Assessment of Low-Flow Sevoflurane and Isoflurane Effects on Renal Function Using Sensitive Markers of Tubular Toxicity

Kharasch, Evan D.; Frink, Edward J.; Zager, Richard A.; Bowdle, T. Andrew; Artu, Man; Nogami, Wallace M.; Adams, A. P.

doi:10.1097/00132586-199804000-00013

Cited by 34 publications

(54 citation statements)

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“…Candidate molecules have included both structural proteins (e.g., renal tubular epithelial, "RTE" antigen; i.e., megalin; see reference 1) and proximal tubular enzymes (e.g., N-acetylglucosaminidase; alkaline phosphatase and ␥-glutamyltransferase). [2][3][4][5][6] A second approach has been to document proximal tubular dysfunction, as denoted by decreased tubular reabsorption of freely filtered low molecular weight proteins (e.g., ␤2 microglobin, lysozyme, and cystatin C). [7][8][9] Third, the approach that recently has received the greatest attention has been quantifying the urinary excretion of renal tubular proteins that are acutely overexpressed in response to AKI.…”

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confidence: 99%

MCP-1 Gene Activation Marks Acute Kidney Injury

Munshi¹,

Johnson²,

Siew³

et al. 2011

Journal of the American Society of Nephrology

136

107

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Monocyte chemoattractant protein 1 (MCP-1) mediates acute ischemic and toxic kidney injury, but whether this can be used as a biomarker of acute kidney injury (AKI) is unknown. We obtained kidney and urine samples from mice with intrarenal (maleate), prerenal (endotoxemia), or postrenal (ureteral obstruction) injury. We also studied the independent effects of uremia without concomitant kidney injury by performing bilateral ureteral transection in mice. Additionally, we obtained urine samples from APACHE II-matched critically ill patients with or without advancing azotemia (n ϭ 10 in each group). We assayed selected samples for MCP-1, MCP-1 mRNA, and for an activating histone mark (H3K4m3) at urinary fragments of the MCP-1 gene and contrasted the results with those obtained for neutrophil gelatinase-associated lipocalin (NGAL), a comparator "AKI biomarker" gene. Maleate increased urinary MCP-1 protein and mRNA more than the corresponding increases in NGAL. Endotoxemia and ureteral obstruction also increased NGAL and MCP-1 gene expression. Uremia, in the absence of renal injury, induced the NGAL gene, but not MCP-1, suggesting the possibility of better specificity of MCP-1 for AKI. Clinical assessments supported the utility of MCP-1 as a biomarker (e.g., nonoverlapping concentrations of urinary MCP-1 in patients with and without AKI). Elevated levels of urinary MCP-1 mRNA and levels of H3K4m3 at the MCP-1 gene supported MCP-1 gene activation in patients with renal injury. In conclusion, these data suggest that MCP-1 has potential as a biomarker of AKI and provide "proof of concept" that urinary histone assessments provide mechanistic insight among patients with kidney disease.

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mentioning

confidence: 99%

MCP-1 Gene Activation Marks Acute Kidney Injury

Munshi¹,

Johnson²,

Siew³

et al. 2011

Journal of the American Society of Nephrology

136

107

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“…The significance of a positive result (increased enzymuria) is questionable because the clinical predictive value of enzymuria is unknown. 22 Our results showed that all groups had positive enzymuria and tubular damage in preoperative period, probably due to arterial disease.…”

Section: Discussionmentioning

confidence: 50%

Enzyme Biomarkers of Renal Tubular Injury in Arterial Surgery Patients

et al. 2011

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Objective: The aim of this study was to verify whether preoperative diabetes, hypertension, and renal function had any relationship with postoperative tubule function in patients submitted to anesthesia for arterial surgery. Methods: Prospective observational study. One hundred and forty-four patients submitted to anesthesia for arterial surgery enrolled consecutively and divided into four groups: G1 -diabetes and hypertension; G2 -diabetes; G3 -hypertension; and G4 -without hypertension or diabetes. Urine was obtained for laboratory analysis of urinary creatinine (Ucr), alkaline phosphatase (AP), g-glutamyltransferase (gGT), and blood for cystatin C and creatinine before the surgery (M1) and 24 h after the surgery (M2). Results: Values of gGT, gGT/Ucr, and AP × gGT/Ucr increased at M2 in G4. Patients without renal function compromise (GFR ≥90 mL/min/1.73 m 2 ) presented increased gGT/Ucr and AP × gGT/Ucr values at M2 and those with slightly compromised renal function (60-89 mL/min/1.73 m 2 ) presented increased gGT values at M2. There was no correlation between deltaCystatin C and deltaAP, deltagGT, deltagGT/Ucr, deltaAP/Ucr, and deltaAP × gGT/Ucr. Conclusions: Diabetes, hypertension, and preoperative renal function seem to interfere in tubular enzymuria immediately after surgery in arteriopathic patients. However, when these markers do not increase in postoperative period, renal dysfunction cannot be discarded.

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“…Al though CpA was shown to exhibit nephrotoxicity in rodents, no significant changes in renal function parameters were reported in surgical patients (5,26,31,32). In a previous study, it was reported that plasma inorganic fluoride concentrations were regularly increased after sevoflurane anesthesia and were not associated with nephrotoxicity.…”

Section: Discussionmentioning

confidence: 99%

“…In rats, it was shown that both degradation products from 150 to 300-ppm/h concentrations could injure rat kidneys and compound A (CpA) caused corticomedullary tubular necrosis loca lized to the proximal tubule (5). However, its effect on the human kidney is not known (6).…”

Section: Introductionmentioning

confidence: 99%

“…Besides, desflurane causes carbon monoxide poisoning by producing carbon monoxide as enflurane and isoflurane do (8). Carbon monoxide can significantly elevate carboxyhemoglobin concentrations and it is not known if carboxyhemoglobin is degraded to difluorovinyl products, which are nephrotoxic (5,12). Desflurane and sevoflurane were reported to have no adverse effects on hepatic metabolic function and most of the clinical studies have shown that low-flow anesthesia with desflurane and sevoflorane did not change renal and hepatic functions as well (13)(14)(15).…”

Section: Introductionmentioning

confidence: 99%

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Biochemical Effects of Low-Flow Anesthesia with Inhalation agents in Patients undergoing Laparoscopic Surgery

Sivaci¹,

Demir²,

Köken³

et al. 2012

Journal of Medical Biochemistry

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Summary: This study was designed to investigate the effects of low-flow anesthesia with sevoflurane and desflurane on renal and hepatic functions in patients undergoing laparoscopic abdominal surgery. Twenty patients with ASA I or II (American Society of Anesthesiologists classification) physi cal scores were included in the study. There were no signifi cant differences between sevoflurane and desflurane groups with respect to age, weight, body mass index, duration of the operation and the anesthesia. In both groups, renal function parameters such as urea, BUN, creatinine and calculated creatinine clearance did not show significant differences at 24 and 48 hours. Homocysteine levels, which showed renal metabolic function, did not change significantly at 24 and 48 hours when compared to baseline le vels in both groups. Transaminases were not significantly different between the two groups from baseline to 24 and 48 hours. These differences between the preoperative and post operative values of biochemical parameters were similar for both anes thetic groups (p>0.05). Low-flow anesthesia did not cause impairment in terms of renal and hepatic functions.

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Assessment of Low-Flow Sevoflurane and Isoflurane Effects on Renal Function Using Sensitive Markers of Tubular Toxicity

Cited by 34 publications

References 0 publications

MCP-1 Gene Activation Marks Acute Kidney Injury

MCP-1 Gene Activation Marks Acute Kidney Injury

Enzyme Biomarkers of Renal Tubular Injury in Arterial Surgery Patients

Biochemical Effects of Low-Flow Anesthesia with Inhalation agents in Patients undergoing Laparoscopic Surgery

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