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Received from the Department of Anesthesiology, Hahnemann Universisty, Philadelphia, Pennsylvania; the Departments of Anesthesiology, Millard Fillmore Hospital, and the State University of New York at Buffalo, Buffalo, New York; and the Clinical Pharmacokinetics Laboratory, Millard Fillmore Hospital, and College of Pharmacy, Department of Pharmaceutics, State University of New York at Buffalo, Buffalo, New York.
Abstract
Urinary excretion of alanine aminopeptidase (AAP) is an extremely sensitive indicator of drug-induced renal tubular damage. The urinary excretion of AAP was determined in patients after enflurane anesthesia with or without concurrent aminoglycoside administration to determine if enfrurane enhances the nephrotoxic potential of aminoglycosides. Twenty-two patients with normal renal function were studied. Ten received enflurane alone, eight received enflurane plus gentamicin or tobramycin, and four patients who underwent nitrous oxide and narcotic anesthesia were the control group. Preoperative values ranged from 1010 to 2461 µU/24 hour. Urinary AAP excretion increased significantly in both enflurane groups 2 days postoperatively (P < 0.025). Patients who received both enflurane and aminoglycosides had significantly greater urinary AAP excretion on postoperative day 2 than did patients given enflurnne alone: 21,342 ± 4074 µU/24 hour and 6336 ± 1496 µU/24 hour, respectively (mean ± SEM, P < 0.005). There was no change in AAP excretion in the control group compared to baseline; on day 3 AAP was 1412 ± 710 µU/24 hour. No changes in blood urea nitrogen or serum creatinine levels were observed. These data suggest that enflurane increases the renal tubular effects of aminoglycosides, possibly increasing the risk of aminoglycoside renal toxicity.
Key Words: ANESTHETICS, VOLATILE—enflurane KIDNEY—tubular function ANTIBIOTICS—aminoglycosides
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