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Acute Renal Failure following Massive Mannitol Infusion
Author(s) -
Jordi Rello,
C. Triginer,
José Marcel Sánchez,
Net A
Publication year - 1989
Publication title -
˜the œnephron journals/nephron journals
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.951
H-Index - 72
eISSN - 2235-3186
pISSN - 1660-8151
DOI - 10.1159/000185786
Subject(s) - medicine , mannitol , nephrology , intensive care medicine , urology , chemistry , organic chemistry
Mannitol is an osmotic diuretic agent widely used in the treatment of cerebral edema and in the prophylaxis of acute renal failure [1]. The kidneys are the major source of excretion of mannitol (90% excreted within 24 h of intravenous administration) [2]. Renal insufficiency will markedly impair excretion, leading to accumulation in extracellular fluid space [1, 2]. Thus, mannitol intoxication has been reported to be a potentially life-threatening complication when mannitol is used unrestrictedly in patients with established renal failure [3, 4]. The aim of this letter is to report on a patient with diabetic nephropa-thy and no known other predisposing factors in whom acute oliguric renal failure occurred as a consequence of infusion of massive quantities of mannitol. A 50 year-old woman arrived at the emergency room with progressive obnubilation and right hemiparesis. She had a history of diabetic nephropathy, and 6 months earlier suffered an episode of acute renal failure due to iodic contrast medium, remaining with a creatinine clearance of 18 ml/min. Intracranial haemorrage was suspected, and 200 g of mannitol was administered as well as thiopental sodium, insulin, ranitidine, and dexamethasone. A computerized tomography scan without contrast medium did not show signs of cerebral bleeding. Serum creatinine was 248 μmol/l, urea 27 mmol/l, Na 130, and K 4.5 mmol/l. Within the first 2 h the patient presented diuresis of 758 ml, though later she was anuric and did not respond to furosemide. Morever, consciousness decreased progressively until the patient entered profound coma. Haemodynamic stability was maintained throughout. During the following 48 h the patient was anuric and presented hypervolaemic signs which led to the institution of peritoneal dialysis. The patient required mechanical ventilation due to Cheyne-Stokes respiration. Twelve hours after Table 1. Laboratory data

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