[Pseudo-Bartter's syndrome induced by surreptitious ingestion of furosemide to lose weight: a case report and possible pathophysiology].

Bartter's syndrome (B.S) is often difficult to distinguish from pseudo-Bartter's syndrome (pseudo-B.S), a condition which may be caused by "loop" diuretics abuse. Although our patient firmly denied ingestion of diuretics or laxatives, all screening of urine samples gave consistently positive results for furosemide, even during hospitalization. A 25-year-old married woman with persistent hypokalemia had many characteristics of B.S, including hypokalemic hypochloremic alkalosis, hyperactivity of the renin-angiotensin-aldosterone system, normotension, insensitivity to the pressor effect of angiotensin II (A.II), increased urinary excretion of prostaglandin E2 and kallikrein, and marked reduction of distal fractional reabsorption of chloride in Henle's loop, as estimated by CH2O/CH2O+C.Cl, under conditions of hypotonic saline diuresis. Furthermore, hypotension occurred with [1-Sar, 8-Ile] A.II and with the angiotensin converting enzyme inhibitor (Captopril). Renal biopsy revealed juxtaglomerular hyperplasia. A tentative diagnosis of B.S was made. Indomethacin (IDM), an inhibitor of prostaglandin synthesis was prescribed and the pressor response to A.II improved. Impaired fractional chloride reabsorption was also improved significantly under IDM, but the value was low compared to the normal. The value for basal plasma human atrial natriuretic polypeptide (hANP) was slightly above the normal ranges and was suppressed by IDM. We conclude that manifestations B.S in this patient may have been fostered significantly by the long-term surreptitious use of furosemide, taken to lose weight. The analysis of urine for detection of diuretics was only finding distinguishing her clinical state from "true" B.S and leading to a final diagnosis. Pathophysiologic relationships between B.S and pseudo-B.S due to furosemide are discussed.