Metabolic mimicry of Bartter's syndrome by covert vomiting: utility of urinary chloride determinations

Bartter's syndrome characteristically exhibits the constellation of hypokalemic alkalosis with moderate kaliuresis, normotensive hyperreninemia, hyperaldosteronism, urinary hyperexcretion of prostaglandin E (PGE) and vascular hyporesponsivity to pressor agents. We describe precise biochemical mimicry of these metabolic abnormalities in a patient with surreptitious repetitive vomiting, in whom simple urinary chloride excretion data subsequently excluded the diagnosis of Bartter's syndrome.