Monday, November 24, 2008

Renal Tubular Acidosis


Oy. These are kind of tricky. Let’s work through it.

Okay…let’s say we have already established that we have a metabolic acidosis, and that the anion gap is not elevated (nor is the osmolar gap). Fine. The next step is to look at the urine anion gap.

Urine Anion Gap (UAG) = [Urine Na + Urine K] – [Urine Cl]

The whole goal of this UAG business is to see how the kidneys are processing NH4+ . The UAG really is a surrogate measurement for NH4+ because we don’t measure it directly. Think about this for a second…if there is lots of NH4+, then we would expect more anions to balance out that positive charge (like more Cl-). So if the UAG is negative, it means we have more Cl than Na and K in the urine and that there is good kidney processing of NH4+. The kidneys are working well here, so think about non-renal causes to your non-anion gap metabolic acidosis – like diarrhea.

Now what if the UAG is positive? Well, then there is a failure of the kidneys to secrete NH4+ in this situation, causing a non-anion gap metabolic acidosis.

Type 1 RTA (distal): usually a more sever metabolic acidocis with HCO3 commonly less than 17 mmol/L from defective H+ secretion. Common etiologies include lupus, Sjogren’s syndrome, multiple myeloma, and medications such as amphotericin.

Type 2 RTA (proximal): less severe acidosis with HCO3 typically above 17 mmol/L. Common etiologies include multiple myeloma, amyloidosis, heavy metal poisoning, and medications like tenofovir, aminoglycosides. You can read more about this here.

Type 4 RTA: this is seen in hypoaldosteronism, and is very common in patients with longstanding diabetes. Hyperkalemia and a mild acidosis is the hallmark.

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