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      Metabolic Syndrome as a Risk Factor for Contrast-Induced Nephropathy in Non-Diabetic Elderly Patients with Renal Impairment

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          Abstract

          Background/Aims: Metabolic syndrome (MS) as a risk factor for contrast-induced nephropathy (CIN) has not been studied. The aim of the present study was to assess the influence of MS on the development of CIN in patients undergoing coronary angiography. Methods: This was a prospective cohort study. A total of 219 non-diabetic patients with reduced kidney function and age ≧60 years were divided into two groups (MS, n = 107 and non-MS, n = 112). CIN was defined as an increase of ≧25% in creatinine over the baseline value within 48 h of angiography. Results: CIN occurred in 14% of the MS group and 3.6% of the non-MS group (p = 0.006). Serum creatinine increased from 1.06 ± 0.17 to 1.12 ± 0.27 mg/dl in the MS group and from 1.03 ± 0.17 to 1.09 ± 0.23 mg/dl in the non-MS group (p < 0.001). MS was a risk indicator of CIN [odds ratio (OR) 4.26; 95% confidence interval (95% CI) 1.19–15.25; p = 0.026). Impaired fasting glucose (OR 4.72; 95% CI 1.53–14.56; p = 0.007), high triglyceride (OR 4.06; 95% CI 1.22–13.44; p = 0.022), and multivessel involvement (OR 3.14; 95% CI 1.07–9.82; p = 0.038) in the MS group were predictors of CIN. Conclusion: Our data support the hypothesis that patients with MS are at risk of developing CIN.

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          Prevalence of the Metabolic Syndrome Among US Adults

          Earl S. Ford, Wayne Giles, William Dietz (2002)
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            The metabolic syndrome is associated with advanced vascular damage in patients with coronary heart disease, stroke, peripheral arterial disease or abdominal aortic aneurysm.

            Ton Rabelink, Jobien Olijhoek, Ale Algra … (2004)
            The metabolic syndrome is associated with an increased risk of cardiovascular disease in patients without a cardiovascular history. We investigated whether the metabolic syndrome is related to the extent of vascular damage in patients with various manifestations of vascular disease. The study population of this cross-sectional survey consisted of 502 patients recently diagnosed with coronary heart disease (CHD), 236 with stroke, 218 with peripheral arterial disease (PAD) and 89 with abdominal aortic aneurysm (AAA). Metabolic syndrome was diagnosed according to Adult Treatment Panel III criteria. Carotid Intima Media Thickness (IMT), Ankle Brachial Pressure Index (ABPI) and albuminuria were used as non-invasive markers of vascular damage and adjusted for age and sex if appropriate. The prevalence of the metabolic syndrome in the study population was 45%. In PAD patients this was 57%; in CHD patients 40%, in stroke patients 43% and in AAA patients 45%. Patients with the metabolic syndrome had an increased mean IMT (0.98 vs 0.92mm, P-value <0.01), more often a decreased ABPI (14% vs 10%, P-value 0.06) and increased prevalence of albuminuria (20% vs 15%, P-value 0.03) compared to patients without this syndrome. An increase in the number of components of the metabolic syndrome was associated with an increase in mean IMT (P-value for trend <0.001), lower ABPI (P-value for trend <0.01) and higher prevalence albuminuria (P-value for trend <0.01). In patients with manifest vascular disease the presence of the metabolic syndrome is associated with advanced vascular damage.
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              Uric acid and the state of the intrarenal renin-angiotensin system in humans.

              Naomi D L Fisher, Olga Gumieniak, Todd S. Perlstein … (2004)
              Experimental hyperuricemia is marked by an activated intrarenal renin-angiotensin system (RAS). The renal vascular response to exogenous angiotensin II (Ang II) provides an indirect measure of intrarenal RAS activity. We tested the hypothesis that the serum uric acid concentration predicts the renal vascular response to Ang II. A total of 249 subjects in high sodium balance had the renal plasma flow (RPF) response to Ang II measured. Para-aminohippuric acid (PAH) clearance was used to estimate RPF. Multivariable regression analysis determined if the serum uric acid concentration independently predicts the RPF response to Ang II. Variables considered included age, gender, race, body mass index (BMI), hypertension status, blood pressure, basal RPF, creatinine clearance, serum insulin, serum glucose, serum high-density lipoprotein (HDL), serum triglycerides, and plasma renin activity (PRA). Uric acid concentration negatively correlated with the RPF response to Ang II (r=-0.37, P < 0.001). In univariate analysis, age, BMI, hypertension, triglycerides, and blood pressure were negatively associated, and basal RPF, HDL, and female gender were positively associated with the RPF response to Ang II. In multivariable analysis, serum uric acid concentration independently predicted the RPF response to Ang II (beta=-5.3, P < 0.001). Serum uric acid independently predicted blunted renal vascular responsiveness to Ang II, consistent with results from experimental hyperuricemia showing an activated intrarenal RAS. This could be due to a direct effect of uric acid or reflect a more fundamental renal process. These data may have relevance to the association of uric acid with risk for hypertension and nephropathy.
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                Author and article information

                Journal
                Journal ID (publisher-id): KBR
                Journal ID (nlm-ta): Kidney Blood Press Res
                Journal ID (doi): 10.1159/issn.1420-4096
                Title: Kidney and Blood Pressure Research
                Publisher: S. Karger AG
                ISSN (Print): 1420-4096
                ISSN (Electronic): 1423-0143
                Publication date Subscription-year: 2006
                Publication date (Print): June 2006
                Publication date (Electronic): 06 June 2006
                Volume: 29
                Issue: 1
                Pages: 2-9
                Affiliations
                Departments of aNephrology, bFirst Cardiology, and cRadiology, Ataturk Training and Research Hospital, Izmir, Turkey; dDepartment of Medicine, Division of Nephrology and eDepartment of Biostatistics, Vanderbilt University School of Medicine, Nashville, Tenn., USA
                Article
                Publisher ID: 92481 Other ID: Kidney Blood Press Res 2006;29:2–9
                DOI: 10.1159/000092481
                PubMed ID: 16582571
                SO-VID: 39e6bbc4-ba72-4a28-9ddf-5c3f8b46a1d1
                Copyright © © 2006 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 : 22 August 2005
                Date accepted : 31 October 2005
                Page count
                Figures: 2, Tables: 3, References: 32, Pages: 8
                Categories
                Subject: Original Paper

                ScienceOpen disciplines: Cardiovascular Medicine,Nephrology
                Keywords: Renal impairment in non-diabetic elderly patients,Coronary angiography,Nephropathy,Contrast media,Metabolic syndrome,Contrast-induced nephropathy
                Data availability:
                ScienceOpen disciplines: Cardiovascular Medicine, Nephrology
                Keywords: Renal impairment in non-diabetic elderly patients, Coronary angiography, Nephropathy, Contrast media, Metabolic syndrome, Contrast-induced nephropathy

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