Cystic fibrosis (CF) is an autosomal recessive disease characterized by loss-of-function mutations in the CF transmembrane conductance regulator (CFTR) gene, which encodes a chloride and bicarbonate channel.1,2 CFTR is expressed in many different organ systems, including sweat glands.3,4 Although people with CF secrete normal primary sweat,3,5 they fail to reabsorb chloride (and sodium), resulting in sweat sodium and chloride concentrations 3-5 times higher than in people without CF.6 Accordingly, excessive sweating, without replenishment of fluids and electrolytes, can result in profound sodium and chloride depletion, secondary hyperaldosteronism, and hypokalemic metabolic alkalosis.