Normal anion gap acidosis

Differential diagnosis

• Hyperalimentation
• Acetazolamide and other carbonic anhydrase inhibitors
• Renal tubular acidosis
• 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 Cl⁻concentration. This scenario can be avoided if formulations such as lactated Ringer’s solution are used instead of normal saline to replace GI losses.
• Ureteroenteric fistula – an abnormal connection between a ureter and the gastrointestinal tract
• Pancreaticoduodenal fistula – an abnormal connection between the pancreas and duodenum
• Spironolactone
• High ostomy output
• 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.