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      The Visceral Adiposity Index Is a Predictor of Incident Chronic Kidney Disease: A Population-Based Longitudinal Study

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          Background and Aims: Visceral adiposity index (VAI), calculated with body mass index, high density lipoprotein-cholesterol, triglycerides and waist circumference, has been proposed as a marker of visceral fat accumulation and dysfunction in adipose tissue. Methods: The impact of VAI on incident chronic kidney disease (CKD) in a historical cohort study of 15,159 (8,260 men and 6,899 women) participants was investigated. CKD was defined when estimated glomerular filtration rate was <60 mL/min/1.73 m<sup>2</sup> or proteinuria (positive: ≥1+). We divided the participants into 2 groups according to sex and into quartiles according to VAI (Q1–4). We performed Cox proportional hazard models, adjusting for age, smoking status, exercise, alcohol consumption, systolic blood pressure, hemoglobin A1c, uric acid, and creatinine. Results: During the median 3.3-year follow-up for men and 3.2-year follow-up for women, 1,078 participants (629 men and 449 women) developed CKD. The 4,000 days cumulative incidence rate of CKD for men and women were 3.7 and 3.9% in Q1, 5.2 and 5.9% in Q2, 6.5 and 7.0% in Q3, and 8.4 and 9.3% in Q4 respectively. Compared to Q1, the hazard ratios of incident CKD in Q2, Q3 and Q4 for men and women were 1.23 (95% CI 0.91–1.66, p = 0.184) and 1.30 (0.87–1.96, p = 0.203), 1.42 (1.06–1.90, p = 0.018) and 1.38 (0.94–2.05, p = 0.105), and 1.51 (1.12–2.02, p = 0.006) and 1.65 (1.12–2.46, p = 0.013) respectively. Additionally, the area under the curve of VAI for incidence of CKD was superior to that of VAI in men (0.595 vs. 0.552, p < 0.001) and equal to in women (0.597 vs. 0.591, p = 0.708). Conclusions: The VAI can be a predictor of incident CKD.

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          Most cited references 17

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          Chronic kidney disease as a global public health problem: approaches and initiatives - a position statement from Kidney Disease Improving Global Outcomes.

          Chronic kidney disease (CKD) is increasingly recognized as a global public health problem. There is now convincing evidence that CKD can be detected using simple laboratory tests, and that treatment can prevent or delay complications of decreased kidney function, slow the progression of kidney disease, and reduce the risk of cardiovascular disease (CVD). Translating these advances to simple and applicable public health measures must be adopted as a goal worldwide. Understanding the relationship between CKD and other chronic diseases is important to developing a public health policy to improve outcomes. The 2004 Kidney Disease Improving Global Outcomes (KDIGO) Controversies Conference on 'Definition and Classification of Chronic Kidney Disease' represented an important endorsement of the Kidney Disease Outcome Quality Initiative definition and classification of CKD by the international community. The 2006 KDIGO Controversies Conference on CKD was convened to consider six major topics: (1) CKD classification, (2) CKD screening and surveillance, (3) public policy for CKD, (4) CVD and CVD risk factors as risk factors for development and progression of CKD, (5) association of CKD with chronic infections, and (6) association of CKD with cancer. This report contains the recommendations from the meeting. It has been reviewed by the conference participants and approved as position statement by the KDIGO Board of Directors. KDIGO will work in collaboration with international and national public health organizations to facilitate implementation of these recommendations.
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            Long-term follow-up after tight control of blood pressure in type 2 diabetes.

            Post-trial monitoring of patients in the United Kingdom Prospective Diabetes Study (UKPDS) examined whether risk reductions for microvascular and macrovascular disease, achieved with the use of improved blood-pressure control during the trial, would be sustained. Among 5102 UKPDS patients with newly diagnosed type 2 diabetes mellitus, we randomly assigned, over a 4-year period beginning in 1987, 1148 patients with hypertension to tight or less-tight blood-pressure control regimens. The 884 patients who underwent post-trial monitoring were asked to attend annual UKPDS clinics for the first 5 years, but no attempt was made to maintain their previously assigned therapies. Annual questionnaires completed by patients and general practitioners were used to follow patients who were unable to attend the clinic in years 1 through 5, and questionnaires were used for all patients in years 6 to 10. Seven prespecified aggregate clinical end points were examined on an intention-to-treat basis, according to the previous randomization categories. Differences in blood pressure between the two groups during the trial disappeared within 2 years after termination of the trial. Significant relative risk reductions found during the trial for any diabetes-related end point, diabetes-related death, microvascular disease, and stroke in the group receiving tight, as compared with less tight, blood-pressure control were not sustained during the post-trial follow-up. No risk reductions were seen during or after the trial for myocardial infarction or death from any cause, but a risk reduction for peripheral vascular disease associated with tight blood-pressure control became significant (P=0.02). The benefits of previously improved blood-pressure control were not sustained when between-group differences in blood pressure were lost. Early improvement in blood-pressure control in patients with both type 2 diabetes and hypertension was associated with a reduced risk of complications, but it appears that good blood-pressure control must be continued if the benefits are to be maintained. (UKPDS 81; Current Controlled Trials number, ISRCTN75451837.) 2008 Massachusetts Medical Society
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              Insulin signaling to the glomerular podocyte is critical for normal kidney function.

              Diabetic nephropathy (DN) is the leading cause of renal failure in the world. It is characterized by albuminuria and abnormal glomerular function and is considered a hyperglycemic "microvascular" complication of diabetes, implying a primary defect in the endothelium. However, we have previously shown that human podocytes have robust responses to insulin. To determine whether insulin signaling in podocytes affects glomerular function in vivo, we generated mice with specific deletion of the insulin receptor from their podocytes. These animals develop significant albuminuria together with histological features that recapitulate DN, but in a normoglycemic environment. Examination of "normal" insulin-responsive podocytes in vivo and in vitro demonstrates that insulin signals through the MAPK and PI3K pathways via the insulin receptor and directly remodels the actin cytoskeleton of this cell. Collectively, this work reveals the critical importance of podocyte insulin sensitivity for kidney function. Copyright © 2010 Elsevier Inc. All rights reserved.

                Author and article information

                Kidney Blood Press Res
                Kidney and Blood Pressure Research
                S. Karger AG
                May 2020
                30 March 2020
                : 45
                : 3
                : 407-418
                aDepartment of Endocrinology and Metabolism, Kyoto Prefectural University of Medicine, Graduate School of Medical Science, Kyoto, Japan
                bDepartment of Gastroenterology, Asahi University Hospital, Gifu, Japan
                Author notes
                *Masahide Hamaguchi, MD, PhD, Department of Endocrinology and Metabolism, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, 465, Kajii cho, Kamigyo-ku, Kyoto 621–8585 (Japan), mhama@koto.kpu-m.ac.jp
                506461 Kidney Blood Press Res 2020;45:407–418
                © 2020 The Author(s) Published by S. Karger AG, Basel

                This article is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License (CC BY-NC-ND). Usage and distribution for commercial purposes as well as any distribution of modified material requires written permission. 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: 4, Tables: 3, Pages: 12
                Research Article


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