Additional mechanisms may also contribute: for example (i) aldosterone activation of the distal nephron, as is to be expected and not uncommonly seen with thiazide-induced hypokalaemia and hyperaldosteronism 122, or (ii) With No lysine protein Kinase (WNK) regulation of the renal outer-medullary potassium channel (ROMK) in the collecting duct and the thiazide-sensitive sodium chloride cotransporter (NCC) in the distal convoluted tubule as has been proposed for the hyperkalaemia seen in Gordon syndrome 123, a Mendelian disorder of thiazide-responsive hypertension and metabolic acidosis. This evidence concerns the gene KCNJ1 and hypertensive disorder.