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Distinguish renal from GI causes of non-anion gap metabolic acidosis
UAG = Urine Na + Urine K - Urine Cl
The UAG is a surrogate for unmeasured urine ammonium (NH4+)
GI loss of HCO3 (diarrhea). Kidneys are compensating by excreting NH4+.
Indeterminate. May need further evaluation.
Renal tubular acidosis. Kidneys cannot excrete adequate NH4+.
NH4+ is excreted with Cl- in urine. High NH4+ means high Cl- which makes UAG negative. Low NH4+ (renal failure) means less Cl-, making UAG positive.
Kidneys increase NH4+ excretion to eliminate acid. This NH4+ pairs with Cl-, increasing urine Cl- and making UAG negative.
In RTA, kidneys cannot produce or excrete adequate NH4+. Less NH4Cl in urine, so UAG stays positive.
Cannot acidify urine. Urine pH >5.5. Hypokalemia. Stones, nephrocalcinosis.
Impaired HCO3 reabsorption. Can acidify urine when HCO3 low. Fanconi syndrome.
Low aldosterone or resistance. Hyperkalemia. Common in diabetics with CKD.
Calculate UAG when a patient has non-anion gap metabolic acidosis (NAGMA) and you need to distinguish GI bicarbonate loss (diarrhea) from renal tubular acidosis.
UAG is most useful in non-anion gap acidosis. In high anion gap acidosis (DKA, lactic acidosis), the cause is usually obvious and UAG adds little value.
Yes. UAG may be misleading with: very low urine Na (volume depletion), ketoacidosis (ketones carry negative charge), or toluene toxicity.
Alternative to UAG. Urine osmolal gap = measured osmolality - calculated osmolality. More directly estimates NH4+. Values >150 suggest adequate NH4+ excretion.
GI secretions (below stomach) are rich in bicarbonate. Diarrhea causes direct HCO3 loss. Kidneys compensate by increasing NH4+ excretion (negative UAG).
Serum potassium (low in Type 1/2, high in Type 4), urine pH, fractional excretion of HCO3, and serum aldosterone levels.
UAG is essentially an indirect measure of urine NH4+. Think: "Negative UAG = Normal NH4+ excretion = GI cause. Positive UAG = Poor NH4+ excretion = Renal cause."