Genetic tubular hypokalemia

Recent progress in molecular genetics have improved our understanding of th e pathophysiology of several inherited diseases characterized by a renal hy pokalemia. Some of these diseases result from inactivating mutations on the main cotransports involved in the reabsorption of sodium, namely the Gitel man and Bartter syndromes, that clinically mimics diuretic abuse with mild hypovolemia and low or normal blood pressure. Conversely some affections ev entually lead to an increase in sodium reabsorption with hypervolemia and a rterial hypertension: Liddle syndrome, apparent mineralocorticoid excess an d dexamethasone suppressible hyperaldosteronism.