- Confirm the patient has a normal-anion-gap (hyperchloremic) metabolic acidosis before using this tool — UAG is not interpretable in high-anion-gap acidosis.
- Enter a spot urine sodium, urine potassium, and urine chloride (all in mEq/L) from the same urine specimen.
- The calculator computes UAG = U_Na + U_K − U_Cl and displays the result with interpretation.
- Review the validity warnings — UAG is unreliable if urine Na < 25 mEq/L, ketonuria is present, or the patient is in AKI.
All computation runs in your browser; no values are stored or transmitted.
When to Use
Use the UAG to narrow the differential of a normal-anion-gap (hyperchloremic) metabolic acidosis — specifically to ask whether the kidneys are appropriately excreting ammonium (NH₄⁺) or not. The UAG is a surrogate for urinary ammonium: because NH₄⁺ is excreted with Cl⁻ but is not directly measured on a standard urine electrolyte panel, a strongly negative UAG (U_Cl far exceeds U_Na + U_K) signals high NH₄⁺ output and therefore intact renal acidification.
Appropriate setting
Adults with confirmed normal-anion-gap metabolic acidosis (serum AG ≤ 12 mEq/L, or corrected for albumin) and a clinical question of diarrhea / GI bicarbonate loss versus distal (type 1) RTA or hypoaldosteronism (type 4 RTA). Most useful when urine pH alone is ambiguous (urine pH > 5.5 is expected in both diarrhea-induced alkaline stool loss and in type 1 RTA during systemic acidosis).
When NOT to rely on it
UAG is invalid in: high-anion-gap metabolic acidosis; ketonuria or hippurate anionuria (unmeasured anions increase U_Cl equivalently and falsely normalize UAG); volume depletion with urine Na < 25 mEq/L (Na avidity trumps Cl secretion); acute kidney injury; toluene intoxication (hippuric acid); and amphotericin B nephropathy. Always interpret with serum context (AG, bicarbonate, albumin, potassium).
Pearls & Pitfalls
Negative UAG = intact renal acidification
A UAG < −10 mEq/L means U_Cl greatly exceeds U_Na + U_K, implying large NH₄⁺-Cl excretion. This is the appropriate renal response to metabolic acidosis and points to an extrarenal (GI) cause — most commonly diarrhea, laxative abuse, or ileostomy output.
Positive UAG = impaired renal NH₄⁺ excretion
A UAG > +10 mEq/L in the context of normal-anion-gap acidosis indicates that the kidney is not appropriately excreting NH₄⁺ — the hallmark of distal (type 1) RTA (inability to lower urine pH below 5.5) or type 4 RTA / hypoaldosteronism (hyperkalemia, reduced aldosterone effect). Proximal (type 2) RTA may show a variable or transiently positive UAG.
Critical pitfalls
(1) Ketonuria invalidates UAG — ketone anions are excreted with Na⁺ rather than Cl⁻, raising U_Na and making UAG falsely positive even when ammonium excretion is adequate. (2) Urine Na < 25 mEq/L — avid Na reabsorption under volume depletion means Na delivery to the collecting duct is too low to reflect ammonium handling; UAG is unreliable. (3) AKI — tubular dysfunction disrupts normal urine electrolyte relationships. (4) Toluene/hippurate — hippurate anions mimic chloride in raising U_Cl, making UAG falsely negative. (5) UAG cannot distinguish type 1 RTA from type 4 RTA — use serum potassium and aldosterone levels for that.
Why Use It
Urine pH is unreliable for distinguishing diarrhea from distal RTA during systemic acidosis because both conditions may produce a urine pH above 5.5 (diarrhea causes K⁺ depletion and aldosterone-driven Na⁺/H⁺ exchange; type 1 RTA cannot acidify regardless). The UAG exploits the fact that ammonium (NH₄⁺) — the kidneys' primary vehicle for excreting an acid load — carries chloride as its counterion. Because routine labs do not measure urine NH₄⁺ directly, the UAG provides an indirect window: a strongly negative UAG signals high Cl⁻ output that can only be accounted for by NH₄Cl excretion, confirming intact distal acidification and pointing the clinician toward a GI source. This distinction has direct therapeutic consequences — diarrhea is managed with volume and bicarbonate replacement, whereas RTA requires long-term alkali therapy and investigation of the underlying cause.
Urine Anion Gap (UAG) Calculator
Enter spot urine sodium, potassium, and chloride from the same specimen. Valid only in normal-anion-gap (hyperchloremic) metabolic acidosis — see the validity warnings above before interpreting the result.
⚕ UAG = U_Na + U_K − U_Cl. Valid only in normal-anion-gap (hyperchloremic) metabolic acidosis with urine Na ≥ 25 mEq/L and no ketonuria. This tool assists clinical interpretation and requires physician assessment of validity in context.
Next Steps
Use the UAG result to guide — not conclude — the workup.
- Negative UAG (GI cause suggested): Confirm diarrhea history, laxative use, or ileostomy output. Check stool electrolytes if the source is unclear. Treat with volume repletion and oral/IV sodium bicarbonate. Correct hypokalemia (common in diarrhea).
- Positive UAG (RTA suggested): Distinguish type 1 from type 4 RTA using serum potassium and aldosterone axis (type 1: hypokalemia, urine pH > 5.5; type 4: hyperkalemia, low aldosterone or aldosterone resistance). Investigate for Sjögren's syndrome, autoimmune conditions, nephrocalcinosis, or obstructive nephropathy for type 1. For type 4, check RAAS axis, adrenal function, and review ACE inhibitors / ARBs / NSAIDs / heparin.
- Indeterminate (−10 to +10): Recheck the validity criteria — ensure urine Na ≥ 25 mEq/L and no ketonuria. Consider urine ammonium measurement if available.
- Refer to nephrology for persistent or complex RTA, or when the cause of normal-anion-gap acidosis remains unclear after initial evaluation.
Evidence & References
Formula
| Quantity | Equation |
|---|---|
| Urine Anion Gap (mEq/L) | U_Na + U_K − U_Cl |
| Negative UAG (e.g. < −10) | High NH₄⁺ excretion → intact renal acidification → GI / extrarenal HCO₃⁻ loss |
| Positive UAG (e.g. > +10) | Low NH₄⁺ excretion → impaired renal acidification → distal RTA or hypoaldosteronism |
| Indeterminate (−10 to +10) | Non-diagnostic; check validity criteria and clinical context |
References
- Goldstein MB, Bear R, Richardson RMA, Marsden PA, Halperin ML. The urine anion gap: a clinically useful index of ammonium excretion. Am J Med Sci. 1986;292(4):198–202.
- Batlle DC, Hizon M, Cohen E, Gutterman C, Gupta R. The use of the urinary anion gap in the diagnosis of hyperchloremic metabolic acidosis. N Engl J Med. 1988;318(10):594–599.
- Halperin ML, Goldstein MB. Fluid, Electrolyte, and Acid-Base Physiology: A Problem-Based Approach. 4th ed. Philadelphia: Saunders; 2010.
