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      Chronic Inflammation and CD16+ Natural Killer Cell Zeta-Chain Downregulation in Hemodialysis Patients

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          Abstract

          Background: Natural killer (NK) cell activity is decreased in hemodialysis (HD) patients. Zeta-chain phosphorylation is an early event that follows the triggering of some NK cell-activating receptors. NK cell zeta-chain is downregulated in patients with cancer due to chronic inflammation. HD is also a chronic inflammatory state. NK cell zeta-chain expression in HD was evaluated. Patients and Methods: Thirty-three HD patients and 30 healthy volunteers were enrolled into the study. The CD3–CD16+ subpopulation was examined, since it corresponds to 90% of all NK cells and has the highest cytotoxicity.NK cell count and zeta-chain mean fluorescence intensity were evaluated with flow cytometry. The inflammatory markers C-reactive protein, IL-6 and tumor necrosis factor-α were measured with ELISA. Results: The inflammatory markers were increased in HD patients. NK cell count did not differ between HD patients and healthy volunteers. NK cell zeta-chain mean fluorescence intensity was decreased in the patient group. Conclusions: Chronic inflammation could be responsible for the NK cell zeta- chain downregulation in HD patients, contributing to the decreased NK cell activity.

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          Mortality caused by sepsis in patients with end-stage renal disease compared with the general population.

          In the United States, infection is second to cardiovascular disease as the leading cause of death in patients with end-stage renal disease (ESRD), and septicemia accounts for more than 75% of this category. This increased susceptibility to infections is partly due to uremia, old age, and comorbid conditions. Although it is intuitive to believe that mortality caused by sepsis may be higher in patients with ESRD compared with the general population (GP), no such data are currently available. We compared annual mortality rates caused by sepsis in patients with ESRD (U.S. Health Care Financing Administration 2746 death notification form) with those in the GP (death certificate). Data were abstracted from the U.S. Renal Data System (1994 through 1996 Special Data request) and the National Center for Health Statistics. Data were stratified by age, gender, race, and diabetes mellitus (DM). Sensitivity analyses were performed to account for potential limitations of the data sources. Overall, the annual percentage mortality secondary to sepsis was approximately 100- to 300-fold higher in dialysis patients and 20-fold higher in renal transplant recipients (RTRs) compared with the GP. Mortality caused by sepsis was higher among diabetic patients across all populations. After stratification for age, differences between groups decreased but retained their magnitude. These findings remained robust despite a wide range of sensitivity analyses. Indeed, mortality secondary to sepsis remained approximately 50-fold higher in dialysis patients compared with the GP, using multiple cause-of-death analyses; was approximately 50-fold higher in diabetic patients with ESRD compared with diabetic patients in the GP, when accounting for underreporting of DM on death certificates in the GP; and was approximately 30-fold higher in RTRs compared with the GP, when accounting for the incomplete ascertainment of cause of death among RTRs. Furthermore, despite assignment of primary cause-of-death to major organ infections in the GP, annual mortality secondary to sepsis remained 30- to 45-fold higher in the dialysis population. Patients with ESRD treated by dialysis have higher annual mortality rates caused by sepsis compared with the GP, even after stratification for age, race, and DM. Consequently, this patient population should be considered at high-risk for the development of lethal sepsis.
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            Are there two types of malnutrition in chronic renal failure? Evidence for relationships between malnutrition, inflammation and atherosclerosis (MIA syndrome).

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              Inflammation-associated immune suppression in cancer: the roles played by cytokines, chemokines and additional mediators.

              Chronic inflammation and presence of inflammatory cells, primarily macrophages, at tumor sites are highly associated with specific malignancies. In these cases, the inflammatory milieu is overloaded with mediators that suppress immune activities at many levels: recognition of tumor-associated antigens, activation, the actual cytolysis of tumor cells and more. Local suppression of leukocyte functions at the inflammatory tumor site further contributes to profound immunosuppression of potential anti-tumor immune functions. The present review discusses the inflammatory setup in tumors and the factors inducing the presence of detrimental inflammatory macrophages at tumor sites. Moreover, the different mediators that contribute to inflammation-associated immune suppression, including primarily cytokines and chemokines but also prostaglandins and oxidants, are described. Bearing in mind the notion that under specific conditions the inflammatory mediators clearly contribute to malignancy, while in others they may exert surveillance missions against tumor cells, the potential therapeutic value of the inflammatory components is discussed.
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                Author and article information

                Journal
                BPU
                Blood Purif
                10.1159/issn.0253-5068
                Blood Purification
                S. Karger AG
                0253-5068
                1421-9735
                2008
                July 2008
                07 May 2008
                : 26
                : 4
                : 317-321
                Affiliations
                aNephrology Department, General Hospital of Serres, Serres, bLaboratory of Hematology and cLaboratory of Biochemistry, Theagenion Anticancer Hospital, Thessaloniki, Greece
                Article
                130068 Blood Purif 2008;26:317–321
                10.1159/000130068
                18463433
                75621956-1a72-4798-a933-4866c658f784
                © 2008 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
                : 03 August 2007
                : 07 December 2007
                Page count
                Figures: 4, References: 28, Pages: 5
                Categories
                Original Paper

                Cardiovascular Medicine,Nephrology
                Hemodialysis,Immune response,Inflammation,Natural killer cell,Zeta-chain

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