In patients with isolated dominant hypomagnesemia, the FXYD2b abnormality causes inadequate Na,K-ATPase-energized transcellular magnesium transport in the distal convoluted tubule via the apical Mg2+ channel TRPM6 and the Na+-Mg2+ exchanger at the basolateral site [18,29]. Here, TRPM6 is linked to familial primary hypomagnesemia.