{'fraction_non_alphanumeric': 0.02547065337763012, 'fraction_numerical': 0.0022148394241417496, 'mean_word_length': 5.598540145985401, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Factitious Bartter's syndrome induced by surreptitious intake of furosemide.

Studies on the electrolyte metabolism and the renin-angiotensin-aldosterone system were made in a 47-year-old female patient with factitious Bartter's syndrome induced by surreptitious use of furosemide. The diagnosis was confirmed later by detection of the diuretic in the urine. In metabolic studies patient exhibited abnormalities similar to those reported in Bartter's syndrome; viz, hypokalemic alkalosis, blunted response to exogenous angiotensin II, which reverted to normal by volume expansion with an albumin solution, and diminished fractional free water clearance per fractional distal sodium delivery. The above data, along with the known pharmacological effects of furosemide, suggest that the abnormality in Na+ or Cl- reabsorption in the ascending limb of Henle's loop is a primary cause of Bartter's syndrome.