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      Call for Papers: Green Renal Replacement Therapy: Caring for the Environment

      Submit here before July 31, 2024

      About Blood Purification: 3.0 Impact Factor I 5.6 CiteScore I 0.83 Scimago Journal & Country Rank (SJR)

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      Metabolic Syndrome in IgA Glomerulonephritis

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          Background/Aims: Metabolic syndrome (MetS) may have an independent impact on the development of chronic kidney disease. This study examines the prevalence of MetS in subjects with IgA glomerulonephritis (IgAGN) and its impact on disease progression in a retrospective fashion. Patients and Methods: Altogether, 174 subjects (104 males) were examined 11 years (first visit) after IgAGN diagnosis and again after 16 years (second visit; 144 subjects responded). Different glomerular filtration markers were utilized. The MetS criteria by Alberti et al. [Circulation 2009;120:1640-1645] were applied, in which the presence of any three of five risk factors (elevated waist circumference, triglycerides, glucose, existence of hypertension, or reduced high-density lipoprotein cholesterol) constitutes the diagnosis. Results: The prevalence of MetS at the first visit was 39%, corresponding to that of the general Finnish population. In univariate analyses, MetS was significantly associated with the progression of IgAGN at the second visit. However, in multivariate analyses, the existence of MetS was not a significant prognostic determinant. Conclusion: The number of subjects with MetS among IgAGN patients and the general population is equal in Finland. MetS does not seem to be an independent prognostic variable.

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          Natural history of primary IgA nephropathy.

          Hesham Mohey, F Berthoux, Aida Afiani (2007)
          Primary IgA nephropathy (IgAN) is the most frequent type of primary glomerulonephritis worldwide. The characteristic presentation is gross hematuria at the time of an infectious episode. A renal biopsy still is mandatory for the diagnosis. The natural history of the disease is characterized by clinical and pathologic progression over time, which can vary from a few years to more than 50 years. It is possible to make a broad prediction at the time of diagnosis of the long-term (20 years) risk of progressive chronic kidney disease, and then to end-stage renal disease requiring renal replacement therapy (20-year cumulative end-stage renal disease risk range, 14%-39%). The 3 major independent risk factors are arterial hypertension, proteinuria more than 1 g/d, and severe renal histopathologic lesions including hyalinosis, crescents, or defined by histopathologic scoring systems. When any clinical risk factors are present, patients should be targeted closely by appropriate treatments in the following order: (1) precise control of hypertension, (2) control of proteinuria when persisting for greater than 1 g/d, and (3) evidence-based treatment where available for severe lesions. This is a symptomatic treatment strategy because pathogenesis and etiology still remain unclear.
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            Metabolic syndrome and the development of CKD in American Indians: the Strong Heart Study.

            Jaime Lucove, Suma Vupputuri, Gerardo Heiss … (2008)
            Metabolic impairments that precede type 2 diabetes, such as metabolic syndrome, may contribute to the development of chronic kidney disease (CKD). This study documents the prevalence and incidence of CKD and the prospective association between metabolic syndrome and CKD in American Indians without diabetes in the Strong Heart Study. Prospective cohort study. American Indians aged 45 to 74 years from 3 geographic regions were recruited by using tribal records and were assessed every 3 years from 1989 to 1999 as part of the Strong Heart Study. Participants with type 2 diabetes, on dialysis therapy, or who received a kidney transplant at baseline examination were excluded. Metabolic syndrome, defined using Adult Treatment Panel III criteria. CKD was measured by using estimated glomerular filtration rate (eGFR) and urinary albumin-creatinine ratio (ACR) dichotomized at conventional cutoff values. The association between metabolic syndrome and incident CKD was evaluated by using multivariable Cox proportional hazards models and binomial regression, with statistical adjustment for confounders (age, sex, study center, education, and smoking). Metabolic syndrome was present in 896 (37.7%) and absent in 1,484 participants (62.3%) at baseline. The prevalence of ACR of 30 mg/g or greater at baseline examination was 12.1%, with 290 new cases and an incidence of 233/10,000 person-years. The prevalence of eGFR less than 60 mL/min/1.73 m(2) was 7.8%, with 189 new cases and an incidence of 138/10,000 person-years. The prevalence of CKD was 17.8%, with 388 new cases and an incidence of 342/10,000 person-years. The adjusted hazard ratio for CKD associated with metabolic syndrome was 1.3 (95% confidence interval [CI], 1.1 to 1.6). Equivalent hazard ratios for ACR greater than 30 mg/g and eGFR less than 60 mL/min/1.73 m(2) were 1.4 (95% CI, 1.0 to 1.9) and 1.3 (95% CI, 1.0 to 1.6), respectively. The relationship between metabolic syndrome and kidney outcomes was stronger in those who developed diabetes during follow-up. Intraindividual variability in serum creatinine and ACR measures may have resulted in some misclassification of participants by outcome status. Metabolic syndrome is associated with an increased risk of developing CKD in American Indians without diabetes. The mechanism through which metabolic syndrome may cause CKD in this population likely is the development of diabetes.
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              Is serum cystatin-C a reliable marker for metabolic syndrome?

              Aude Servais, Philippe Giral, Maguy Bernard … (2008)
              Chronic kidney disease and metabolic syndrome are recognized as major cardiovascular risk factors. It has been shown that cystatin C has a stronger association with mortality risk than creatinine-based estimations of glomerular filtration rate. We measured cystatin values in dyslipidemic patients and looked for correlations between renal function, cystatin, and metabolic syndrome. There were 925 dyslipidemic patients prospectively included in this cross-sectional study and evaluated over 10 months. Each visit included clinical and biological assessment. Most patients exhibited cardiovascular risk factors other than dyslipidemia: hypertension in 34%, diabetes in 11%, and smoking in 18%. Mean triglycerides were 149 +/- 136 mg/dL, mean high-density lipoprotein cholesterol 54 +/- 14 mg/dL, and low-density lipoprotein 167 +/- 48 mg/dL. Metabolic syndrome was present in 238 (26%) patients. Plasma creatinine did not differ between control group and metabolic syndrome patients (80 +/- 26 vs 82 +/- 20 micromol/L, respectively, P = .2), but creatinine clearance evaluated by abbreviated Modification of Diet in Renal Disease Study formula was lower in the metabolic syndrome group than in the non-metabolic-syndrome group (83.3 +/- 18.8 mL/min/1.73 m(2) vs 86.8+/-16.9 mL/min/1.73 m(2), respectively, P < .007). Cystatin value was significantly higher in metabolic syndrome patients than in others (0.86 +/- 0.23 vs 0.79 +/- 0.20 mg/L, respectively, P < .0001), independently of serum creatinine level and creatinine clearance. Furthermore, there was a progressive increase in cystatin, as a function of the number of metabolic syndrome components. Our study shows that cystatin is associated with metabolic syndrome in dyslipidemic patients. Cystatin may be an interesting marker of metabolic syndrome and of increased cardiovascular and renal risk.
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                Author and article information

                Journal
                Journal ID (publisher-id): NNE
                Journal ID (pmc): NNE
                Journal ID (doi): 10.1159/issn.1664-5529
                Title: Nephron Extra
                Publisher: S. Karger AG
                ISSN (Electronic): 1664-5529
                Publication date Subscription-year: 2014
                Publication date Collection: May – August 2014
                Publication date (Electronic): 19 August 2014
                Volume: 4
                Issue: 2
                Pages: 138-145
                Affiliations
                Schools of aMedicine and bHealth Sciences, University of Tampere, and cDepartment of Internal Medicine, Tampere University Hospital, Tampere, and dDepartment of Laboratory Medicine, Central Hospital of Savonlinna, Savonlinna, Finland
                Author notes
                *Kati Kaartinen, Kapteeninkatu 8 E 26, FI-00140 Helsinki (Finland), E-Mail kati.kaartinen@elisanet.fi
                Article
                Publisher ID: 365591 Pmcid ID: PMC4164079 Other ID: Nephron Extra 2014;4:138-145
                DOI: 10.1159/000365591
                PMC ID: PMC4164079
                PubMed ID: 25337083
                SO-VID: 77e55804-308c-457c-9c27-5dc684c5fc28
                Copyright © © 2014 S. Karger AG, Basel
                License:

                Open Access License: This is an Open Access article licensed under the terms of the Creative Commons Attribution-NonCommercial 3.0 Unported license (CC BY-NC) ( http://www.karger.com/OA-license), applicable to the online version of the article only. Distribution permitted for non-commercial purposes only. 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.

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                Figures: 1, Tables: 5, Pages: 8
                Categories
                Subject: Original Paper

                ScienceOpen disciplines: Cardiovascular Medicine,Nephrology
                Keywords: Creatinine,Cystatin-C,IgA glomerulonephritis,Metabolic syndrome,Estimated glomerular filtration rate
                Data availability:
                ScienceOpen disciplines: Cardiovascular Medicine, Nephrology
                Keywords: Creatinine, Cystatin-C, IgA glomerulonephritis, Metabolic syndrome, Estimated glomerular filtration rate

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