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      Hemostasis, Platelet Functions, Serotonin and Serum Lipids during Omega-3 Fatty Acid Treatment in Patients with Glomerulonephritis

      a , a , b , b , a

      Nephron

      S. Karger AG

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          A controlled trial of fish oil in IgA nephropathy. Mayo Nephrology Collaborative Group.

          The n-3 fatty acids in fish oil affect eicosanoid and cytokine production and therefore have the potential to alter renal hemodynamics and inflammation. The effects of fish oil could prevent immunologic renal injury in patients with IgA nephropathy. In a multicenter, placebo-controlled, randomized trial we tested the efficacy of fish oil in patients with IgA nephropathy who had persistent proteinuria. The daily dose of fish oil was 12 g; the placebo was a similar dose of olive oil. Serum creatinine concentrations, elevated in 68 percent of the patients at base line, and creatinine clearance were measured for two years. The primary end point was an increase of 50 percent or more in the serum creatinine concentration at the end of the study. Fifty-five patients were assigned to receive fish oil, and 51 to receive placebo. According to Kaplan-Meier estimation, 3 patients (6 percent) in the fish-oil group and 14 (33 percent) in the placebo group had increases of 50 percent or more in their serum creatinine concentrations during treatment (P = 0.002). The annual median changes in the serum creatinine concentrations were 0.03 mg per deciliter (2.7 mumol per liter) in the fish-oil group and 0.14 mg per deciliter (12.4 mumol per liter) in the placebo group. Proteinuria was slightly reduced and hypertension was controlled to a comparable degree in both groups. The cumulative percentage of patients who died or had end-stage renal disease was 40 percent in the placebo group after four years and 10 percent in the fish-oil group (P = 0.006). No patient discontinued fish-oil treatment because of adverse effects. In patients with IgA nephropathy, treatment with fish oil for two years retards the rate at which renal function is lost.
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            Serotonin (5-hydroxytryptamine, 5-HT) enhances migration of rat aortic smooth muscle cells through 5-HT2 receptors.

             K Tamura (1997)
            The effects of serotonin on migration of cultured rat aortic smooth muscle cells (SMC) were studied to clarify the role of this substance in the pathogenesis of atherosclerosis. Serotonin alone did not stimulate SMC migration but stimulated it at physiological concentrations in the presence of other migration factors such as SMC-derived migration factor, platelet-derived migration factor and fibronectin. Checker-board analysis revealed that the serotonin effect was chemotactic. Moreover, serotonin effects were completely abolished by a selective inhibitor of the 5-HT2 receptor (MCI-9042), indicating that serotonin effects were mediated through the 5-HT2 receptor pathway. Finally, serotonin effects were also abolished by a phospholipase C inhibitor, U73122, suggesting that the 5-HT2 receptor mediated signal of serotonin was transduced by PLC. The results suggest that platelet-derived serotonin plays some role in the SMC dominant neointima formation.
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              Author and article information

              Journal
              NEF
              Nephron
              10.1159/issn.1660-8151
              Nephron
              S. Karger AG
              1660-8151
              2235-3186
              1998
              September 1998
              04 September 1998
              : 80
              : 1
              : 94-96
              Affiliations
              Departments of a Nephrology and b Pharmacodynamics, Medical University, Białystok, Poland
              Article
              45140 Nephron 1998;80:94–96
              10.1159/000045140
              9730718
              © 1998 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.

              Page count
              Figures: 1, Tables: 1, References: 21, Pages: 3
              Product
              Self URI (application/pdf): https://www.karger.com/Article/Pdf/45140
              Categories
              Letter to the Editor

              Cardiovascular Medicine, Nephrology

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