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      Individualized Risk Management in Diabetics: How to Implement Best Practice Guidelines – Design and Concept of the IRIDIEM Studies

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          Abstract

          The prevalence of type 2 diabetes mellitus is rising rapidly in all developed countries, particularly in the growing population of persons >50 years of age. As a dangerous consequence, this is accompanied by a proportionate increase in the incidence of chronic renal disease. Evidence-based medicine has shown that tight blood glucose control can delay the onset and retard the progression of diabetic complications, and while it is a challenge to closely manage the complexity of diabetes, it is more difficult to effectively treat the multiple associated comorbidities that develop. Best practice guidelines support early intervention and aggressive treatment of hypertension, hyperglycaemia, proteinuria, hypercholesterolemia, and anaemia. To date, guideline-based management has been proven to be difficult. This article describes the concept of the IRIDIEM studies. The objective of these studies is to endorse and facilitate the use of current best practice guidelines for the management of frequent comorbid diseases and established risk factors in the treatment of type 2 diabetes associated with chronic kidney disease. Additionally, IRIDIEM will assess the impact of this improved disease management model on the progression of chronic kidney disease that can result from electronically prompting clinicians with evidence-based treatment advice.

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          Most cited references 13

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          End-stage renal failure in type 2 diabetes: A medical catastrophe of worldwide dimensions.

          The incidence of patients with end-stage renal failure and diabetes mellitus type 2 as a comorbid condition has increased progressively in the past decades, first in the United States and Japan, but subsequently in all countries with a western lifestyle. Although there are explanations for this increase, the major factor is presumably diminishing mortality from hypertension and cardiovascular causes, so that patients survive long enough to develop nephropathy and end-stage renal failure. This review summarizes the striking differences between countries against the background of a similar tendency of an increasing incidence in all countries. Survival on renal replacement therapy continues to be substantially worse for patients with type 2 diabetes. A major reason for this observation is that patients enter renal replacement programs with cardiovascular morbidity acquired in the preterminal phase of renal failure. It is argued that the challenge for the future will be better patient management in earlier phases of diabetic nephropathy to attenuate or prevent progression, as well as cardiovascular complications.
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            Pathogenesis, prevention, and treatment of diabetic nephropathy.

             M. J. Cooper (1998)
            It is likely that the pathophysiology of diabetic nephropathy involves an interaction of metabolic and haemodynamic factors. Relevant metabolic factors include glucose-dependent pathways such as advanced glycation, increased formation of polyols, and activation of the enzyme, protein kinase C. Specific inhibitors of the various pathways are now available, enabling investigation of the role of these processes in the pathogenesis of diabetic nephropathy and potentially to provide new therapeutic approaches for the prevention and treatment of diabetic nephropathy. Haemodynamic factors to consider include systemic hypertension, intraglomerular hypertension, and the role of vasoactive hormones, such as angiotensin II. The mainstay of therapy remains attaining optimum glycaemic control. Antihypertensive therapy has a major role in slowing the progression of diabetic nephropathy. Agents that interrupt the renin-angiotensin system such as angiotensin-converting enzyme inhibitors and angiotensin II receptor antagonists may be particularly useful as renoprotective agents in both the hypertensive and normotensive context.
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              The relationship between hemoglobin levels and diabetic retinopathy.

              This study evaluates the relationship between hemoglobin levels and diabetic retinopathy. Hemoglobin values measured in 1991 and 1992 were collected from 1691 subjects attending a diabetic clinic in Oulu, Finland, and the mean values for the two years were used in the analyses. A classification of retinopathy, based on non-mydriatic photographs taken in 1991 and 1992, was used as the outcome variable. Multiple logistic regression analyses, controlled for serum creatinine levels, proteinuria, and other prognostic factors associated with diabetes, showed that the odds ratio of having any retinopathy was 2.0 (95% confidence interval 1.2-3.3) among subjects with a hemoglobin level of less than 12 g/dl, as compared with those having a hemoglobin level > or = 12 g/dl. Among the retinopathic subjects with low hemoglobin levels, the relative odds of having a severe retinopathy rather than a mild one was 5.3 (2.3-12.6). We conclude that subjects with normocytic anemia tended to have an increased risk of retinopathy, especially of the severe form.
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                Author and article information

                Journal
                KBR
                Kidney Blood Press Res
                10.1159/issn.1420-4096
                Kidney and Blood Pressure Research
                S. Karger AG
                1420-4096
                1423-0143
                2004
                April 2004
                12 August 2004
                : 27
                : 3
                : 127-133
                Affiliations
                aRenal Division, Ghent University Hospital, Ghent, Belgium; bDepartment of Renal Medicine, Kent and Canterbury Hospital, Canterbury, UK; c2nd Department of Internal Medicine, Research Institute and Diabetes Center, Athens University Medical School, University Hospital ‘Attikon’, Athens, Greece; dDiabetes and Endocrinology Day Centre, Guy’s & St. Thomas’ Trust, London, UK; eDepartment of Diabetology, Krankenanstalt Rudolfstiftung, Vienna, Austria
                Article
                78155 Kidney Blood Press Res 2004;27:127–133
                10.1159/000078155
                15114029
                © 2004 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: 1, Tables: 2, References: 45, Pages: 7
                Product
                Self URI (application/pdf): https://www.karger.com/Article/Pdf/78155
                Categories
                Clinical Study

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