Urine Anion Gap Calculator (Na + K − Cl)

1. Read one reporting unit for a single urine specimen.
2. Read sodium, potassium, and chloride from that specimen.
3. Add sodium and potassium.
4. Subtract chloride and retain the raw signed result.
5. Apply the one-decimal display contract only at the end.

It does not read serum electrolytes or bicarbonate, a serum anion gap, blood gas, urine pH, measured urine osmolality, urine ammonium, urine volume, a 24-hour collection, kidney function, symptoms, history, diagnosis, or treatment information.

The equation describes the charge difference in one urine sample. Mixing different voids, dates, time points, or unit systems creates a number that represented no single specimen. Editing an electrolyte or changing the unit clears the same-specimen confirmation and stale result as a software safety measure.[3, 8]

Raw UAG may be positive, zero, or negative. The formatter shows one decimal; a nonzero raw magnitude below 0.05 can therefore display as 0.0 while the audit retains the original number. A displayed zero is not a normal range, clinical category, or proof that no physiologic difference exists.

In normal-plasma-anion-gap metabolic acidosis, the original 24-hour data reported urine ammonium = −0.8 × UAG + 82 with r = 0.97. That historical relationship motivated use of UAG as an indirect index; it is not this calculator's conversion equation, and this page never outputs an estimated NH₄⁺ value.[1]

The study included 38 patients with altered distal urinary acidification, 8 patients with diarrhea, and 7 healthy participants given NH₄Cl. Mean UAG was about −27 ± 9.8 mmol/L in the loaded healthy group and −20 ± 5.7 mmol/L in the diarrhea group, while each altered-acidification group had a positive mean. The authors called UAG a rough initial index in hyperchloremic metabolic acidosis—not a universal classifier for an arbitrary urine sample.[3]

The historical observations came from selected acidotic cohorts, whereas this form does not confirm any serum acid-base state. A positive result does not automatically establish RTA, a negative result does not establish diarrhea, and zero is not an intermediate diagnosis. No green, yellow, red, positive-disease, or negative-disease label is generated.

Uribarri and Oh argued in 2021 that steady-state UAG principally reflects sodium, potassium, and chloride intake and output, with selective losses and nonsteady state disrupting that balance; they disputed a general ammonium relationship. That critical analysis does not mean every expert abandoned UAG. A 2023 review retains it only as a rough initial bedside marker in selected metabolic-acidosis evaluation while favoring direct ammonium for precision.[6, 8]

Direct urine NH₄⁺ is a separate laboratory measurement. UAG contains only sodium, potassium, and chloride. The 2022 review supports broader direct ammonium availability, and the 2023 review likewise favors direct measurement when a precise assessment is needed. This page does not reverse-engineer a fictional ammonium concentration from its result.[7, 8]

Sodium avidity and low distal sodium delivery can limit acidification interpretation. When urine sodium is below approximately 20 mmol/L, using UAG to infer NH₄⁺ is often considered unreliable. This is static evidence context—not an input threshold or automatic warning—and this calculator never diagnoses volume depletion or RTA from sodium.[2, 4]

Bicarbonate is an unmeasured urine anion in Na + K − Cl. Bicarbonaturia or urine pH above about 6.5 can distort the expected UAG–ammonium relationship, and high urine pH alone cannot diagnose distal RTA. This form has no urine-pH or bicarbonate input.[4]

NH₄⁺ need not be excreted only with chloride. Ketoacids, hippurate, D-lactate, salicylate-related anions, and other unmeasured anions can prevent the expected negative UAG even when ammonium excretion rises. The page does not automatically interpret diabetic ketoacidosis, toluene exposure, D-lactic acidosis, or salicylate-related states.[4, 6]

Water flow changes urine concentrations, so polyuria or rapid physiologic change can weaken a spot calculation. Diet and food additives alter sodium, potassium, chloride, and unmeasured-anion balance. One spot UAG cannot reconstruct 24-hour electrolyte intake or excretion.[4, 6]

Raphael 2018 studied 1,044 AASK participants. Standard UAG had a weak direct correlation with measured urine ammonium (r = 0.18). Low directly measured ammonium was associated with ESRD or death, but standard-UAG tertiles did not reproduce that relationship. The authors judged standard UAG a poor CKD surrogate and preferred direct ammonium; this CKD result must not be mechanically extended to every acute acid-base setting.[5]

The urine osmolal gap uses measured minus calculated urine osmolality and can provide different indirect information when ammonium accompanies a nonchloride anion. Kim 1996 and later reviews found useful correlations in selected chronic-acidosis cohorts, but UOG remains an estimate affected by other unmeasured osmoles. This page lacks measured urine osmolality, urea, and glucose and therefore cannot calculate UOG.[4, 8, 9]

Reliability may be reduced when inputs are not from one specimen, the unit is wrong, normal-gap/hyperchloremic metabolic acidosis has not been established, urine sodium is low, polyuria or nonsteady state is present, bicarbonaturia or high urine pH exists, ammonium accompanies ketoacid, hippurate, D-lactate or another nonchloride anion, CKD is present, diet or electrolyte intake changes, fluids or diuretics precede sampling, collection or assay error occurs, or the sign is considered without the absolute electrolytes.

It cannot determine direct urine NH₄⁺, net acid excretion, UOG, the presence or type of metabolic acidosis, distal/proximal/type 4 RTA, diarrhea or GI bicarbonate loss, CKD cause or severity, or any alkali, potassium, fluid, medicine, dialysis, referral, or other treatment decision.