For Publishers
DiscoveryMetadataPeer reviewHostingPublishing
For Researchers
JoinPublishReviewCollect
Register
Blog
About
Search
Advanced search
My ScienceOpen
Search
For Publishers
For Researchers
Blog
About
36
views
41
references
 Top references
cited by
2
    
0 reviews
 Review
0
comments
 Comment
0
recommends
+1 Recommend
0 collections
    0
    shares
      218
      similar
       All similar
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Effects of Dietary Protein and Fat Contents on Renal Function and Inflammatory Cytokines in Rats with Adriamycin-Induced Nephrotic Syndrome

      research-article

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          The effects of dietary protein and fat on renal function-related blood and urine parameters, such as albumin, urinary protein,and inflammatory cytokines were investigated in adriamycin- (ADR) induced nephrotic syndrome rats. ADR (2 mg/kg BW) was injected i.p. weekly for six weeks to develop nephrotic syndrome; thereafter rats were fed low-protein/high-fat (LPHF) or high-protein/low-fat (HPLF) diets for five weeks. Renal function-related blood and urine parameters were measured before and after dietary intervention. Serum levels of albumin, TG, and creatinine were significantly higher in the LPHF group than in the HPLF group. Serum levels of albumin were low and urinary protein excretion protein was high in HPLF group. BUN and UUN levels were higher in the HPLF group than in the LPHF. Urinary excretion of creatinine was significantly higher in the HPLF group than in the LPHF group. Serum inflammatory cytokine levels did not differ between the two groups, however the levels of IL-6, TNF- α , and IL-13 in splenocyte supernatants were significantly higher in the LPHF group than in the HPLF group. We confirmed that protein and fat contents in diet affect renal function-related blood and urine parameters and splenocyte inflammatory cytokine levels in ADR-induced nephrotic syndrome rats.

          Related collections

          Most cited references41

          • Record: found
          • Abstract: found
          • Article: not found

          The impact of protein intake on renal function decline in women with normal renal function or mild renal insufficiency.

          Meir J. Stampfer, Donna Spiegelman, Eric L. Knight … (2003)
          In individuals with moderate to severe renal insufficiency, low protein intake may slow renal function decline. However, the long-term impact of protein intake on renal function in persons with normal renal function or mild renal insufficiency is unknown. To determine whether protein intake influences the rate of renal function change in women over an 11-year period. Prospective cohort study. Nurses' Health Study. 1624 women enrolled in the Nurses' Health Study who were 42 to 68 years of age in 1989 and gave blood samples in 1989 and 2000. Ninety-eight percent of women were white, and 1% were African American. Protein intake was measured in 1990 and 1994 by using a semi-quantitative food-frequency questionnaire. Creatinine concentration was used to estimate glomerular filtration rate (GFR) and creatinine clearance. In multivariate linear regression analyses, high protein intake was not significantly associated with change in estimated GFR in women with normal renal function (defined as an estimated GFR > or = 80 mL/min per 1.73 m2). Change in estimated GFR in this subgroup over the 11-year period was 0.25 mL/min per 1.73 m2 (95% CI, -0.78 to 1.28 mL/min per 1.73 m2) per 10-g increase in protein intake; the change in estimated GFR was 1.14 mL/min per 1.73 m2 (CI, -3.63 to 5.92 mL/min per 1.73 m2) after measurement-error adjustment for protein intake. In women with mild renal insufficiency (defined as an estimated GFR > 55 mL/min per 1.73 m2 but <80 mL/min per 1.73 m2), protein intake was significantly associated with a change in estimated GFR of -1.69 mL/min per 1.73 m2 (CI, -2.93 to -0.45 mL/min per 1.73 m2) per 10-g increase in protein intake. After measurement-error adjustment, the change in estimated GFR was -7.72 mL/min per 1.73 m2 (CI, -15.52 to 0.08 mL/min per 1.73 m2) per 10-g increase in protein intake, an association of borderline statistical significance. High intake of nondairy animal protein in women with mild renal insufficiency was associated with a significantly greater change in estimated GFR (-1.21 mL/min per 1.73 m2 [CI, -2.34 to -0.33 mL/min per 1.73 m2] per 10-g increase in nondairy animal protein intake). High protein intake was not associated with renal function decline in women with normal renal function. However, high total protein intake, particularly high intake of nondairy animal protein, may accelerate renal function decline in women with mild renal insufficiency.
          Article 0 comments Cited 112 times – based on 0 reviews     Review now
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Dietary protein restriction and the progression of chronic renal disease: what have all of the results of the MDRD study shown? Modification of Diet in Renal Disease Study group.

            Patrícia S Klahr, A Caggiula, Kenneth Levey … (1999)
            The Modification of Diet in Renal Disease (MDRD) Study was the largest randomized clinical trial to test the hypothesis that protein restriction slows the progression of chronic renal disease. However, the primary results published in 1994 were not conclusive with regard to the efficacy of this intervention. Many physicians interpreted the failure of the MDRD Study to demonstrate a beneficial effect of protein restriction over a 2- to 3-yr period as proving that this therapy does not slow disease progression. The authors believe that this viewpoint is incorrect, and is the result of misinterpretation of inconclusive evidence as evidence in favor of the null hypothesis. Since then, numerous secondary analyses of the MDRD Study have been undertaken to clarify the effect of protein restriction on the rate of decline in GFR, urine protein excretion, and onset of end-stage renal disease. This review describes some of the principles of secondary analyses of randomized clinical trials, presents the results of these analyses from the MDRD Study, and compares them with results from other randomized clinical trials. Although these secondary results cannot be regarded as definitive, the authors conclude that the balance of evidence is more consistent with the hypothesis of a beneficial effect of protein restriction than with the contrary hypothesis of no beneficial effect. Until additional data become available, physicians must continue to make recommendations in the absence of conclusive results. The authors suggest that physicians incorporate the results of these secondary analyses into their interpretation of the findings of the MDRD Study.
            Article 0 comments Cited 65 times – based on 0 reviews     Review now
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              T regulatory cell function in idiopathic minimal lesion nephrotic syndrome.

              Richard Johnson, Eduardo H. Garin, Clive Wasserfall … (2009)
              The purpose of this study was to test the hypothesis that, in idiopathic minimal lesion nephrotic syndrome (IMLNS), the T regulatory (T reg) cell suppressor mechanism is deficient, thereby enhancing cytokine release by T effector cells. Twenty-one patients with IMLNS, eight healthy controls and two patients with nephrotic syndrome and membranoproliferative glomerulonephritis were studied. The percentage of T reg cells was similar in the healthy controls and in patients with IMLNS in relapse or in remission. Thymidine incorporation in autologous T effector cells, as well as expression of the regulatory cytokine interleukin (IL)-10, was significantly reduced in patients in relapse when compared with patients in remission and healthy subjects. IL-2 expression was also reduced in patients in relapse but did not achieve statistical significance. In a different set of experiments, T cells, from subjects with IMLNS in remission, when stimulated with antiCD3-antiCD28 antibodies, secreted increased levels of cytokines. No such increase in cytokines was observed when cells from healthy controls were stimulated with same mitogen. The impaired T reg cell function observed in these patients may have pathogenic and therapeutic implications, because it could explain the persistence of the proposed pathogenic cytokines observed in the patients with IMLNS.
              Article 0 comments Cited 55 times – based on 0 reviews     Review now
                Bookmark
                All references

                Author and article information

                Journal
                Journal ID (nlm-ta): Mediators Inflamm
                Journal ID (publisher-id): MI
                Title: Mediators of Inflammation
                Publisher: Hindawi Publishing Corporation
                ISSN (Print): 0962-9351
                ISSN (Electronic): 1466-1861
                Publication date (Print): 2011
                Publication date (Electronic): 24 May 2011
                Volume: 2011
                Electronic Location Identifier: 945123
                Affiliations
                1Department of Medical Nutrition, Graduate School of East-West Medical Science, Kyung Hee University, Seocheon-dong, Giheung-gu, Yongin, Gyeonggi-do 446-701, Republic of Korea
                2Research Institute of Medical Nutrition, Kyung Hee University, Heikidong, Seoul 130-701, Republic of Korea
                Author notes

                Academic Editor: Alex Kleinjan

                Article
                DOI: 10.1155/2011/945123
                PMC ID: 3136151
                PubMed ID: 21822358
                SO-VID: c0c2e4d9-8506-49d3-b19e-bbbf0009b89d
                Copyright © Copyright © 2011 Su Yeon Kim et al.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 9 October 2010
                Date accepted : 3 March 2011
                Categories
                Subject: Research Article

                ScienceOpen disciplines: Immunology
                Data availability:
                ScienceOpen disciplines: Immunology

                Comments

                Comment on this article

                scite_

                Similar content218

                See all similar

                Cited by2

                See all cited by

                Most referenced authors205

                See all reference authors