RENAL-FUNCTION IN PATIENTS WITH HIGH SERUM FLUORIDE CONCENTRATIONS AFTER PROLONGED SEVOFLURANE ANESTHESIA

Background In studies of methoxyflurane-induced nephrotoxicity, renal- concentrating impairment has been observed only when serum inorganic f luoride concentrations exceed 50 mu M. Prolonged sevoflurane anesthesi a can result in serum inorganic fluoride concentrations in excess of 5 0 mu M. The authors compared renal function after prolonged sevofluran e anesthesia with that after isoflurane anesthesia. In addition, they measured urinary excretion of N-acetyl-beta-glucosaminidase (NAG), a s ensitive index of renal tubular damage, during the S-day period after anesthesia. Methods: Thirty-four healthy patients who underwent either sevoflurane (23 patients) or isoflurane (11 patients) anesthesia at a total gas flow of 61/min for orthopedic surgery scheduled to last at least 5 h were studied. At 16.5 h after cessation of anesthesia, patie nts were administered 10 units of vasopressin and urine was collected frequently thereafter for evaluation of urinary osmolality. In additio n, urinary excretion of NAG was measured before and on days 1-3 after anesthesia. Based on whether peak fluoride concentrations exceeded 50 mu M, 23 patients anesthetized with sevoflurane were assigned to a sev oflurane(high)group (>50 mu M) or a sevoflurane(low) (<50 mu M) group. Results: The eight patients in the sevoflurane(high) group had a mean peak fluoride concentration of 57.5 +/- 4.3 mu M. A significant, albe it weak, inverse correlation was found between peak fluoride concentra tion and maximal urinary osmolality after the injection of vasopressin (r = -0.42, P < 0.05). Mean maximum urinary osmolality tended to be l ower in the sevoflurane(high) group (681 +/- 60 mOsm/kg) than in the o ther two groups after administration of vasopressin, although the diff erence among the three groups did not quite reach a statistical signif icance (P = 0.068). One patient had a transient concentrating defect ( maximum urinary osmolality = 390 mOsm/kg) on day 1 after anesthesia. U rinary excretion of NAG in both the sevoflurane(high) and sevoflurane( low) groups was greater on days 2 and 3 after anesthesia than before a nesthesia. The increase in urinary NAG excretion was dose related with sevoflurane, but there was no difference in results of routine labora tory renal tests on days 2 and 3 after anesthesia among the three grou ps. Conclusions: The authors concluded that sevoflurane anesthesia res ults in increased serum fluoride concentration, a tendency toward decr eased maximal ability to concentrate urine, and increased excretion of NAG. However, the increase in urinary NAG excretion was not indicativ e of clinically significant renal damage in these patients with no pre existing renal disease.