kidneys compensate after a few days by forming new HCO3-. The pH is now in normal range again - are we still saying the patient has acidosis? In other words: Is acidosis/alkalosis dependent on the blood pH?
@13Cyko38
5 жыл бұрын
And I still dont understand why you would end up with more Cl- in RTA 4. In our slides it sais something with reduced ammonia genesis. So what i though is: 1. RTA 4 causes Hyperkalemia 2. Hyperkalemia (H+/K+ Exchange) causes increase in IC pH 3. Increased IC pH leads to decreased ammonia genesis. 4. Thuss there is Less ammonium in the tubule -> less NH4CL can be formed and thus less Cl - is excreted. Does this make any sense?
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