Metabolic Acidosis and Renal Failure

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I'm wondering if someone can help me understand better exactly what kinds of metabolic states can lead to an acidosis in a patient with renal failure.

Specifically, I recently was involved in taking care of a patient who had bloodwork indicating metabolic acidosis for a number of days (pH hovering between 7.15-7.25, bicarb between 10-20, pCO2 mostly normal or a bit low). This is despite bicarb supplementation (oral, then IV gtt). Labs indicated slowly worsening renal function with Cr worsening from 5 to 8 or so. No dialysis yet. The patient was also simultaneously being treated for an infection and possible myxedema.

Here's where I get confused. The patient's anion gap was elevated, somewhere around 20. At the same time, the patient's lactic acid level was normal. We had no reason to suspect ketosis. No diarrhea. And no additional toxins or acidifying drugs that I know of.

So... my understanding has always been that a metabolic acidosis caused primarily by bicarb loss would be accompanied by a low or normal anion gap. The easy assumption for me to make given the normal lactic acid level was that the patient's acidosis was due to renal failure and likely due to renal bicarb loss.

But if the acidosis was primarily due to bicarb loss, then why the elevated anion gap?

Alternatively, if the anion gap did in fact indicate that some other acid was present in the patient, what acid was it?

The patient did have an elevated blood uric acid level (around 8). Could that cause a moderate to severe acidosis despite bicarb supplementation? Or does myxedema mess around with your electrolytes enough to alter the anion gap/prevent chloride for compensating for bicarb loss? Or am I missing something entirely?

Sorry for writing a novel. Could anyone help me understand this better?

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Uremia is in the MUDPILES, so an elevated uric acid puts that on the table. Too much bicarb can also make high gap acidosis persist or worsen.

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Uremia is in the MUDPILES, so an elevated uric acid puts that on the table. Too much bicarb can also make high gap acidosis persist or worsen.

Thanks for responding.

I was wondering if anyone has seen a blood uric acid level of 8 correspond to a pH in the 7.15-7.2 range without another acid present. It doesnt seem high enough to account for that pH to me, but i dont have a strong sense of how strong an acid it is.

Also, my understanding had been that bicarb administration during a high anion gap acidosis can contribute to the acidosis (like you said) but via encouraging the production of lactic acid. So im still surprised to see a normal LA level. Is this normal? Am i taking a rule of thumb too literally?

Thanks

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Good discussion. I don't think uremia (azotemia, whatever the nomenclature is currently) is diagnosed by an elevated uric acid alone; I believe it's some combination of Na, K, alk phos and total kidney function. I'd also be curious if the patient had a mixed picture like a hidden respiratory acidosis superimposed on the HAGMA that could be causing it to persist.

What efforts were made to improve renal function? And did you notice any changes as it improved (if it did at all) compared to before?

I'll have to review my bicarb-lactate controversy literature lol. Intensivists and ED docs seem to hate it now unless they're trying to push the pt away from an arrythmogenic acidosis.

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The patient is in metabolic acidosis due to renal failure. The high anion gap tell you that there is an excess of anion, or acids, in the blood. This is typical of renal failure. The anions typically in excess with high gap acidosis are considered unmeasured anions like lactate, phosphates, sulfates, urates, glycol, the list goes on and on. Yes low bicarb is part of the clinical picture with renal failure but you're giving it more attention than it deserves. You're correct in that the patients acidosis is due to renal failure, hence no elevated lactic( seen with sepsis), no serum ketone (seen with DKA). The pats renal failure is allowing acids to accumulate like the phosphates and ammonia and as you mentioned uric acid. The pt will need dialysis for the acidosis to improve.

Hope this helped.

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I'll have to review my bicarb-lactate controversy literature lol. Intensivists and ED docs seem to hate it now unless they're trying to push the pt away from an arrythmogenic acidosis.

Agreed, our docs really only it with hyperkalemia when we are trying to buy some time.

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