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      The Effect of the Antioxidant Drug “U-74389G” on Creatinine Levels during Ischemia Reperfusion Injury in Rats

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          Abstract

          Objective: The aim of this experimental study was to examine the effect of the antioxidant drug “U-74389G” on a rat model using an ischemia reperfusion protocol. The effect of U-74389G was studied biochemically by measuring mean blood creatinine levels. Materials and Methods: Forty rats were used in the study. Creatinine levels were measured at 60 min of reperfusion (groups A and C) or at 120 min of reperfusion (groups B and D), where groups A and B were controls and groups C and D received U-74389G administration. Results: U-74389G administration significantly decreased the predicted creatinine levels by 21.02 ± 5.06% (p = 0.0001). Reperfusion time non-significantly increased the predicted creatinine levels by 4.20 ± 6.12% (p = 0.4103). However, U-74389G administration and reperfusion time together produced a significant combined effect in decreasing the predicted creatinine levels by 11.69 ± 3.16% (p = 0.0005). Conclusion: Independent of reperfusion time, U-74389G administration significantly decreased the creatinine levels in an ischemic rat model. This study demonstrates that short-term U-74389G administration improves renal function by increasing creatinine excretion.

          Most cited references13

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          Limitations of creatinine as a filtration marker in glomerulopathic patients.

          To determine the reliability of creatinine as a measure of the glomerular filtration rate (GFR), we compared the simultaneous clearance of creatinine to that of three true filtration markers of graded size in 171 patients with various glomerular diseases. Using inulin (radius [rs] = 15 A) as a reference marker, we found that the fractional clearance of 99mTc-DTPA (rs = 4 A) was 1.02 +/- 0.14, while that of a 19 A rs dextran was 0.98 +/- 0.13, with neither value differing from unity. In contrast, the fractional clearance (relative to inulin) of creatinine (rs = 3 A) exceeded unity, averaging 1.64 +/- 0.05 (P less than 0.001), but could be lowered towards unity by acute blockade of tubular creatinine secretion by IV cimetidine. Cross-sectional analysis of all 171 patients revealed fractional creatinine secretion to vary inversely with GFR. This inverse relationship was confirmed also among individual patients with either deteriorating (N = 28) or remitting (N = 26) glomerular disease, who were studied longitudinally. As a result, changes in creatinine relative to inulin clearance were blunted considerably or even imperceptible. We conclude that true filtration markers with rs less than 20 A, including inulin, are unrestricted in glomerular disease, and that creatinine is hypersecreted progressively by remnant renal tubules as the disease worsens. Accordingly, attempts to use creatinine as a marker with which to evaluate or monitor glomerulopathic patients will result in gross and unpredictable overestimates of the GFR.
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            Relationship between duration of brain death and hemodynamic (in)stability on progressive dysfunction and increased immunologic activation of donor kidneys.

            Consistent difference in graft survival after renal transplantation has been shown when cadaveric transplants are compared to the living related donor situation, in favor of the latter. Recently, evidence has been put forward that brain death has significant effects on the donor organ quality. In this study, we aimed to assess the relation between brain death-induced hemodynamic instability in combination with the duration of brain death on the function and immunogenicity status of potential donor kidneys. In Wistar rats, short-term (1 hour) or long-term (6 hours) brain death in the presence or absence of hemodynamic stability was applied. Sham-operated rats served as controls (1 hour and 6 hours). Organ function was studied by monitoring serum creatinine, lactate dehydrogenase (LDH), lactate, and total protein content. Expression of cell adhesion molecules [intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1)] and the influx of leukocytes in the kidney assessed the immunologic status of the kidney. Progressive organ dysfunction was most pronounced in hemodynamically unstable brain-dead donors reflected by increased serum creatinine levels. Regardless of hemodynamic status, a progressive inflammatory activation by cell adhesion molecule expression and an influx of leukocytes could be observed in kidneys of brain-dead rats compared with nonbrain-dead controls. Brain death causes progressive kidney dysfunction. Also, inflammatory responses reflecting tissue injury are caused by brain death. When hemodynamic instability in the brain-dead donor is not corrected, kidney dysfunction is enhanced and immune activation occurs faster and is more profound. The observed changes may predispose the graft for additional ischemia/reperfusion injury during the transplant process and hence accelerate rejection of the graft after transplantation.
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              Ischemia/Reperfusion-Induced Renal Failure in Rats as a Model for Evaluating Cell Therapies

              Chronic renal failure is a devastating disease that leads to a multitude of complications. Cell therapy has emerged as a potential treatment modality for renal failure. However, efficacy testing on systemic renal function has been challenging due to the limited availability of reliable models that are fully characterized. In this study, we investigated the possibility of using renal ischemia/reperfusion (I/R) injury as a viable model for testing cell therapies. We examined functional and pathological changes in rat kidneys that were exposed to different ischemia times. Male Lewis rats were divided into five groups. Renal failure was induced by clamping both renal pedicles for combinations of 60, 75, and 90 min, followed by reperfusion. Age-matched healthy rats served as controls. Blood was collected at regular intervals for serum chemistry, and kidneys were harvested at the same intervals for histomorphological assessment. Serum creatinine levels of the animals with I/R injury increased significantly after 3 days and returned to normal levels at 4 weeks. Histologically, kidney tissue showed progressive glomerular and tubular deterioration with varying degrees of fibrosis. Animals exposed to 75- and 90-min ischemia combination times consistently generated more severe injury than the 60-min ischemia period. However, these groups resulted in a high mortality rate. A model in which one kidney is exposed to a shorter ischemia time (60 or 90 min) resulted in sustained renal damage with a lower mortality rate. This study shows that kidneys exposed to I/R result in renal tissue damage as well as decreased renal function. This model can be used to study both the short-term and longer-term effects of kidney disease by varying the length of the ischemic time. In particular, the use of longer ischemic times (75 and 90 min) could be used to study new therapies for acute renal disease, whereas shorter ischemic times (60 min) could be used to study therapies for chronic renal insufficiency.
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                Author and article information

                Journal
                CUR
                CUR
                10.1159/issn.1661-7649
                Current Urology
                Curr Urol
                S. Karger AG (Basel, Switzerland karger@ 123456karger.com http://www.karger.com )
                1661-7649
                1661-7657
                May 2016
                20 May 2016
                : 9
                : 2
                : 73-78
                Affiliations
                aDepartment of Obstetrics & Gynecology, Mesologi County Hospital, Etoloakarnania; bDepartment of Obstetrics & Gynecology, Aretaieion Hospital; cDepartment of Surgery, Ippokrateion General Hospital, Athens University, Attiki, Greece; dExperimental Research Centre ELPEN Pharmaceuticals, S.A. Inc., Co.
                Article
                CUR2015009002073 PMC4911526 Curr Urol 2015;9:73-78
                10.1159/000442857
                PMC4911526
                27390579
                90ce232b-5f4e-40ec-87ae-1f20da6fc21b
                © 2016 S. Karger AG, Basel

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher or, in the case of photocopying, direct payment of a specified fee to the Copyright Clearance Center. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                History
                : 14 April 2015
                : 09 June 2015
                Page count
                Tables: 8, References: 29, Pages: 6
                Categories
                Original Paper

                Medicine,General social science
                Ischemia,U-74389G,Creatinine,Reperfusion
                Medicine, General social science
                Ischemia, U-74389G, Creatinine, Reperfusion

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