The Anion Gap Calculator computes the unmeasured anion difference from sodium, chloride, and bicarbonate, with optional albumin correction. Classifies metabolic acidosis as high-gap (MUDPILES) vs. normal-gap (hyperchloremic) — the first and most important step in any acid-base workup.
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A patient presents with metabolic acidosis on blood gas. What's causing it? The first question every clinician asks is: what's the anion gap? The calculator for anion gap provides both the standard and albumin-corrected gap in seconds, instantly separating the two main categories of metabolic acidosis and pointing toward the underlying diagnosis.
The anion gap (AG) represents the concentration of unmeasured anions in serum:
AG = Na⁺ − (Cl⁻ + HCO₃⁻)
Normal range: 8–12 mEq/L (using this 3-variable formula). Some labs include potassium: AG = (Na⁺ + K⁺) − (Cl⁻ + HCO₃⁻), giving a normal of 10–16 mEq/L — always verify which formula your institution uses before interpreting results. The gap reflects primarily albumin (the dominant unmeasured anion), phosphate, sulfate, and organic acids. When unmeasured acids accumulate (ketones, lactate, toxins), the gap widens because HCO₃⁻ is consumed buffering H⁺ while Cl⁻ remains unchanged.
Albumin is the most important unmeasured anion — each 1 g/dL reduction in albumin below 4.0 g/dL decreases the AG by approximately 2.5 mEq/L. Hypoalbuminemia (common in critically ill, cirrhotic, and malnourished patients) masks a truly elevated AG:
Corrected AG = Measured AG + 2.5 × (4.0 − albumin g/dL)
A patient with AG = 12 mEq/L and albumin = 2.0 g/dL has a corrected AG = 12 + 2.5 × 2 = 17 mEq/L — significantly elevated, revealing a high-gap acidosis that the uncorrected value obscured. Failing to correct for albumin is one of the most common errors in acid-base analysis in the ICU. Use this online calculator to apply both formulas simultaneously. The delta ratio calculator extends the analysis to mixed acid-base disorders.
An elevated AG (corrected AG above 12 mEq/L) indicates accumulation of unmeasured acids. The classic causes are recalled with MUDPILES:
When metabolic acidosis occurs with a normal AG, the mechanism is direct HCO₃⁻ loss or failure of H⁺ excretion without organic acid accumulation — compensated by Cl⁻ retention. Causes include diarrhea (GI bicarbonate loss), renal tubular acidosis (RTA types 1, 2, and 4), carbonic anhydrase inhibitors (acetazolamide), and early uremic acidosis. The urine anion gap [(Na⁺ + K⁺) − Cl⁻ in urine] helps distinguish renal from GI causes: a positive urine AG suggests impaired NH₄⁺ excretion (RTA); a negative urine AG suggests GI loss. The urine anion gap calculator and electrolyte calculators provide complementary tools for acid-base analysis.
The anion gap is calculated as Na+ - (Cl- + HCO3-). The albumin-corrected anion gap adds 2.5 mEq/L for each 1 g/dL reduction in albumin below 4.0: Corrected AG = AG + 2.5 x (4.0 - albumin). This correction prevents hypoalbuminemia from masking a significant anion gap acidosis in critically ill patients.
Normal anion gap is 8-12 mEq/L (or 3-12 when using corrected AG). An elevated AG indicates accumulation of unmeasured acids (MUDPILES differential). A normal AG with low bicarbonate indicates hyperchloremic metabolic acidosis (diarrhea, RTA). A low AG can occur with hypoalbuminemia, lithium toxicity, or paraproteinemias. Always use the albumin-corrected AG in hypoalbuminemic patients.
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Markedly elevated AG of 27 with low bicarbonate is classic for DKA. Check glucose, ketones, and pH to confirm.
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Raw AG of 15 appears borderline, but corrected AG of 20 reveals significant anion gap acidosis hidden by hypoalbuminemia. Check lactate.
The anion gap is the difference between the principal measured cation (sodium) and the principal measured anions (chloride and bicarbonate): AG = Na - (Cl + HCO3). It represents unmeasured anions in the blood, primarily albumin, phosphate, and sulfate. Normal is 8-12 mEq/L.
MUDPILES is a mnemonic for causes of elevated anion gap metabolic acidosis: Methanol, Uremia, Diabetic ketoacidosis, Propylene glycol, Isoniazid/Iron, Lactic acidosis, Ethylene glycol, and Salicylates. Lactic acidosis and DKA are the most common causes in clinical practice.
Albumin is the largest contributor to the normal anion gap. Each 1 g/dL decrease in albumin reduces the AG by approximately 2.5 mEq/L. In hypoalbuminemic patients (ICU, malnutrition), an elevated AG can be masked and appear falsely normal. Correction prevents missing significant acidosis.
A non-anion gap (hyperchloremic) metabolic acidosis has normal AG but low bicarbonate, with chloride rising to maintain electroneutrality. Causes include diarrhea, renal tubular acidosis, normal saline infusion, and carbonic anhydrase inhibitors. The AG is normal because no unmeasured acids accumulate.
A low AG (below 3) is uncommon but can result from severe hypoalbuminemia, lithium intoxication (lithium is an unmeasured cation), IgG myeloma or paraproteinemia (cationic paraproteins), or laboratory error (including bromide interference with chloride measurement).
Some formulas include potassium: AG = (Na + K) - (Cl + HCO3), which gives a normal range of 12-16. Most clinical practice and guidelines use the formula without potassium because potassium varies narrowly and its inclusion does not improve diagnostic accuracy.
The delta-delta (delta gap) compares the change in AG above normal to the change in bicarbonate below normal. A ratio of 1-2 suggests pure AGMA. A ratio above 2 suggests concurrent metabolic alkalosis. A ratio below 1 suggests concurrent non-AG metabolic acidosis. It identifies mixed acid-base disorders.
The osmolal gap (measured minus calculated osmolality) identifies unmeasured osmoles, particularly toxic alcohols (methanol, ethylene glycol). When AG is elevated, a simultaneous elevated osmolal gap suggests toxic alcohol ingestion. As the parent alcohol is metabolized to acid, the osmolal gap falls while the AG rises.
Yes. Severe dehydration (hemoconcentration), alkalosis (which increases lactate production and albumin charge), and laboratory error can elevate the AG without true metabolic acidosis. Always correlate with pH and bicarbonate to confirm acidosis before pursuing the AGMA differential.
AG is a cornerstone of acid-base analysis in the ICU. It is used to classify metabolic acidosis, identify occult acidosis (especially with albumin correction), monitor treatment response (trending AG in DKA or toxic ingestions), and detect mixed acid-base disorders when combined with the delta-delta analysis.
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