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Can anyone explain why RTA causes non-anion gap acidosis and CKD causes high anion gap acidosis?
Thank you
Thank you
RTA NAGMA V CKD HAGMA
- Thread starter coreytayloris
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No one? No step 1 genius willing to take up the mantle? 🙂
So as you know there are a few different types of RTA. I'll address type I and II since I think they are most salient here. So the basic idea with these is either you are not reabsorbing your bicarb enough in the proximal tubule (Type II [proximal]) and thus you have an increase in unbuffered H+ ions, or alternately you have a problem secreting your H+ ions in the distal tubules (Type I [distal]). I won't go into the causes and pathophysiology of these but there is a pretty decent explanation here https://medicine.ucsf.edu/education/resed/Chiefs_cover_sheets/renal tubular acidosis.pdf. Remember that with these the defect is in the tubules, this will come up later. So with these you can imagine that you will not get an anion gap acidosis because you are loosing bicarb and replacing it with chloride and such [type I] or with type II you are not excreting you H+ ions or making NH4+ sufficiently so again you have a build up of H+. And other acids are being filtered through the glomeruli as normalish.
Now, in CKD you are getting significant decrease in GFR because you are damaging glomeruli and everything (later in the disease). So, now you will get a buildup of waste product acids like H2SO4 which is from sulphur containing amino acids, and other such waste product acids. These then create the gap acidosis. Now note, this does not occur until later in the disease when the GFR drops below 20ml/min. Before that you would see a Cl- based non-anion gap metabolic acidosis similar to what is seen in RTA due to decreased ability to secrete NH4+ and reabsorb bicarb. Hopefully that helps. Here are some articles on it that may help as well. http://www.uptodate.com/contents/pa...-metabolic-acidosis-in-chronic-kidney-disease http://www.anaesthesiamcq.com/AcidBaseBook/ab8_3.php http://fitsweb.uchc.edu/student/selectives/TimurGraham/Uremia.html
Now, in CKD you are getting significant decrease in GFR because you are damaging glomeruli and everything (later in the disease). So, now you will get a buildup of waste product acids like H2SO4 which is from sulphur containing amino acids, and other such waste product acids. These then create the gap acidosis. Now note, this does not occur until later in the disease when the GFR drops below 20ml/min. Before that you would see a Cl- based non-anion gap metabolic acidosis similar to what is seen in RTA due to decreased ability to secrete NH4+ and reabsorb bicarb. Hopefully that helps. Here are some articles on it that may help as well. http://www.uptodate.com/contents/pa...-metabolic-acidosis-in-chronic-kidney-disease http://www.anaesthesiamcq.com/AcidBaseBook/ab8_3.php http://fitsweb.uchc.edu/student/selectives/TimurGraham/Uremia.html
Cations should equal anions for electrical neutrality, we have an anion gap since we're not measuring every single charged particle in the body. Consider:
Na + unmeasured cations (UC) = Cl + HCO3 + unmeasured anions (UA)
which would be
Na - (Cl + HCO3) = UA - UC
Measuring the left side of the equation gives us the answer to UA - UC, which is the anion gap and should normally be under 12, since there are more anions, as opposed to cations, that we don't measure. Big examples would be albumin, citrate, phosphate. So, eg, you'd have to adjust the AG downwards in hypoalbuminemia.
When you get MA due to losing HCO3 (eg RTA), the body replaces it with Cl. Fit this idea into the equation above, and you'll see the measured anion gap will stay normal.
When you get MA due to addition of an acid, you end up with an increase in the AG. Consider the body generating an excess of lactic acid, which dissociates to release H ions. This gets buffered by HCO3, which decreases and we end up with MA. However, the loss of the negative bicarbonate is balanced by the presence of the negatively charged conjugate base from lactic acid. Hence theres no need to increase Cl. Of the values measured in the equation above, HCO3 will decrease, and nothing else. Hence the measured AG increases.
To summarize,
normal AG = due to loss of HCO3
increased AG = due to addition of acid
Na + unmeasured cations (UC) = Cl + HCO3 + unmeasured anions (UA)
which would be
Na - (Cl + HCO3) = UA - UC
Measuring the left side of the equation gives us the answer to UA - UC, which is the anion gap and should normally be under 12, since there are more anions, as opposed to cations, that we don't measure. Big examples would be albumin, citrate, phosphate. So, eg, you'd have to adjust the AG downwards in hypoalbuminemia.
When you get MA due to losing HCO3 (eg RTA), the body replaces it with Cl. Fit this idea into the equation above, and you'll see the measured anion gap will stay normal.
When you get MA due to addition of an acid, you end up with an increase in the AG. Consider the body generating an excess of lactic acid, which dissociates to release H ions. This gets buffered by HCO3, which decreases and we end up with MA. However, the loss of the negative bicarbonate is balanced by the presence of the negatively charged conjugate base from lactic acid. Hence theres no need to increase Cl. Of the values measured in the equation above, HCO3 will decrease, and nothing else. Hence the measured AG increases.
To summarize,
normal AG = due to loss of HCO3
increased AG = due to addition of acid
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