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

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      Association of Metabolic Syndrome with Microalbuminuria in Non-Hypertensive Type 2 Diabetic Patients

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          Abstract

          Background: Several studies have shown that metabolic syndrome contributed to the development of incident chronic kidney disease in the general population. We evaluated the cross-sectional association between metabolic syndrome and microalbuminuria in patients with type 2 diabetes. We excluded patients with hypertension to distinguish the effects of metabolic syndrome from those of hypertension. Methods: A total of 642 non-hypertensive patients with type 2 diabetes were recruited. Metabolic syndrome was assessed according to the NCEP Guidelines and Asian-Pacific criteria for abdominal obesity. Results: Among all patients, 37.2% were diagnosed as having metabolic syndrome, and these patients had a higher prevalence of microalbuminuria than those without metabolic syndrome (19.7 vs. 13.6%, p = 0.044). There was a graded association between metabolic score and the prevalence of microalbuminuria (p = 0.006 for trend). After adjustment for sex, age, smoking status, C-reactive protein, and HbA<sub>1c</sub>, patients with metabolic syndrome had increased odds of 1.58 (95% CI 1.01–2.47) for microalbuminuria. An increment in metabolic score was found to increase the risk of microalbuminuria by 1.34-fold (95% CI 1.07–1.66, p = 0.008). Conclusion: This study demonstrated that metabolic syndrome was associated with an increased risk of microalbuminuria in non-hypertensive patients with type 2 diabetes.

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          The metabolic syndrome, inflammation, and risk of cognitive decline.

          Kristine Yaffe, Alka M. Kanaya, Karla Lindquist … (2004)
          Several studies have reported an association between the metabolic syndrome and cardiovascular disease. Despite an increasing awareness that cardiovascular risk factors increase risk of cognitive decline and dementia, there are few data on the metabolic syndrome and cognition. To determine if the metabolic syndrome is a risk factor for cognitive decline and if this association is modified by inflammation. A 5-year prospective observational study conducted from 1997 to 2002 at community clinics at 2 sites. A total of 2632 black and white elders (mean age, 74 years). Association of the metabolic syndrome (measured using National Cholesterol Education Program guidelines) and high inflammation (defined as above median serum level of interleukin 6 and C-reactive protein) with change in cognition (Modified Mini-Mental State Examination [3MS]) at 3 and 5 years. Cognitive impairment was defined as at least a 5-point decline. Compared with those without the metabolic syndrome (n = 1616), elders with the metabolic syndrome (n = 1016) were more likely to have cognitive impairment (26% vs 21%, multivariate adjusted relative risk [RR], 1.20; 95% confidence interval [CI], 1.02-1.41). There was a statistically significant interaction with inflammation and the metabolic syndrome (P = .03) on cognitive impairment. After stratifying for inflammation, those with the metabolic syndrome and high inflammation (n = 348) had an increased likelihood of cognitive impairment compared with those without the metabolic syndrome (multivariate adjusted RR, 1.66; 95% CI, 1.19-2.32). Those with the metabolic syndrome and low inflammation (n = 668) did not exhibit an increased likelihood of impairment (multivariate adjusted RR, 1.08; 95% CI, 0.89-1.30). Stratified multivariate random-effects models demonstrated that participants with the metabolic syndrome and high inflammation had greater 4-year decline on 3MS (P = .04) compared with those without the metabolic syndrome, whereas those with the metabolic syndrome and low inflammation did not (P = .44). These findings support the hypothesis that the metabolic syndrome contributes to cognitive impairment in elders, but primarily in those with high level of inflammation.
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            Microalbuminuria predicts clinical proteinuria and early mortality in maturity-onset diabetes.

            C E Mogensen (1984)
            We studied whether microalbuminuria (30 to 140 micrograms of albumin per milliliter) would predict the later development of increased proteinuria and early mortality in Type II diabetics. During 1973, morning urine specimens of diabetic clinic patients 50 to 75 years of age whose disease had been diagnosed the age of 45 were examined for albumin level by radioimmunoassay. Seventy-six patients with albumin concentrations of 30 to 140 micrograms per milliliter were identified for long-term follow-up. They were compared with normal controls, diabetic patients with lower albumin concentrations (75 patients with concentrations less than 15 micrograms per milliliter and 53 with concentrations of 16 to 29 micrograms per milliliter), and 28 diabetic patients with higher concentrations (greater than 140). Age, duration of diabetes, treatment method, fasting blood glucose level, blood pressure, height, and weight were determined for the four diabetic groups. After nine years the group with albumin concentrations of 30 to 140 micrograms per milliliter was more likely to have clinically detectable proteinuria (greater than 400 micrograms per milliliter) than were the groups with lower concentrations. Mortality was 148 per cent higher in this group than in normal controls--comparable to the increase (116 per cent) in the group with heavy proteinuria (albumin levels greater than 140 micrograms per milliliter). In addition, mortality was increased 76 per cent in the group with albumin levels of 16 to 29 micrograms per milliliter and 37 per cent in the group with levels below 15. We conclude that microalbuminuria in patients with Type II diabetes is predictive of clinical proteinuria and increased mortality.
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              Clinical practice. Nephropathy in patients with type 2 diabetes.

              Giuseppe Remuzzi, Arrigo Schieppati, Piero Ruggenenti (2002)
              Article 0 comments Cited 112 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (publisher-id): NEC
                Journal ID (nlm-ta): Nephron Clin Pract
                Journal ID (doi): 10.1159/issn.1660-2110
                Title: Nephron Clinical Practice
                Publisher: S. Karger AG
                ISSN (Electronic): 1660-2110
                Publication date Subscription-year: 2007
                Publication date (Print): July 2007
                Publication date (Electronic): 22 May 2007
                Volume: 106
                Issue: 3
                Pages: c98-c103
                Affiliations
                aDepartment of Medicine, Division of Nephrology, and bCenter for Health Promotion, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea
                Article
                Publisher ID: 102996 Other ID: Nephron Clin Pract 2007;106:c98–c103
                DOI: 10.1159/000102996
                PubMed ID: 17522477
                SO-VID: 3d066621-5ab4-4269-a9a4-b8bb43300b26
                Copyright © © 2007 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 : 19 June 2006
                Date accepted : 22 January 2007
                Page count
                Figures: 2, Tables: 3, References: 28, Pages: 1
                Categories
                Subject: Original Paper

                ScienceOpen disciplines: Cardiovascular Medicine,Nephrology
                Keywords: Metabolic syndrome,Microalbuminuria,Abdominal obesity,Diabetes type 2
                Data availability:
                ScienceOpen disciplines: Cardiovascular Medicine, Nephrology
                Keywords: Metabolic syndrome, Microalbuminuria, Abdominal obesity, Diabetes type 2

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