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      Effects of Dietary Conjugated Linoleic Acid in Advanced Experimental Polycystic Kidney Disease

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          Abstract

          Background/Aims: Several dietary interventions, including those involving conjugated linoleic acid (CLA), slow progression of polycystic kidney disease (PKD) when initiated in the early stages of disease in Han:SPRD- cy rats. However, in humans, kidney disease is often undetected until extensive renal injury has developed. The objective of this study therefore was to determine whether initiating dietary CLA intervention in advanced PKD would slow disease progression. Methods: Adult male Han:SPRD- cy rats with advanced kidney disease were fed diets with or without 1% CLA for 16 weeks. Disease progression was assessed by serum urea, proteinuria, and creatinine clearance, and morphological and immunohistochemical measurements for pathologic change. Results: Renal injury was lower in the PKD rats given CLA compared to those given the control diet as indicated by a reduction in inflammation (42% less), fibrosis (28% less), oxidative damage (30% less) and proliferating cells (35% less). Diet had no effect on body, kidney, or liver weight, serum urea, serum creatinine, creatinine clearance, proteinuria, or cyst volume. Conclusions: Late dietary intervention with CLA reduced some disease-associated pathologies, but did not alter renal function in adult Han:SPRD- cy rats. The long-term anti-inflammatory, antioxidant, and antiproliferative benefits of CLA in advanced kidney disease remain to be determined.

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          Kidney disease as a risk factor for recurrent cardiovascular disease and mortality.

          Bonnie MacLeod, Daniel E Weiner, Hocine Tighiouart … (2004)
          Chronic kidney disease (CKD) is highly prevalent in the United States and is an independent risk factor for adverse cardiovascular disease (CVD) and all-cause mortality outcomes in patients with acute coronary syndromes. Few studies have evaluated the effect of CKD on cardiovascular events in a diverse community-based population with underlying CVD. Data for subjects with preexisting CVD were pooled from 4 publicly available, community-based, longitudinal studies: Atherosclerosis Risk in Communities, Cardiovascular Health Study, Framingham Heart Study, and Framingham Offspring Study. CKD was defined as an estimated glomerular filtration rate less than 60 mL/min/1.73 m2 (<1 mL/s/1.73 m2). The primary study outcome was a composite of myocardial infarction (MI), fatal coronary heart disease (CHD), stroke, and all-cause mortality. The secondary outcome included only MI and fatal CHD. A total of 4,278 subjects satisfied inclusion criteria, and 759 subjects (17.7%) had CKD. Mean follow-up was 86 months. The primary and secondary outcomes were observed in 1,703 (39.8%) and 857 subjects (20.0%), respectively. Incidence rates for the primary and secondary outcomes were greater in persons with CKD compared with those without CKD (62.5% versus 34.9% and 30.6% versus 17.8%, respectively). Adjusted hazard ratios for the primary and secondary outcomes were 1.35 (95% confidence interval [CI], 1.21 to 1.52) and 1.32 (95% CI, 1.12 to 1.55), respectively. The presence of CKD in a community-based population with preexisting CVD is associated with an increased risk for recurrent CVD outcomes. This increased risk persists after adjustment for traditional CVD risk factors.
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            Determination of serum creatinine by a direct colorimetric method

            Gunnar Tiderström, Dick Heinegård (1973)
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              Autosomal-dominant polycystic kidney disease in the rat.

              Benjamin Cowley, Seshagirirao Gudapaty, Amy Kraybill … (1993)
              Kaspareit-Rittinghausen described a rodent model of inherited polycystic kidney disease (PKD), the Han:SPRD rat [1, 2], in which heterozygotes develop renal cysts and renal failure (in males) over several months, whereas homozygous animals develop rapidly progressive renal enlargement that leads to death in a few weeks. In this study, we examined selected elements of the pathogenesis of this disease in heterozygotes and homozygotes from birth to advanced disease. Heterozygous male rats developed slowly progressive renal cystic disease with interstitial fibrosis and azotemia seen by six months of age. Female heterozygotes developed slowly progressive renal cystic disease, but did not develop interstitial fibrosis or azotemia. Epithelial cells lining cyst cavities showed various degrees of morphologic immaturity. Cyst walls also developed basement membrane thickening, especially in areas of cellular immaturity, suggesting an interrelationship between this basement membrane thickening and cellular dedifferentiation. Thickened basement membranes were associated with increased immunoreactivity for type IV collagen, laminin, and fibronectin. Homozygous rats developed massive renal enlargement, marked azotemia, and died near three weeks of age. Renal c-myc proto-oncogene expression was elevated in homozygous cystic infants and in adult heterozygotes. In situ hybridization showed high levels of c-myc mRNA in cyst epithelia, suggesting abnormal regulation of cellular proliferation in the cells lining cysts, as seen in other models of PKD. The Han:SPRD rat is the only well-documented animal model of inherited PKD with an autosomal-dominant inheritance pattern and appears to have several features which resemble human ADPKD.
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                Author and article information

                Journal
                Journal ID (publisher-id): NEE
                Journal ID (nlm-ta): Nephron Exp Nephrol
                Journal ID (doi): 10.1159/issn.1660-2129
                Title: Cardiorenal Medicine
                Publisher: S. Karger AG
                ISSN (Electronic): 1660-2129
                Publication date Subscription-year: 2008
                Publication date (Print): November 2008
                Publication date (Electronic): 08 September 2008
                Volume: 110
                Issue: 2
                Pages: e44-e48
                Affiliations
                Departments of aHuman Nutritional Sciences and bPediatrics and Child Health, University of Manitoba, and cManitoba Institute of Child Health, Winnipeg, Man., Canada
                Article
                Publisher ID: 153244 Other ID: Nephron Exp Nephrol 2008;110:e44
                DOI: 10.1159/000153244
                PubMed ID: 18776722
                SO-VID: 0d71481c-3c36-4d24-86cc-cfd7f3eba300
                Copyright © © 2008 S. Karger AG, Basel
                License:

                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
                Date received : 21 December 2007
                Date accepted : 24 June 2008
                Page count
                Tables: 3, References: 33, Pages: 1
                Categories
                Subject: Original Paper

                ScienceOpen disciplines: Cardiovascular Medicine,Nephrology
                Keywords: Linoleic acid, conjugated,Polycystic kidney disease,Dietary treatment,Histology, kidney,Chronic kidney disease, advanced
                Data availability:
                ScienceOpen disciplines: Cardiovascular Medicine, Nephrology
                Keywords: Linoleic acid, conjugated, Polycystic kidney disease, Dietary treatment, Histology, kidney, Chronic kidney disease, advanced

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