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Sevoflurane and postoperative renal function: are omitted clinical data of concern?

The recent article by Goldberg et al. (1) addressing possible sevoflurane induced nephrotoxicity omits important details that may suggest more likely causes of their findings. The authors’ thesis that sevoflurane may cause renal toxicity is based on two patients (Patients 318 and 323) who underwent prolonged intraabdominal surgery and had postoperative increases in serum creatinine. Because of the small sample size, if the increases in postoperative serum creatinine were, in fact, unrelated to sevoflurane, there is a considerable probability that both patients ended up in the sevoflurane group simply by chance. The increase in creatinine of 0.2 mg/dL in Patient 318 could represent assay variability or postoperative intravascular dehydration. The coefficient of variation for creatinine at the laboratory doing the analysis, evidence of low urine output after surgery, and the duration of the creatinine increase would help clarify this issue. The time course of the increase in serum creatinine from 0.8 to 1.6 mg/dL in Patient 323 was not presented. If this patient truly had suffered renal damage to the extent that the serum creatinine doubled, it is unlikely that this injury would have resolved quickly. Fluoride-induced nephrotoxicity results in polyuria due to a loss of concentrating ability, but this patient had poor urine output and received furosemide. This patient also had concurrent hyperglycemia, but the glucose value and its treatment were omitted from the paper. The Goldberg study was part of a multicenter trial, but the number of sites and total enrollment are not stated. This may have helped put the results of their sample in its proper context. Were the authors aware of the data analysis from the entire study, and, if so, were the results they report representative of the entire database?