Impaired renal function in a patient with diuretic abuse

Abstract

A 31-year-old woman was diagnosed as having Bartter's syndrome in 1978, although suspicions remained that she had been taking diuretics surreptitiously. Careful observation and repeated urinary drug analyses revealed no clue that she had been taking diuretics, until 20 years later, when the urine samples at last disclosed traces of furosemide. At this time she showed proteinuria, of 2 g/day, and hypercholesteremia. The glomerular filtration rate had decreased to 66 ml/min per 1.73 m². The 24-h urinary concentrations of β₂-microglobulin, N-acetyl-β-d-glucosaminidase (NAG) activity, and other urinary enzymes that are indicators of damage in proximal tubular cells, were increased, showing proximal tubular damage. The function of the loop of Henle was evaluated by a hypotonic saline loading test. The fractional distal chloride reabsorption, an index of the solute conservation rate in the loop of Henle, was 65.4%, which was lower than the normal value (88.9 ± 6.2%). The maximal urinary concentrating ability was 357 mOsm/kg·H₂O, and a short ammonium chloride loading test showed impairment in the acidification of the urine. The third renal biopsy specimens showed some obsolescent glomeruli, marked juxtaglomerular cell hyperplasia, intraluminal calcification, interstitial infiltration of lymphocytes with fibrosis, and thickening of arteriolar walls with narrow lumens. Patients often attempt to hide their use of diuretics from medical staff, leading to them to make a misdiagnosis of Bartter's syndrome. Although the patient described here has not experienced life-threatening adverse effects from furosemide abuse, some findings appear to be irreversible, suggesting the deterioration of renal function. Patients should realize that longstanding abuse of diuretics causes not only metabolic abnormalities but also the risk of renal damage.