Idiopathic edema patients abusing diuretics are occasionally becoming dependent to such a degree on increasing doses of diuretics that their withdrawal results in severe cardiorespiratory failure, occasionally even pulmonary edema. Two such patients are described and 1 is investigated in depth as to the mechanism of the diuretic abuse-induced excessive tubular avidity for sodium. An extreme diuretic-induced secondary hyperaldosteronism and atrial natriuretic factor suppression, although tapering off when diuretics are stopped, results in a continuous tubular sodium hyper-reabsorption. Since the most affected patient was deprived of the benefits of converting enzyme inhibitors because of their side effects, the only way to partially overcome this condition was a generous combination of several diuretics acting at several segments of the nephron. This contrasted with a similar patient who was relatively well controlled by a converting enzyme inhibitor combined with lower dose diuretics. Diuretic abuse-induced secondary hyperaldosteronism and diuretic resistance are apparently best prevented by converting enzyme inhibitors. When nonpharmacological preventive measures fail, converting enzyme inhibitors are preferable to diuretics as the first-choice treatment of idiopathic edema patients.

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