Laxative abuse is the most likely cause of this patient's acid-base and electrolyte abnormalities. She has a normal anion gap metabolic acidosis in the setting of physical examination findings consistent with low/normal extracellular fluid status and low/normal blood pressure. The etiology of a normal anion gap metabolic acidosis is typically due to either the inability of the kidney to excrete acid (renal tubular acidosis) or loss of bicarbonate, usually through the gastrointestinal tract. Differentiating the cause of a normal anion gap metabolic acidosis may be accomplished by measurement of the urine anion gap, which is calculated as follows: (UNa + UK − UCl). The urine anion gap is a surrogate method of estimating the ability of the kidney to excrete an acid load. The normal physiologic response to systemic acidosis is an increase in urine acid excretion resulting in an increase in urine ammonium, which is difficult to measure clinically. However, because ammonium carries a positive charge, chloride is excreted into the urine in equal amounts with ammonium to maintain electrical neutrality. Therefore, the amount of chloride in the urine reflects the amount of ammonium present, with a positive urine anion gap suggesting a kidney source of acid loss, and a negative urine anion gap is consistent with gastrointestinal bicarbonate loss. The negative urine anion gap in this patient (-6 mEq/L [6 mmol/L]) indicates a gastrointestinal cause of her normal anion gap metabolic acidosis, and laxative abuse is a likely explanation. In addition, hypokalemia combined with low urine potassium indicates appropriate renal compensation to attempt to retain filtered potassium.
The vomiting associated with bulimia nervosa leads to loss of gastric acid with a resulting metabolic alkalosis, not metabolic acidosis.
Active diuretic use leads to kidney potassium wasting and a metabolic alkalosis, as does Gitelman syndrome, a defect that mimics the clinical picture of thiazide diuretic use.
Renal causes of normal anion gap metabolic acidosis are due to specific defects in renal handling of bicarbonate reclamation or in hydrogen ion secretion. Type 1 (hypokalemic distal) renal tubular acidosis is caused by a defect in hydrogen secretion by the distal tubule and is associated with a positive urine anion gap, a high urine potassium secretion, and hypokalemia.