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      The Relationship of Microalbuminuria with Metabolic Syndrome

      a , b , a

      Nephron Clinical Practice

      S. Karger AG

      Microalbuminuria, Metabolic syndrome

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          Abstract

          Background/Aims: Microalbuminuria and the metabolic syndrome are risk factors for cardiovascular disease. The aim of this study is to examine the prevalence of microalbuminuira and to document the relationship of microalbuminuria with the metabolic syndrome in a large population of Korean subjects. Methods: We examined the cross-sectional association of microalbuminuria with the components of the metabolic syndrome and with other cardiovascular risk factors in 6,588 Korean adults who took part in a health examination program. Results: The prevalence of microalbuminuria was 4.2% in the non-metabolic syndrome group (n = 5,902), and 14.4% in the metabolic syndrome group (n = 686). The odds ratio of microalbuminuria in the adults with the metabolic syndrome compared with those adults without the metabolic syndrome was 1.53 (1.13–2.07 95% CI). In the multiple logistic regression analysis, as compared with the subjects without an elevated blood pressure, a low high-density lipoprotein cholesterol level, a high triglyceride level, a high plasma glucose level and a large waist circumference, the odds ratios for microalbuminuria with these components, after adjustment was made for the body mass index, the high-sensitivity C-reactive protein level and the homeostasis model assessment, were 2.17 (95% CI 1.71–2.76), 2.84 (95% CI 1.55–5.21), 1.30 (95% CI 1.03–1.65) and 2.68 (95% CI 2.04–3.51), respectively. The corresponding multivariate-adjusted odds ratios of microalbuminuria for the participants with 1, 2, 3, and 4 and 5 components of metabolic syndrome were 1.79 (95% CI 1.24–2.59), 2.35 (95% CI 1.58–3.51), 3.23 (95% CI 2.07–5.25), and 4.22 (95% CI 2.13–8.35), respectively. Conclusion: There was a significantly graded relationship between the number of metabolic syndrome components and the corresponding prevalence of microalbuminuria. These findings suggest microalbuminuria is strongly related with the components of the metabolic syndrome.

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          Most cited references 14

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          The homeostasis model in the San Antonio Heart Study.

          Both insulin resistance and decreased insulin secretion have been shown to predict the development of NIDDM. However, methods to assess insulin sensitivity and secretion are complicated and expensive to apply in epidemiological studies. The homeostasis model assessment (HOMA) has been suggested as a method to assess insulin resistance and secretion from the fasting glucose and insulin concentrations. However, this method has not been extensively evaluated, particularly in different ethnic groups. We applied the HOMA model to cross-sectional analyses of the San Antonio Heart Study (n = 2,465). HOMA insulin resistance (IR) was very strongly correlated with fasting insulin (r = 0.98) and HOMA beta-cell function (beta-cell) was moderately correlated with the 30-min increment in insulin concentration over the 30-min increment in glucose concentration (delta I30/delta G30) in an oral glucose tolerance test (OGTT) (r = 0.44). NIDDM was characterized by both high HOMA IR and low HOMA beta-cell function. In Mexican-Americans, HOMA IR in NIDDM subjects was 9.5 compared with 2.7 in normal glucose tolerance (NGT) subjects. In contrast, HOMA beta-cell function showed only small differences in Mexican-Americans (176 NIDDM; 257 NGT). However, the delta I30/delta G30 (pmol/mmol) showed much larger differences (75 NIDDM; 268 NGT). When modeled separately, impaired glucose tolerance (IGT) was characterized by high HOMA IR and high HOMA beta-cell function. However, when analyzed in the same regression model, high HOMA IR and low HOMA beta-cell function characterized subjects with IGT. These results were similar in both ethnic groups. Mexican-Americans had increased insulin resistance (as judged by both HOMA IR and fasting insulin) and insulin secretion (by HOMA beta-cell and delta I30/delta G30) relative to non-Hispanic whites. We conclude that HOMA provides a useful model to assess insulin resistance and beta-cell function in epidemiological studies in which only fasting samples are available and that, further, it is critical to take into account the degree of insulin resistance in assessing insulin secretion by the HOMA model.
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            Prospective analysis of the insulin-resistance syndrome (syndrome X).

            Many studies have shown that hyperinsulinemia and/or insulin resistance are related to various metabolic and physiological disorders including hypertension, dyslipidemia, and non-insulin-dependent diabetes mellitus. This syndrome has been termed Syndrome X. An important limitation of previous studies has been that they all have been cross sectional, and thus the presence of insulin resistance could be a consequence of the underlying metabolic disorders rather than its cause. We examined the relationship of fasting insulin concentration (as an indicator of insulin resistance) to the incidence of multiple metabolic abnormalities in the 8-yr follow-up of the cohort enrolled in the San Antonio Heart Study, a population-based study of diabetes and cardiovascular disease in Mexican Americans and non-Hispanic whites. In univariate analyses, fasting insulin was related to the incidence of the following conditions: hypertension, decreased high-density lipoprotein cholesterol concentration, increased triglyceride concentration, and non-insulin-dependent diabetes mellitus. Hyperinsulinemia was not related to increased low-density lipoprotein or total cholesterol concentration. In multivariate analyses, after adjustment for obesity and body fat distribution, fasting insulin continued to be significantly related to the incidence of decreased high-density lipoprotein cholesterol and increased triglyceride concentrations and to the incidence of non-insulin-dependent diabetes mellitus. Baseline insulin concentrations were higher in subjects who subsequently developed multiple metabolic disorders. These results were not attributable to differences in baseline obesity and were similar in Mexican Americans and non-Hispanic whites. These results support the existence of a metabolic syndrome and the relationship of that syndrome to multiple metabolic disorders by showing that elevations of insulin concentration precede the development of numerous metabolic disorders.
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              Microalbuminuria in the US population: third National Health and Nutrition Examination Survey.

              Microalbuminuria (MA) is associated with adverse health outcomes in diabetic and hypertensive adults. The prevalence and clinical significance of MA in nondiabetic populations is less clear. The purpose of this study was to generate national estimates of the prevalence of MA in the US population. Untimed urinary albumin concentrations (UACs) and creatinine concentrations were evaluated in a nationally representative sample of 22,244 participants aged 6 years and older. Persons with hematuria and menstruating or pregnant women were excluded from analysis. The percent prevalence of clinical proteinuria (UAC > or = 300 mg/L) was similar for males and females. However, the prevalence of MA (urinary albumin-creatinine ratio [ACR], 30 to 299 mg/g) was significantly lower in males (6.1%) compared with females (9.7%). MA prevalence was greater in children than young adults and increased continuously starting at 40 years of age. MA prevalence was greater in non-Hispanic blacks and Mexican Americans aged 40 to 79 years compared with similar-aged non-Hispanic whites. MA prevalence was 28.8% in persons with previously diagnosed diabetes, 16.0% in those with hypertension, and 5.1% in those without diabetes, hypertension, cardiovascular disease, or elevated serum creatinine levels. In adults aged 40+ years, after excluding persons with clinical proteinuria, albuminuria (defined as ACR > or = 30 mg/g) was independently associated with older age, non-Hispanic black and Mexican American ethnicity, diabetes, hypertension, and elevated serum creatinine concentration. MA is common, even among persons without diabetes or hypertension. Age, sex, race/ethnicity, and concomitant disease contribute to the variability of MA prevalence estimates. Copyright 2002 by the National Kidney Foundation, Inc.
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                Author and article information

                Journal
                NEC
                Nephron Clin Pract
                10.1159/issn.1660-2110
                Nephron Clinical Practice
                S. Karger AG
                1660-2110
                2006
                September 2006
                21 June 2006
                : 104
                : 2
                : c85-c93
                Affiliations
                aDivision of Nephrology and bOccupational Medicine, Sungkyunkwan University, School of Medicine, Kangbuk Samsung Hospital, Seoul, Korea
                Article
                93995 Nephron Clin Pract 2006;104:c85–c93
                10.1159/000093995
                16785740
                © 2006 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: 2, Tables: 5, References: 22, Pages: 1
                Product
                Self URI (application/pdf): https://www.karger.com/Article/Pdf/93995
                Categories
                Original Paper

                Cardiovascular Medicine, Nephrology

                Microalbuminuria, Metabolic syndrome

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