KCNJ1 and familial primary hypomagnesemia: Hypomagnesemia appears to modulate both sodium–potassium adenosine triphosphatase pump (Na-K-ATPase) function and the basolateral membrane as well as the flow of potassium out of the apical renal outer medullary potassium channel (ROMK) channels leading to enhanced renal K+ excretion [10].