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

Goldberg, Michael E.; Cantillo, Joaquin; Gratz, Irwin; Deal, Edward; Vekeman, Denis; McDougall, Robert J; Afshar, Mary; Zafeiridis, Andreas; Larijani, Ghassem E.

doi:10.1213/00000539-199902000-00040

Cited by 51 publications

(7 citation statements)

References 18 publications

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“…Although transient nephrotoxicity was demonstrated by Eger et al [19] and Goldberg et al [20] with respectively 80-160 ppm/h and 240 ppm-h of CA exposure in humans, the majority of publications demonstrate no nephrotoxicity in humans with the use of sevoflurane in combination with any kind of absorbent [21][22][23]. The results of this study, together with the results from our laboratory study [9], confirm these observations.…”

Section: Discussionsupporting

confidence: 83%

Inspiratory Carbon Monoxide and Compound A Concentrations During Desflurane and Sevoflurane Anesthesia in Humans: An Observational Study

Keijzer¹,

Pérez²,

Lange³

2008

TOATJ

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Section: Discussionsupporting

confidence: 83%

Inspiratory Carbon Monoxide and Compound A Concentrations During Desflurane and Sevoflurane Anesthesia in Humans: An Observational Study

Keijzer¹,

Pérez²,

Lange³

2008

TOATJ

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“…In animal and human studies, increased urinary alpha GST (α-GST), a proximal tubule cystosolic enzyme, has been reported in response to Compound A, a nephrotoxic metabolite of sevofluorane (Kharasch et al, 1997;Goldberg et al, 1999). Pai et al (2005) reported increased urinary levels of α-GST and pi-GST, a distal tubule cytosolic enzyme, in male patients but not female patients following amphotericin B administration.…”

Section: Urinary Proteins With Enzymatic Activitymentioning

confidence: 99%

Biomarkers of nephrotoxic acute kidney injury

2008

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Acute kidney injury (AKI) is a common condition with significant associated morbidity and mortality. Epidemiologic data suggest that a significant proportion of AKI cases are at least partially attributable to nephrotoxin exposure. This is not surprising given intrinsic renal susceptibility to toxicant-induced injury, a consequence of the unique physiologic and biochemical properties of the normally functioning kidney. A number of pathophysiologic mechanisms have been identified that mediate toxic effects on the kidney, resulting in a variety of clinical syndromes ranging from subtle changes in tubular function to fulminant renal failure. Unfortunately, standard metrics used to diagnosis and monitor kidney injury, such as blood urea nitrogen and serum creatinine, are insensitive and nonspecific, resulting in delayed diagnosis and intervention. Considerable effort has been made to identify biomarkers that will allow the earlier diagnosis of AKI. Further characterization of these candidate biomarkers will clarify their utility in the setting of acute nephrotoxicity, define new diagnostic and prognostic paradigms for kidney injury, facilitate clinical trials, and lead to novel effective therapies.

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“…Eger et al sowie Goldberg et al berichteten von vorübergehender Albumin-und Enzymurie (α-GST, π-GST) nach 4-bzw. 8-stündiger Exposition gegenüber Compound A [7,8,15].Auch Higuchi et al berichteten von einer milden, vorübergehenden Proteinurie während Sevoflurannarkosen unter Low-flow-Bedingungen [16].Allerdings wurde in keiner dieser Studien Veränderung von Harnstoff und Kreatinin im Serum oder der Kreatininclearance berichtet.…”

Section: Zusammenfassungunclassified

Einfluss von niedrigem Alkalimetallgehalt im Atemkalk auf Compound-A-Bildung während Low-flow-Narkosen mit Sevofluran

Reichle¹,

Conzen²,

Czerner³

et al. 2001

Der Anaesthesist

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The alkali hydroxide content in soda lime induces Compound A formation from Sevoflurane (Sevo). This study was designed to answer the question if the use of potassium hydroxide-free Soda Lime (SL) would lead to lower Compound A levels as compared to Sodasorb (SO). A total of 30 patients scheduled for elective laparoscopic cholecystectomy received Sevo anaesthesia under low-flow conditions (0.8 l/min fresh gas flow). Each absorbent was used in 15 patients, but 3 patients of the SO group were excluded due to technical problems with Compound A analysis. Hemodynamic parameters, parameters of ventilation and gas concentrations were documented. Compound A concentrations were measured by gas chromatography from gas samples before Sevo application and 20, 40, 60, 90 and 120 min after low-flow start. Mean endtidal Sevo concentrations were 1.94 +/- 0.17 (SO) and 1.97 +/- 0.15 (SL) vol %, the total anaesthetic exposition was 1.52 +/- 0.36 (SO) and 1.64 +/- 0.47 (SL) MAC-h (n.s). The maximum Compound A concentration was significantly higher in SL group (19.6 +/- 2.8 vs. 11.7 +/- 4.1 ppm, p < 0.001). Therefore, elimination of potassium hydroxide from carbon dioxide absorbents alone did not lead to a reduction of Compound A formation during low-flow anaesthesia.

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

Cited by 51 publications

References 18 publications

Inspiratory Carbon Monoxide and Compound A Concentrations During Desflurane and Sevoflurane Anesthesia in Humans: An Observational Study

Inspiratory Carbon Monoxide and Compound A Concentrations During Desflurane and Sevoflurane Anesthesia in Humans: An Observational Study

Biomarkers of nephrotoxic acute kidney injury

Einfluss von niedrigem Alkalimetallgehalt im Atemkalk auf Compound-A-Bildung während Low-flow-Narkosen mit Sevofluran

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