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      The Inflammatory Cascade in Acute Ischemic Renal Failure

      review-article
      Nephron
      S. Karger AG
      Leukocytes, Nitric oxide, Kidney, Acute renal failure, Ischemia-reperfusion, Cytokines, Inflammation, Polymorphoneutrophils

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          Abstract

          The pathogenesis of human acute ischemic renal failure is complex. Studies in animals have revealed a number of factors that could contribute to the injury associated with acute ischemic renal failure. Despite these discoveries, we have yet to devise a therapeutic regimen that will ameliorate or prevent acute renal failure in humans. Nevertheless we have made great strides in understanding mechanisms that contribute to acute ischemic renal failure. An important component is the contribution of the inflammatory cascade brought about by tissue reperfusion following an ischemic period. This review summarizes recent studies that implicate the inflammatory cells in the development of renal injury associated with acute ischemic renal failure. Because of the complex overlapping pathways involved in the inflammatory cascade, blocking single molecules is unlikely to be successful in reducing renal injury. Rather broadly abrogating the inflammatory cascade is likely to yield the greatest success in the treatment and prevention of acute ischemic renal failure.

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          Author and article information

          Journal
          NEF
          Nephron
          10.1159/issn.1660-8151
          Nephron
          S. Karger AG
          1660-8151
          2235-3186
          2002
          February 2002
          30 January 2002
          : 90
          : 2
          : 133-138
          Affiliations
          Department of Medicine, University of Virginia, Charlottesville, Va., USA
          Article
          49032 Nephron 2002;90:133–138
          10.1159/000049032
          11818695
          6bd911bd-0913-498c-9723-db2e87422e65
          © 2002 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. 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
          Page count
          Figures: 3, References: 47, Pages: 6
          Categories
          Distinguished Scientists Lecture Series. Section Editors: Chan, J.C.M.; Krieg, R.J., Jr.; Scheinmann, J.I. (Richmond, Va.)

          Cardiovascular Medicine,Nephrology
          Leukocytes,Nitric oxide,Kidney,Acute renal failure,Ischemia-reperfusion,Cytokines,Inflammation,Polymorphoneutrophils

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