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• W2067029447 abstract "In Response: Mazze correctly notes that, although markers indicating renal injury increased in the 4-h study, the increases were small, transient, and generally within normal limits for awake humans. Thus, Mazze argues, our 4-h study provides no valid evidence that sevoflurane caused renal injury. We disagree and offer several counterarguments. First, Mazze argues that normal limits for laboratory markers of renal integrity are not validated in anesthetized humans. We disagree. We have demonstrated that the values established in normal awake patients do not differ from those found in volunteers anesthetized with desflurane [1,2]. If Mazze argues that sevoflurane (Compound A) does not injure human kidneys, then he also must argue that desflurane improves renal health. Second, as to valid evidence that 4 h of 1.25 minimum alveolar anesthetic concentration (MAC) sevoflurane anesthesia induced transient mild renal injury, consider that we found increases with sevoflurane or differences between sevoflurane and desflurane in markers of injury for several aspects of nephron integrity: creatinine (glomerular filtration rate), urinary albumin (leakage through glomerular membranes), and urinary alpha-glutathione-S-transferase (alpha-GST; indicates injury to proximal tubules) [3,4]. We found that these measures of injury increased with increasing duration of sevoflurane (but not desflurane) anesthesia [1,2]. In addition, with 8 h of sevoflurane (but not desflurane) anesthesia, glucosuria occurred [1], which, like increased alpha-GST, indicates tubular injury. One might dismiss one of these findings, but not the coincidence of several factors (all except creatinine) increasing in a dose-related manner. As noted by Mazze, serum creatinine increased a maximum of 0.11 mg/dL after 4 h of anesthesia with sevoflurane, and, on the first day after anesthesia, serum creatinine was 0.14 mg/dL greater than after desflurane anesthesia (P < 0.005). We calculate that 0.11 mg/dL equals 11% of the preanesthetic value of 0.99 mg/dL. Assuming constant creatinine production, an 11% increase reflects a 10% decrease in glomerular filtration rate. A 10% decrease in glomerular filtration rate may impress the reader as more clinically relevant (less absurd) than an 0.11-mg/dL increase in creatinine. Large decreases in glomerular filtration rate (i.e., one third) may produce only small increases in creatinine (i.e., 0.5 mg/dL above a normal value of 1.0 mg/dL). In eight of the nine volunteers in the 4-h study, average urinary excretion of albumin was greater after sevoflurane anesthesia than after desflurane anesthesia (P < 0.05). Albuminuria correlates with other evidence (including histologic evidence) of both transient and permanent renal injury in humans [5,6], injury from both drugs and disease. Average urinary albumin for the first 5 days after 4 h of sevoflurane anesthesia increased from preanesthetic control values (P < 0.05), a transient increase indicating increased leakiness of the glomerular membrane. This did not result from anesthesia per se because it was not seen in volunteers given desflurane for 4 h [2] or 8 h [1]. The absence of changes in urinary albumin with desflurane addresses the issue of what constitutes normal values after anesthesia per se in humans. Although Mazze infers otherwise from the paper of Kharasch et al. [7], Kharasch et al.'s work is muddied by the coincident effects of surgery and drugs other than sevoflurane or isoflurane. Regarding alpha-GST, this measure correlates with injury in animals [3] and injury to human kidneys [4]. It is not broadly applied clinically because it is more difficult and expensive to perform than measurement of serum creatinine. That does not diminish its validity as a sensitive marker of proximal tubular injury. At a 2-L/min inflow rate, 1.25 MAC sevoflurane increases urinary alpha-GST after both 4-h [2] and 8-h anesthetic exposures [1]. Again to the issue of what constitutes a normal value, consider that neither 4 h nor 8 h of desflurane anesthesia increases urinary alpha-GST. Third, Mazze challenges our recommendation that we abandon serum creatinine as the (sole) measure of renal injury in future studies of the renal effects of sevoflurane and replace it with more appropriate measures. Our position is unchanged because variables that do not reflect injury to the kidney may increase creatinine, and creatinine may not increase in the presence of injury: 1. Creatinine increases minimally with mild to moderate glomerular injury that decreases glomerular filtration rate (see above), and may remain (as in our study) within the normal range of values [8]. 2. Glomerular injury (e.g., by gold) may allow leakage of proteins through the glomerular membrane without influencing total glomerular filtration rate [5]. Such injury produces albuminuria without altering creatinine or creatinine clearance. 3. Creatinine values provide minimal information about tubular integrity. Compound A injures tubules as well as glomeruli [9-12]. 4. Serum creatinine can increase in the absence of injury to the kidney. Eating meat increases creatinine [13,14]; thus, as in our and other studies, the decrease in appetite after anesthesia should decrease creatinine. Creatinine increases with dehydration sufficient to decrease renal blood flow (prerenal azotemia) [8], and with obstruction of ureteral outflow (postrenal azotemia) [8]. Similarly, Kharasch et al. [7] and Bito et al. [15] demonstrate that serum creatinine is not a sufficient measure of renal injury: creatinine did not increase in either study, but these studies revealed evidence of injury by proteinuria [7] and enzymuria [15]. As in our studies, their patients probably had a decrease in protein intake, a dietary change that would decrease serum creatinine. Mazze asserts that there has not been an increased incidence of adverse renal effects in the 20 million sevoflurane administrations to date. Similarly, at the October 1997 ASA/Anesthesiology-sponsored symposium on sevoflurane and desflurane toxicity, Kharasch asked why renal toxicity has not been reported in anesthesia journals or to the Food and Drug Administration, as has the severe hepatic injury rarely caused by halothane [16] and the severe renal injury produced by methoxyflurane [17,18]. As we have noted [2], the threshold for nephrotoxicity of Compound A in the average human seems to be approximately 150 ppm-h (e.g., 50 ppm breathed for 3 h). A small fraction of the 20 million patients reached that threshold because their procedure was short, because inflow rates were high [diminishing Compound A concentrations [19]], and/or because concentrations of sevoflurane were low [19]. Of that small fraction, injury was rarely noted (and still more rarely reported) because the injury was likely subclinical, the patient was discharged without examination of renal integrity, and/or only serum creatinine was used to measure renal integrity. Reports to the Food and Drug Administration and to journals reveal rare cases of disaster because disaster forces itself to the attention of attending physicians. Such is not the case with subtle injury. However, studies focused on the problem-studies such as our reports-readily reveal such injury. We can debate the clinical significance of apparently transient injury. Injury from several nephrotoxins (e.g., nonsteroidal antiinflammatory drugs, cisplatin, cyclosporin, gold) may resolve if the insult is not repeated. However, if the insult is repeated, injury can become permanent [5,6]. We agree with Mazze and Jamison [20] that sevoflurane should not be used in patients with impaired renal function and wonder whether this also applies to patients, particularly the elderly, undergoing major intraabdominal, thoracic, and vascular surgery, in which renal function may be compromised by impaired volume status or mechanical restriction of abdominal or thoracic aorta blood flow. Further, the anesthesia practitioner usually has insufficient preoperative evidence concerning which patient has impaired renal function [21]. We contend that our report provides valid evidence that 4 h of 1.25 MAC sevoflurane anesthesia administered to volunteers at a 2-L/min inflow rate induces transient mild renal injury. Our findings should be considered in the context of other information on this issue. One would have to believe in an astonishing coincidence to find that the dose-related albuminuria, glucosuria, and enzymuria in humans resulting from exposure to Compound A [1,2,22,23] does not reflect injury. The coincidence becomes more astonishing when one considers that these measures of injury plus histological evidence of injury are also seen in rats [11], occurring at the same threshold for injury-150 ppm-h-found in humans [2]. Whether the administration of sevoflurane at a 2-L/min flow endangers public health remains to be determined. However, flows lower than 2 L/min increase Compound A exposure in a flow-dependent manner [19] and thereby increase the likelihood of clinically relevant toxicity. Edmond I Eger II, MD Richard B. Weiskopf, MD Department of Anesthesia; University of California-San Francisco; San Francisco, CA 94143-0464 Paid consultants to Ohmeda, PPD." @default.
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• W2067029447 title "No Evidence of Sevoflurane-Induced Renal Injury in Volunteers" @default.
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