Dose of Compound A, Not Sevoflurane, Determines Changes in the Biochemical Markers of Renal Injury in Healthy Volunteers

Abstract

We examined the dose-response relationship of sevoflurane/Compound A and urinary excretion of albumin, glucose, and alpha-GST. Sevoflurane exposure for 8 h at a 2-L/min inflow rate produces transient albuminuria and enzymuria in healthy volunteers when the dose of Compound A exceeds 240 ppm-h (30 ppm for 8 h).

Case report: proximal tubule impairment following volatile anesthetic exposure

“…1998; Goldberg et al. 1999) in addition to surgical patients, suggesting that the observed glycosuria is related to anesthesia rather than clinical confounders such as may occur in surgical patients. Glycosuria has been frequently observed following the use of sevoflurane (Eger et al.…”

“…1997; Goldberg et al. 1999; Ebert and Arain 2000) and resolving within seven to 14 days (Eger et al. 1997b; Ebert et al.…”

“…1998; Goldberg et al. 1999). The time-course of proteinuria parallels that of glycosuria, typically abating within 7 days (Eger et al.…”

“…1998; Goldberg et al. 1999). As with glycosuria, desflurane appears to induce less proteinuria than sevoflurane (Eger et al.…”

Effect of sevoflurane on grafted kidney function in renal transplantation

“…In human volunteers, compound A, at concentrations ranging from 150 to 342 ppm-h after sevoflurane administration, induced transient abnormalities in urine biochemical markers [4,5]. Furthermore, compound A exposures of 240 ppm-h from sevoflurane resulted in albuminuria and increased excretion of α-glutathione-S-transferase (a biochemical marker in urine) [7]. Additionally, surgical patients with low-flow sevoflurane anesthesia were exposed to compound A at 214 ppm-h and exhibited mild, transient proteinuria and increased excretion of N-acetyl-β-D-glucosaminidase (a lysosomal enzyme located in the proximal renal tubule) [8].…”