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      Relationship between Microfibrillar-Associated Protein 4 Levels and Subclinical Myocardial Damage in Chronic Kidney Disease

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          Abstract

          Introduction: Chronic kidney disease (CKD) is a widespread health problem, in which mortality is most frequently due to cardiovascular diseases. Microfibrillar-associated protein 4 (MFAP4) is an extracellular matrix protein. MFAP4 is involved in several biological processes, particularly the maintenance of vascular integrity and extracellular matrix remodeling. Our review of the literature revealed no data concerning MFAP4 levels in CKD and its relationship with myocardial functions. Objective: The purpose of this study was therefore to investigate MFAP4 levels in CKD, parameters affecting these, and the relationship with myocardial functions. Materials and Methods: Seventy-nine CKD patients and 30 healthy controls were included in the study. Routine biochemical tests and echocardiography were performed once demographic data had been recorded. Blood specimens were collected for MFAP4 analysis, and the results were subjected to statistical analysis. Results: MFAP4 levels were significantly higher in the patient group than in the control group ( p< 0.001). Doppler parameters revealed more frequent LV diastolic impairment in the patient group. Tissue Doppler systolic velocity and global longitudinal strain were significantly impaired, revealing the subclinical LV systolic dysfunction in CKD patients. MFAP4 elevation in the patient group was positively correlated with aortic root (AR), global circumferential strain (GCS), and GCS rate. Conclusion: Our results showed MFAP4 elevation in CKD for the first time in the literature, and that this elevation may be related to GCS and AR dilation. We think that, once supported by further studies, MFAP4 may constitute a marker in the evaluation of myocardial functions in CKD.

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          Most cited references 19

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          Chronic kidney disease: effects on the cardiovascular system.

          Accelerated cardiovascular disease is a frequent complication of renal disease. Chronic kidney disease promotes hypertension and dyslipidemia, which in turn can contribute to the progression of renal failure. Furthermore, diabetic nephropathy is the leading cause of renal failure in developed countries. Together, hypertension, dyslipidemia, and diabetes are major risk factors for the development of endothelial dysfunction and progression of atherosclerosis. Inflammatory mediators are often elevated and the renin-angiotensin system is frequently activated in chronic kidney disease, which likely contributes through enhanced production of reactive oxygen species to the accelerated atherosclerosis observed in chronic kidney disease. Promoters of calcification are increased and inhibitors of calcification are reduced, which favors metastatic vascular calcification, an important participant in vascular injury associated with end-stage renal disease. Accelerated atherosclerosis will then lead to increased prevalence of coronary artery disease, heart failure, stroke, and peripheral arterial disease. Consequently, subjects with chronic renal failure are exposed to increased morbidity and mortality as a result of cardiovascular events. Prevention and treatment of cardiovascular disease are major considerations in the management of individuals with chronic kidney disease.
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            Elastic fibres.

            Elastic fibres are essential extracellular matrix macromolecules comprising an elastin core surrounded by a mantle of fibrillin-rich microfibrils. They endow connective tissues such as blood vessels, lungs and skin with the critical properties of elasticity and resilience. The biology of elastic fibres is complex because they have multiple components, a tightly regulated developmental deposition, a multi-step hierarchical assembly and unique biomechanical functions. However, their molecular complexity is at last being unravelled by progress in identifying interactions between component molecules, ultrastructural analyses and studies of informative mouse models.
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              Prevalent left ventricular hypertrophy in the predialysis population: identifying opportunities for intervention.

              Left ventricular hypertrophy (LVH) is present in over 70% of patients commencing dialysis. It is an independent risk factor for cardiac death, which is the cause of death in approximately 45% of patients in dialysis. The prevalence of LVH in patients earlier in the course of renal insufficiency is unknown. As part of a prospective longitudinal study evaluating the progression of comorbid diseases in patients with progressive renal disease, we evaluated LVH. In 175 consecutive patients attending a renal insufficiency clinic we obtained technically adequate echocardiograms and estimated left ventricular mass index (LVMI) using two-dimensional targeted M-mode echocardiography. We calculated LVMI using the American Society of Echocardiography cube formula method regressed to anatomic validation. The population consisted of 115 men and 60 women ranging in age from 20 to 82 years (mean age, 51.5 years). The mean creatinine was 403 +/- 207 micro mol/L (+/-SD), representing a creatinine clearance (Ccr) of 25.5 +/- 17 mL/min. Left ventricular hypertrophy was defined as LVMI greater than 131 g/m(2) in men and greater than 100 g/m(2) in women, and was present in 38.9% of the population studied. We demonstrate that the prevalence of LVH increased with progressive renal decline: 26.7% of patients with Ccr greater than 50 mL/min had LVH, 30.8% of those with Ccr between 25 and 49 mL/min had LVH, and 45.2% of patients with severe renal impairment (Ccr <25 L/min) had LVH (P = 0.05). The mean LVMI was significantly different among the three groups (97.5 g/m(2) v 114.4 g/m(2), respectively; P < 0.001). Univariate analyses revealed that age, hemoglobin, systolic blood pressure and Ccr were significantly different between the groups with and without LVH. The logistic regression model confirmed the findings of the univariate analysis: an increase in age of 5 years was associated with an increase of 3% in risk of LVH (P = 0.0094), as was an increase in systolic blood pressure of 5 mm Hg (P = 0.0018). For each 10 g/L decrease in hemoglobin, the risk of LVH increased by 6% (P = 0.0062), and for each 5 mL/min decline in Ccr the risk increased by 3% (P = 0.0168). We demonstrate the high prevalence of LVH in patients with renal insufficiency prior to the need for dialysis, which is associated with severity of renal impairment, and identify two modifiable factors (systolic blood pressure and anemia) as important predictors of LVH. We suggest that future studies should focus on interventions aimed at attenuating the impact of these factors.
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                Author and article information

                Journal
                CRM
                Cardiorenal Med
                10.1159/issn.1664-5502
                Cardiorenal Medicine
                S. Karger AG
                1664-3828
                1664-5502
                2020
                July 2020
                08 April 2020
                : 10
                : 4
                : 257-265
                Affiliations
                aDepartment of Internal Medicine, Tekirdağ Namık Kemal University School of Medicine, Tekirdağ, Turkey
                bDepartment of Nephrology, Tekirdağ Namık Kemal University School of Medicine, Tekirdağ, Turkey
                cDepartment of Cardiology, Tekirdağ Namık Kemal University School of Medicine, Tekirdağ, Turkey
                dDepartment of Biochemistry, Tekirdağ Namık Kemal University School of Medicine, Tekirdağ, Turkey
                Author notes
                *Dr. Gülsüm Özkan, Department of Nephrology, Tekirdağ Namık Kemal University School of Medicine, TR–59000 Tekirdağ (Turkey), gulsumozkan78@hotmail.com
                Article
                506827 Cardiorenal Med 2020;10:257–265
                10.1159/000506827
                32268335
                © 2020 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: 3, Pages: 9
                Categories
                Research Article

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