Urinary potassium wasting can result from a number of different causes including: 1) genetic defects in tubular sodium reabsorption increasing distal sodium delivery, a key regulator of potassium excretion, 2) hypomagnesemia, which decreases tonic inhibition of secretory potassium channels, 3) varied forms of hyperaldosteronism leading to upregulation of sodium and potassium conductances in the connecting tubule and collecting duct, or 4) increase in urinary anions (e.g. bicarbonate) that are excreted with countercations such as potassium to maintain electroneutrality. Here, KCNA3 is linked to hyperaldosteronism.