Non-anion gap metabolic acidosis

A young woman developed a symptomatic non-anion gap metabolic acidosis, with dyspnea and confusion, believed to have been caused by topiramate [295 ]. She was given intravenous fluids and sodium bicarbonate and was later intubated. After topiramate withdrawal, she recovered completely over 72 hours. 

In a 37-year-old woman who took a massive topiramate ingestion there was prolonged coma, with normal vital signs and a non-anion gap metabolic acidosis [300 ]. 

Shiber JR. Severe non-anion gap metabolic acidosis induced by topiramate a case report J Emerg Med 2010 38(4) 494-6. 

Electrolyte balance Aminoglycosides cause fluid, electrolyte, and acid-base disorders by altering renal tubular function in several ways, leading to hypokalemia and acidosis or alkalosis. Stimulation of the calcium-sensing receptor has been reported to cause a Bartter-like syndrome (hypokalemic metabolic alkalosis, hypomagnesemia, hypocalcemia, and normal serum creatinine concentrations). More rarely, a proximal renal tubular acidosis (Fanconi syndrome non-anion gap metabolic acidosis) can develop. The mechanisms have been summarized [4 ]. 

A non-anion gap acidosis (hyperchloremic acidosis anion gap <16 mEq/L) is characterized by an acidosis where the anion gap is unchanged from the patient s baseline. This occurs as the decrease in serum bicarbonate is equaled by the rise in serum chloride [3]. Bicarbonate is typically lost from the gastrointestinal tract (i.e., diarrhea) or through the kidneys (i.e., renal tubular acidosis) [4]. Although a few metabolic disorders result in a non-anion gap acidosis (i.e., Fanconi-Bickel syndrome, OMIM 227810), a non-anion gap acidosis is typically not the result of an inborn error of metabolism. 

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