At present, careful screening for primary aldosteronism should be included in the search for a remediable type of hypertension in any work-up of a hypertensive patient. Since the first description of primary aldosteronism by Conn in 1954, an increasing number of cases with adrenocortical tumor have been recognized. Any degree of hypertension in the presence of a reliable and preferably repeated demonstration of hypokalemia and alkalosis, especially when accompanied by nocturnal polyuria, paresthesias, weakness, and headaches, should suggest primary aldosteronism.1 It must be noted that in patients restricted to less than 50 mEq. of sodium per day, the usually characteristic hypokalemic alkalosis may correct itself by the decrease in the sodium ions available for aldosteroneinduced exchange of the potassium and hydrogen ions in the distal tubule. Valuable findings corroborative of primary aldosteronism are moderate hypernatremia, unresponsiveness of the renal concentrating mechanism to vasopressin, and renal potassium wastage.