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      Drug Design, Development and Therapy (submit here)

      This international, peer-reviewed Open Access journal by Dove Medical Press focuses on the design and development of drugs, as well as the clinical outcomes, patient safety, and programs targeted at the effective and safe use of medicines. Sign up for email alerts here.

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      Does remifentanil attenuate renal ischemia–reperfusion injury better than dexmedetomidine in rat kidney?

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          Abstract

          Background

          Ischemia–reperfusion (I/R) injury is a common cause of patient morbidity and mortality in the perioperative period. Patients undergoing long-lasting, abdominal, and urogenital surgeries with risk factors such as advanced age, peripheral artery disease, diabetes mellitus, renovascular disease, and congestive heart failure are candidates for acute kidney injury (AKI) due to impaired renal perfusion and decreased functional renal reserve. Pharmacological agents with multiple functions and anti-oxidative and anti-inflammation properties may be promising preventative strategies for AKI. Recently, dexmedetomidine (dex) has been postulated to have renoprotective effects.

          Objectives

          We aimed to investigate the protective effects of an intravenous anesthetic remifentanil in renal I/R injury in the rat in comparison with dex.

          Materials and methods

          A total of 30 Sprague Dawley adult rats were randomly assigned into five groups: the control group (group C, n=6), the sham group (group Sh, n=6, saline-infused rats without I/R injury), the saline group (group S, n=6, saline-infused rats with I/R injury), the remifentanil-treated group (group REM, n=6), and the dexmedetomidine-treated group (group DEX, n=6). The infusions (saline, remifentanil, and dex) were started after anesthesia induction and right nephrectomy and continued until the end of the surgical procedure. In I/R injury groups, the left renal artery and vein were occluded together by a clamp for 30 minutes and reperfusion lasted for 30 minutes. The rats were sacrificed after reperfusion, and the left kidney tissue was harvested. Blood samples were drawn from all animals to evaluate plasma neutrophil gelatinase-associated lipocalin (NGAL) at the beginning, 15 minutes after ischemia, 15 minutes after reperfusion, and 6 hours after the surgical procedure (T0, T1, T2, and T3, respectively).

          Results

          The plasma NGAL levels exhibited increase at T1, T2, and T3 compared to the levels at T0 in group S ( P<0.05). In group REM, there was a significant increase in plasma NGAL levels at T3 in comparison to those at T0, T1, and T2. The plasma NGAL levels at T2 in group S were significantly higher than those at T2 in group DEX ( P<0.05). The groups S and REM showed significantly higher plasma NGAL levels at T3 compared to those at T0 ( P<0.05). Upon histological examination, there was no difference among the study groups when left kidneys were evaluated ( P>0.05).

          Conclusion

          The NGAL levels and histopathological findings reflected protection by dex against renal I/R injury. However, the same exact results could not be mentioned for remifentanil depending on our study results.

          Most cited references40

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          The outcome of neutrophil gelatinase-associated lipocalin-positive subclinical acute kidney injury: a multicenter pooled analysis of prospective studies.

          Michael Haase, Prasad Devarajan, Anja Haase-Fielitz … (2011)
          The aim of this study was to test the hypothesis that, without diagnostic changes in serum creatinine, increased neutrophil gelatinase-associated lipocalin (NGAL) levels identify patients with subclinical acute kidney injury (AKI) and therefore worse prognosis. Neutrophil gelatinase-associated lipocalin detects subclinical AKI hours to days before increases in serum creatinine indicate manifest loss of renal function. We analyzed pooled data from 2,322 critically ill patients with predominantly cardiorenal syndrome from 10 prospective observational studies of NGAL. We used the terms NGAL(-) or NGAL(+) according to study-specific NGAL cutoff for optimal AKI prediction and the terms sCREA(-) or sCREA(+) according to consensus diagnostic increases in serum creatinine defining AKI. A priori-defined outcomes included need for renal replacement therapy (primary endpoint), hospital mortality, their combination, and duration of stay in intensive care and in-hospital. Of study patients, 1,296 (55.8%) were NGAL(-)/sCREA(-), 445 (19.2%) were NGAL(+)/sCREA(-), 107 (4.6%) were NGAL(-)/sCREA(+), and 474 (20.4%) were NGAL(+)/sCREA(+). According to the 4 study groups, there was a stepwise increase in subsequent renal replacement therapy initiation-NGAL(-)/sCREA(-): 0.0015% versus NGAL(+)/sCREA(-): 2.5% (odds ratio: 16.4, 95% confidence interval: 3.6 to 76.9, p < 0.001), NGAL(-)/sCREA(+): 7.5%, and NGAL(+)/sCREA(+): 8.0%, respectively, hospital mortality (4.8%, 12.4%, 8.4%, 14.7%, respectively) and their combination (4-group comparisons: all p < 0.001). There was a similar and consistent progressive increase in median number of intensive care and in-hospital days with increasing biomarker positivity: NGAL(-)/sCREA(-): 4.2 and 8.8 days; NGAL(+)/sCREA(-): 7.1 and 17.0 days; NGAL(-)/sCREA(+): 6.5 and 17.8 days; NGAL(+)/sCREA(+): 9.0 and 21.9 days; 4-group comparisons: p = 0.003 and p = 0.040, respectively. Urine and plasma NGAL indicated a similar outcome pattern. In the absence of diagnostic increases in serum creatinine, NGAL detects patients with likely subclinical AKI who have an increased risk of adverse outcomes. The concept and definition of AKI might need re-assessment. Copyright © 2011 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.
          Article 0 comments Cited 203 times – based on 0 reviews     Review now
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            Neutrophil Gelatinase-Associated Lipocalin: A Novel Early Urinary Biomarker for Cisplatin Nephrotoxicity

            Jaya Mishra, Kiyoshi Mori, Qing Ma … (2004)
            Background: Cisplatin is one of the most widely used chemotherapeutic agents, but the risk of nephrotoxicity frequently hinders the use of higher doses to maximize its antineoplastic effects. The lack of early biomarkers has impaired our ability to initiate potential therapeutic or preventive interventions in cisplatin nephrotoxicity in a timely manner. In this study, we have explored the expression and urinary excretion of neutrophil gelatinase-associated lipocalin (NGAL) in a mouse model of cisplatin-induced nephrotoxic injury. Methods: Mice were subjected to intraperitoneal injections of 20 mg/kg (high dose) or 5 mg/kg (low dose) cisplatin. The expression of NGAL was measured in the kidney and urine by Western analysis and immunofluorescence, and compared to changes in serum creatinine and urinary N-acetyl-β- D -glucosaminidase (NAG). Results: Cisplatin resulted in tubule cell necrosis and apoptosis following the high dose, but not the low dose. By Western analysis, NGAL protein was rapidly induced in the kidney within 3 h of high-dose cisplatin. By immunofluorescence, NGAL was induced predominantly in proximal tubule cells in a punctate cytoplasmic distribution, reminiscent of a secreted protein. NGAL was easily detected in the urine by Western analysis within 3 h of cisplatin administration in a dose- and duration-dependent manner. By comparison, changes in urinary NAG or serum creatinine were not evident until 96 h after cisplatin. Using defined concentrations of purified recombinant NGAL, urinary NGAL excretion following cisplatin administration was quantified to be in the 20–80 ng/ml range. Conclusion: The results indicate that NGAL represents an early and quantitative urinary biomarker for cisplatin nephrotoxicity.
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              Dexmedetomidine: current role in anesthesia and intensive care.

              Joana Afonso, Flávio Reis (2015)
              To update and review the application of dexmedetomidine in anesthesia and intensive care. This study is a comprehensive review of clinical uses, pharmacology, pharmacokinetics, mechanism of action and adverse effects of dexmedetomidine. The effective use of sedative-hypnotic agents and analgesics is an integral part of comfort and safety of patients. Dexmedetomidine is a potent and highly selective α-2 adrenoceptor agonist with sympatholytic, sedative, amnestic, and analgesic properties, which has been described as a useful and safe adjunct in many clinical applications. It provides a unique "conscious sedation", analgesia, without respiratory depression. The current reviewed uses include sedation at Intensive Care Unit-ICU (both adult and pediatric), emergency department, regional and general anesthesia, neurosurgery, sedation for pediatric procedures, awake fiber-optic intubation, cardiac surgery and bariatric surgery. Dexmedetomidine offers a unique ability of providing both sedation and analgesia without respiratory depression. It is a new agent with a wide safety margin, excellent sedative capacity and moderate analgesic properties. Although its wide use is currently in patients of surgical and non-surgical intensive care units, dexmedetomidine seems to have promising future applications in neuroprotection, cardioprotection and renoprotection. More detailed studies are required to define its role as sedative in critical, neurosurgical and pediatric patients, as anesthesia adjunct and sedative during procedures. Copyright © 2012 Elsevier Editora Ltda. All rights reserved.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Drug Des Devel Ther
                Journal ID (iso-abbrev): Drug Des Devel Ther
                Journal ID (publisher-id): Drug Design, Development and Therapy
                Title: Drug Design, Development and Therapy
                Publisher: Dove Medical Press
                ISSN (Electronic): 1177-8881
                Publication date Collection: 2017
                Publication date (Electronic): 08 March 2017
                Volume: 11
                Pages: 677-683
                Affiliations
                [1 ]Anesthesiology and Reanimation Department
                [2 ]General Surgery Department, Atatürk Training and Research Hospital
                [3 ]Biochemistry Department, Faculty of Medicine, Gazi University
                [4 ]Pathology Department, Atatürk Training and Research Hospital
                [5 ]General Surgery Clinic, Faculty of Medicine, Yıldırım Beyazıt University, Ankara, Turkey
                Author notes
                Correspondence: E Erkılıç, Ahmet Taner Kışlalı mh Park cd Rönesans evleri A-11 Çayyolu Ankara 06530, Turkey, Tel +90 505 366 3491, Email eerkilic72@ 123456yahoo.com
                Article
                Publisher ID: dddt-11-677
                DOI: 10.2147/DDDT.S126701
                PMC ID: 5352155
                SO-VID: 2387270f-3a04-4e74-83e3-f629eb442be2
                Copyright © © 2017 Erkılıç et al. This work is published and licensed by Dove Medical Press Limited
                License:

                The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

                History
                Categories
                Subject: Original Research

                ScienceOpen disciplines: Pharmacology & Pharmaceutical medicine
                Keywords: ischemia–reperfusion,dexmedetomidine,remifentanil,neutrophil gelatinase-associated lipocalin
                Data availability:
                ScienceOpen disciplines: Pharmacology & Pharmaceutical medicine
                Keywords: ischemia–reperfusion, dexmedetomidine, remifentanil, neutrophil gelatinase-associated lipocalin

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