Loading...
Printed on 6/29/2026
For informational purposes only. This is not medical advice.
The Urine Anion Gap (UAG) helps differentiate between extrarenal (GI) and renal causes of non-anion gap metabolic acidosis (NAGMA — first confirm with [Anion Gap Calculator](/tools/anion-gap) and [ABG Interpreter](/tools/abg-interpreter)). It is calculated as Urine Na + Urine K − Urine Cl. A negative UAG indicates high urinary ammonium (NH4+) excretion, suggesting the kidneys are working properly and the acidosis is from GI losses (e.g., diarrhea). A positive UAG suggests the kidneys cannot excrete adequate ammonium, pointing to renal tubular acidosis (RTA). This is a key tool in the workup of hyperchloremic metabolic acidosis. Assess renal function severity with [eGFR Calculator](/tools/egfr-calculator).
Formula: UAG = Urine Na (mEq/L) + Urine K (mEq/L) − Urine Cl (mEq/L)
Save your results with a free account
Keep a history of calculations, favorite tools, and access your dashboard anytime.
Collect a spot urine sample and measure sodium, potassium, and chloride concentrations simultaneously with a blood sample to confirm non-anion gap metabolic acidosis.
Apply the formula: Urine Anion Gap = urine sodium + urine potassium − urine chloride (all in mEq/L). The result is a surrogate for urinary ammonium (NH4+) excretion.
Positive UAG (+10 to +20 or greater) indicates impaired renal ammonium excretion, pointing to renal tubular acidosis (RTA). Negative UAG (−20 to −50) indicates high urinary ammonium, meaning the kidneys are responding normally — the acidosis is likely from GI bicarbonate loss such as diarrhea.
Nephrologists, hospitalists
The UAG is the first-line test to distinguish GI bicarbonate loss (negative UAG, kidney working well) from renal tubular acidosis (positive UAG, kidney failing to excrete acid) in a patient with non-anion gap metabolic acidosis.
Nephrologists
When UAG is positive, combine with urine pH and serum potassium to subtype: Type 1 RTA shows urine pH >5.5 with hypokalemia; Type 4 RTA (hypoaldosteronism) shows urine pH often <5.5 with hyperkalemia.
Internal medicine, nephrology
UAG is a standard component of the hyperchloremic metabolic acidosis workup in hospitalized patients, providing rapid, inexpensive guidance using only a spot urine sample.
Nephrology clinic teams
In patients with unexplained chronic acidosis or recurrent kidney stones, the UAG helps determine whether impaired renal acid excretion is contributing to the underlying disorder.
Nephrologists, ophthalmologists
Acetazolamide and other carbonic anhydrase inhibitors cause a non-anion gap metabolic acidosis. The UAG can confirm impaired distal ammonium excretion in this iatrogenic setting.
The UAG is an indirect estimate of urinary NH4+ because ammonium is not routinely measured. NH4+ is excreted with chloride, so high NH4+ raises urine chloride and makes the UAG negative. A negative UAG means the kidney is working hard to excrete acid.
A negative UAG (typically −20 to −50 mEq/L) indicates the kidneys are responding appropriately to acidosis with high ammonium excretion. This points away from RTA and toward extrarenal bicarbonate loss, most commonly diarrhea.
A positive UAG (>0 mEq/L) in NAGMA means the kidney cannot excrete adequate ammonium, indicating RTA or hypoaldosteronism. Further workup with urine pH and serum potassium is needed to differentiate Type 1 from Type 4 RTA.
The UAG is only valid when the serum anion gap is normal. If an elevated anion gap acidosis is present, unmeasured anions in the urine confound the calculation. Always confirm NAGMA first using the serum anion gap calculator.
When urine sodium is <20 mEq/L (as in severe volume depletion), low sodium delivery to the collecting duct limits tubular function. The UAG becomes unreliable in this setting — consider the urine osmolal gap instead.
Acetoacetate is an unmeasured urinary anion that is excreted with sodium rather than NH4+. In patients with significant ketonuria (DKA, fasting ketosis), the UAG will be falsely elevated and cannot reliably diagnose RTA.
When the UAG is unreliable (low urine Na, ketonuria), use the urine osmolal gap instead: UOG = measured urine osmolality − [2×(uNa + uK) + urea/2.8 + glucose/18]. UOG >100 mOsm/kg suggests high ammonium excretion (GI cause).
Type 1 (distal) RTA cannot acidify urine below pH 5.5 even in systemic acidosis, a hallmark diagnostic finding. Combined with a positive UAG and hypokalemia, this pattern strongly supports the diagnosis of distal RTA.
Type 4 RTA from hypoaldosteronism (common in diabetic nephropathy and CKD) presents with positive UAG, hyperkalemia, and urine pH often <5.5. The hyperkalemia itself suppresses renal ammoniagenesis, reducing NH4+ excretion.
In suspected Type 4 RTA, a spot urine potassium-to-creatinine ratio >200 mEq/g suggests inappropriate potassium wasting from a different cause. Combined with UAG interpretation, this helps narrow the tubular defect.
Urine anion gap was validated by Batlle et al. (NEJM 1988) as a clinical tool to estimate urinary ammonium. Normal values and diagnostic cutoffs are discussed in standard nephrology references including Brenner & Rector's The Kidney (10th ed.). RTA classification follows Rodríguez-Soriano's framework (Pediatr Nephrol 2002) and Halperin & Goldstein.
The urine anion gap result is interpreted in the context of a patient who has a non-anion gap metabolic acidosis (NAGMA), characterized by low serum bicarbonate with a normal serum anion gap. A negative urine anion gap (typically -20 to -50 mEq/L) indicates that the kidneys are appropriately excreting ammonium (NH4+) in response to the acidosis. Since NH4+ is excreted with chloride, high ammonium excretion raises urine chloride relative to sodium plus potassium, pulling the gap negative. This pattern points to an extrarenal cause of the acidosis, most commonly diarrhea or other gastrointestinal bicarbonate losses.
A positive urine anion gap (greater than 0 mEq/L) in the setting of NAGMA indicates that the kidneys are failing to appropriately increase ammonium excretion. This points to a renal tubular acidosis (RTA). Type 1 (distal) RTA is characterized by impaired hydrogen ion secretion in the distal tubule, resulting in a urine pH typically above 5.5 and hypokalemia. Type 4 (hyperkalemic) RTA results from aldosterone deficiency or resistance and presents with hyperkalemia and a urine pH below 5.5.
A urine anion gap near zero is indeterminate and may require additional testing, such as the urine osmolar gap, which is a more direct estimate of urinary ammonium and can be helpful when the UAG result is equivocal.
Use the urine anion gap as part of the diagnostic workup for non-anion gap metabolic acidosis. After confirming NAGMA (low bicarbonate, normal serum anion gap, and hyperchloremia), the key clinical question is whether the acidosis is due to renal or extrarenal causes. The urine anion gap answers this question by indirectly estimating whether the kidneys are appropriately excreting ammonium.
The most common clinical scenarios include: distinguishing diarrhea-induced bicarbonate loss (negative UAG) from renal tubular acidosis (positive UAG); evaluating unexplained hyperchloremic metabolic acidosis in hospitalized patients; and working up possible Type 1 or Type 4 RTA in patients with persistent metabolic acidosis of unclear etiology. It is a simple, inexpensive test that requires only a spot urine sample for sodium, potassium, and chloride.
The urine anion gap is only valid in the setting of non-anion gap metabolic acidosis. It should not be used when the serum anion gap is elevated, as the filtered unmeasured anions in the urine can confound the calculation. It is also unreliable in patients with significant ketonuria or other organic anions in the urine (e.g., hippurate from toluene exposure), as these anions are excreted with sodium rather than ammonium and can falsely elevate the UAG.
The test assumes that the major unmeasured cation in urine is ammonium. In patients with very low urine sodium (such as those who are volume-depleted), the UAG may be unreliable because low sodium delivery to the collecting duct limits the ability to interpret the gap. In these cases, the urine osmolar gap may be a better alternative for estimating urinary ammonium.
Polyuria and very dilute urine can also affect results. Additionally, certain medications such as lithium (an unmeasured cation in urine) can interfere with the calculation. The UAG provides a qualitative assessment of ammonium excretion and should always be interpreted alongside the clinical picture, serum potassium, urine pH, and other laboratory findings.
Disclaimer: This tool is for educational and informational purposes only. It is not a substitute for professional medical advice, diagnosis, or treatment. Always consult a qualified healthcare provider with questions about your health.
April 21, 2026 · trust-baseline
Clinical trust metadata enabled for this tool page with structured review/version fields.
Calculate anion gap and albumin-corrected anion gap to evaluate metabolic acidosis, narrow differential diagnosis, and monitor treatment response.
OpenNephrologyCalculate the Fractional Excretion of Sodium (FENa) to differentiate pre-renal azotemia (FENa <1%) from intrinsic renal disease such as ATN (FENa >2%) in acute kidney injury.
OpenClinicalInterpret arterial blood gas (ABG) results to identify acid-base disorders. Determines primary disorder and compensation status from pH, pCO₂, and HCO₃⁻.
Open