REN and Hypokalemia: Increased activity of the epithelial sodium channel (ENaC) is the final common abnormality in several forms of hypertension: primary aldosteronism, glucocorticoid remediable aldosteronism, Liddle’s syndrome and 11-β-hydroxysteroid dehydrogenase-2 deficiency.1 Activating mutations of either the β- or γ-ENaC subunits can result in Liddle’s syndrome,2,3 in which constitutive reabsorption of sodium leads to hypertension and hypokalaemia in the presence of low plasma levels of renin and aldosterone.