Thank you to HH and Katie for co-presenting a case of a young woman with T1DM, CKD presenting with a severe non-anion gap metabolic acidosis with a pH of 7 and a Bicarb of 6! Overall, it was felt that her initial presentation was 2/2 to a mix of GI losses given her profound diarrhea and renal losses of bicarb in early renal dysfunction.
- When calculating the serum anion gap, there’s no need to correct serum sodium for hyperglycemia. The osmotic pull of water would dilute all of the electrolytes in an equal manner, so the sodium, potassium, and chloride are all relatively dilute, and the anion gap calculation would not change.
- When trying to determine where a patient is losing bicarbonate – you can calculate a urine anion gap UAG – see more below.
- In a patient with normally functioning kidneys, they will secrete ketones in their urine. In patients with DKA, this can eventually result in a non-anion gap acidosis.
- Remember risk factors for central pontine demyelination with rapid correction > 10 in 24 hours include: very low sodium levels < 110 (in most cases), premenopausal females and severe malnutrition.
Urine Anion Gap (UAG)
Na + K – Cl = Ur Anion Gap (this is calculating unmeasured anions NH4+ primarily)
- Assumes that the patient is volume replete (Una > 20) and is without an anion gap acidosis
- If UAG + in setting of non-gap metabolic acidosis this suggests the kidneys are FAILING to excrete ammonia à renal tubular acidosis
- DDx: RTAs (see below)
- If UAG zero or negative, suggests bicarbonate losses from GI tract (this means the kidneys are appropriately getting rid of NH4+ to compensate for acidosis).
- DDx: GI losses (diarrhea or fistulas), early renal failure& ingestions
- These labs must be interpreted in the context of patient’s presentation and there are not strict cut-offs.
- Depending on the severity of the metabolic acidosis, if you have normal kidneys, the urine anion gap should be even more negative (kidney is responding appropriately to excrete NH4+).
- If you have severe metabolic acidosis, and the urine anion gap is zero or only slightly negative, this suggests a mixed picture – in that there are GI losses, but the kidney’s are not responding as robustly as they should to get rid of NH4+. With excretion of NH4+ the CL- amount increases and this should drive the equation above more and more negative.
Non-Gap Acidosis Ddx
- GI losses of HCO3- Diarrhea, fistulas/drainage
- Proximal (Type II): decreased reabsorption & then loss of HCO3-
- Distal (Type I): defect in H+ excretion (hence profound acidosis)
- Hypoaldo (Type IV): acidosis 2/2 to inability to excrete acid
- Early renal failure – impaired generation of NH4+ (this is the KEY to understanding the physiology per above)!
- Ingestions – acetazolamine, sevelamer, toluene
- Dilution – rapid infusion of bicarb free IVFs
- Post-hypocapnia – Rapid correction of respiratory alkalosis -> renal wasting og HCO3 needs to be regenerated
|Location||Type||Acidosis||UAG||U pH||FeHco3||Serum K|
|Distal||I||Severe||+||> 5.3||< 3%||Variable|
|Hypoaldo||IV||Mild||+||> 5.3||< 3%||HIGH|