Electrolyte disorders such as hypomagnesemia and hypokalemia can result from excessive urinary losses. Rarely, this is due to loss-of-function mutations in genes such as those encoding tubular transporters or ion channels. In Gitelman syndrome (GS), mutant NCCT (encoded by SLC12A3) in the distal convoluted tubule leads to hypokalemia, metabolic alkalosis, hypomagnesemia, and hypocalciuria.1 Because thiazide diuretics block NCCT, thiazide challenge can probe NCCT function in patients thought to have GS.