21
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Bicarbonates for the Prevention of Postoperative Renal Failure in Endovascular Aortic Aneurysm Repair: A Randomized Pilot Trial

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Purpose. Contrast-induced nephropathy (CIN) can contribute to acute kidney injury (AKI) in patients undergoing endovascular aortic aneurysm surgery. We evaluated the incidence of AKI together with the evolution of early biomarkers of renal injury in patients receiving bicarbonates or NaCl 0.9%. Methods. This study involved endovascular aortic aneurysm surgery patients. Group A ( n = 17) received bicarbonates 3 mL/kg/h for 1 h before the procedure and then 1 mL/kg/h until 6 h after surgery, whereas group B ( n = 17) received NaCl 0.9% using the same protocol. Biomarkers of renal injury from urine (interleukin-18 (IL-18), neutrophil gelatinase-associated lipocalin (NGAL), N-acetyl- β-D-glucosaminidase (NAG), and kidney injury molecule 1 (KIM-1)) and blood (NGAL, cystatin C) were measured at baseline and 3, 24, and 48 h postoperatively. Results. AKI occurred in 1 patient (2.9%), in the bicarbonates group. IL-18, NAG, NGAL, and KIM-1 significantly rose in both groups after the surgery. There was a greater rise in NGAL and IL-18 after 3 h in the bicarbonates versus NaCl 0.9% group: 1115% versus 240% increase ( P = 0.03) and 338% increase versus 1.4% decrease ( P = 0.01). Conclusions. Despite significant elevation in biomarkers of renal injury, we demonstrated a low rate of AKI following endovascular aortic surgery.

          Related collections

          Most cited references 50

          • Record: found
          • Abstract: found
          • Article: not found

          A simple risk score for prediction of contrast-induced nephropathy after percutaneous coronary intervention: development and initial validation.

          We sought to develop a simple risk score of contrast-induced nephropathy (CIN) after percutaneous coronary intervention (PCI). Although several risk factors for CIN have been identified, the cumulative risk rendered by their combination is unknown. A total of 8,357 patients were randomly assigned to a development and a validation dataset. The baseline clinical and procedural characteristics of the 5,571 patients in the development dataset were considered as candidate univariate predictors of CIN (increase >or=25% and/or >or=0.5 mg/dl in serum creatinine at 48 h after PCI vs. baseline). Multivariate logistic regression was then used to identify independent predictors of CIN with a p value 75 years, anemia, and volume of contrast) were assigned a weighted integer; the sum of the integers was a total risk score for each patient. The overall occurrence of CIN in the development set was 13.1% (range 7.5% to 57.3% for a low [ or=16] risk score, respectively); the rate of CIN increased exponentially with increasing risk score (Cochran Armitage chi-square, p < 0.0001). In the 2,786 patients of the validation dataset, the model demonstrated good discriminative power (c statistic = 0.67); the increasing risk score was again strongly associated with CIN (range 8.4% to 55.9% for a low and high risk score, respectively). The risk of CIN after PCI can be simply assessed using readily available information. This risk score can be used for both clinical and investigational purposes.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Prevention of contrast-induced nephropathy with sodium bicarbonate: a randomized controlled trial.

            Contrast-induced nephropathy remains a common complication of radiographic procedures. Pretreatment with sodium bicarbonate is more protective than sodium chloride in animal models of acute ischemic renal failure. Acute renal failure from both ischemia and contrast are postulated to occur from free-radical injury. However, no studies in humans or animals have evaluated the efficacy of sodium bicarbonate for prophylaxis against contrast-induced nephropathy. To examine the efficacy of sodium bicarbonate compared with sodium chloride for preventive hydration before and after radiographic contrast. A prospective, single-center, randomized trial conducted from September 16, 2002, to June 17, 2003, of 119 patients with stable serum creatinine levels of at least 1.1 mg/dL (> or =97.2 micromol/L) who were randomized to receive a 154-mEq/L infusion of either sodium chloride (n = 59) or sodium bicarbonate (n = 60) before and after iopamidol administration (370 mg iodine/mL). Serum creatinine levels were measured at baseline and 1 and 2 days after contrast. Patients received 154 mEq/L of either sodium chloride or sodium bicarbonate, as a bolus of 3 mL/kg per hour for 1 hour before iopamidol contrast, followed by an infusion of 1 mL/kg per hour for 6 hours after the procedure. Contrast-induced nephropathy, defined as an increase of 25% or more in serum creatinine within 2 days of contrast. There were no significant group differences in age, sex, incidence of diabetes mellitus, ethnicity, or contrast volume. Baseline serum creatinine was slightly higher but not statistically different in patients receiving sodium bicarbonate treatment (mean [SD], 1.71 [0.42] mg/dL [151.2 [37.1] micromol/L] for sodium chloride and 1.89 [0.69] mg/dL [167.1 [61.0] micromol/L] for sodium bicarbonate; P =.09). The primary end point of contrast-induced nephropathy occurred in 8 patients (13.6%) infused with sodium chloride but in only 1 (1.7%) of those receiving sodium bicarbonate (mean difference, 11.9%; 95% confidence interval [CI], 2.6%-21.2%; P =.02). A follow-up registry of 191 consecutive patients receiving prophylactic sodium bicarbonate and meeting the same inclusion criteria as the study resulted in 3 cases of contrast-induced nephropathy (1.6%; 95% CI, 0%-3.4%). Hydration with sodium bicarbonate before contrast exposure is more effective than hydration with sodium chloride for prophylaxis of contrast-induced renal failure.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              NGAL is an early predictive biomarker of contrast-induced nephropathy in children.

              We hypothesized that neutrophil gelatinase-associated lipocalin (NGAL) is an early predictive biomarker of contrast-induced nephropathy (CIN). We prospectively enrolled 91 children (age 0-18 years) with congenital heart disease undergoing elective cardiac catheterization and angiography with contrast administration (CC; Ioversol). Serial urine and plasma samples were analyzed in a double-blind fashion by NGAL enzyme-linked immunosorbent assay (ELISA). CIN, defined as a 50% increase in serum creatinine from baseline, was found in 11 subjects (12%), but detection using increase in serum creatinine was only possible 6-24 h after CC. In contrast, significant elevation of NGAL concentrations in urine (135 +/- 32 vs. 11.6 +/- 2 ng/ml without CIN, p < 0.001) and plasma (151 +/- 34 vs. 36 +/- 4 without CIN, p < 0.001) were noted within 2 h after CC in those subjects. Using a cutoff value of 100 ng/ml, sensitivity, specificity, and area under the receiver-operating characteristic (ROC) curve for prediction of CIN were excellent for the 2-h urine NGAL (73%, 100%, and 0.92, respectively) and 2-h plasma NGAL (73%, 100%, and 0.91, respectively). By multivariate analysis, the 2-h NGAL concentrations in the urine (R (2) = 0.52, p < 0.0001) and plasma (R (2) = 0.72, p < 0.0001) were found to be powerful independent predictors of CIN. Patient demographics and contrast volume were not predictive of CIN.
                Bookmark

                Author and article information

                Journal
                Anesthesiol Res Pract
                Anesthesiol Res Pract
                ARP
                Anesthesiology Research and Practice
                Hindawi Publishing Corporation
                1687-6962
                1687-6970
                2013
                12 June 2013
                : 2013
                Affiliations
                1Anesthesiology Department, University of Montreal Hospital Centre, 3840 St. Urbain Street, Montréal, QC, Canada H2W 1T8
                2Department of Anesthesiology, Maisonneuve-Rosemont Hospital, 5415 Boulevard de l'Assomption, Montréal, QC, Canada H1T 2M4
                3Nephrology Department and Guy-Bernier Research Centre, Maisonneuve-Rosemont Hospital, Canada
                4Vascular Surgery Department, University of Montreal Hospital Centre, 3840 St. Urbain Street, Montréal, QC, Canada H2W 1T8
                5Radiology Department, University of Montreal Hospital Centre, 3840 St. Urbain Street, Montréal, QC, Canada H2W 1T8
                6Department of Pharmacology, University of Montreal, 3840 St. Urbain Street, Montréal, QC, Canada H2W 1T8
                Author notes
                *Véronique Brulotte: verobrulotte@ 123456hotmail.com

                Academic Editor: Peter Andrews

                Article
                10.1155/2013/467326
                3694372
                23840204
                Copyright © 2013 Véronique Brulotte et al.

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                Categories
                Research Article

                Anesthesiology & Pain management

                Comments

                Comment on this article