Normal anion gap acidosis

Normal anion gap acidosis is an acidosis that is not accompanied by an abnormally increased anion gap.

Normal anion gap acidosis
Other namesNon-anion gap acidosis
SpecialtyEndocrinology, nephrology 

The most common cause of normal anion gap acidosis is diarrhea with a renal tubular acidosis being a distant second.

Differential diagnosis

The differential diagnosis of normal anion gap acidosis is relatively short (when compared to the differential diagnosis of acidosis):

  • Hyperalimentation (e.g. from TPN containing ammonium chloride)
  • Acetazolamide and other carbonic anhydrase inhibitors
  • Renal tubular acidosis[1]
  • Diarrhea: due to a loss of bicarbonate. This is compensated by an increase in chloride concentration, thus leading to a normal anion gap, or hyperchloremic, metabolic acidosis. The pathophysiology of increased chloride concentration is the following: fluid secreted into the gut lumen contains higher amounts of Na+ than Cl; large losses of these fluids, particularly if volume is replaced with fluids containing equal amounts of Na+ and Cl, results in a decrease in the plasma Na+ concentration relative to the Clconcentration. This scenario can be avoided if formulations such as lactated Ringer’s solution are used instead of normal saline to replace GI losses.[2]
  • Ureteroenteric fistula – an abnormal connection (fistula) between a ureter and the gastrointestinal tract
  • Pancreaticoduodenal fistula – an abnormal connection between the pancreas and duodenum
  • Spironolactone
  • High ostomy output[1]
  • Hyperparathyroidism – can cause hyperchloremia and increase renal bicarbonate loss, which may result in a normal anion gap metabolic acidosis. Patients with hyperparathyroidism may have a lower than normal pH, slightly decreased PaCO2 due to respiratory compensation, a decreased bicarbonate level, and a normal anion gap.[3]

As opposed to high anion gap acidosis (which involves increased organic acid production), normal anion gap acidosis involves either increased production of chloride (hyperchloremic acidosis) or increased excretion of bicarbonate.

See also


  1. "Metabolic Acidosis: Acid-Base Regulation and Disorders: Merck Manual Professional". Retrieved 2008-12-04.
  2. Jean-Louis Vincent; Abraham Edward; Kochanek Patrick (8 July 2011). "Acid-base disorders". Textbook of Critical Care. Elsevier. ISBN 143771367X.
  3. Coe FL (August 1974). "Magnitude of metabolic acidosis in primary hyperparathyroidism". Arch. Intern. Med. 134 (2): 262–5. doi:10.1001/archinte.1974.00320200072008. PMID 4843192.
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