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      Erythropoietin Resistance in Patients with Chronic Kidney Disease: Current Perspectives

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          Abstract

          Anemia is a frequent complication of chronic kidney disease, and its primary cause is erythropoietin deficiency. After diagnosis, treatment begins with administration of an erythropoiesis-stimulating agent (ESA). However, some patients present with resistance to ESA, which needs to be reversed, as it can increase the risk of death in patients with kidney disease. Therefore, we provide a discussion of the current literature regarding the factors that can modify the response to this class of drugs and the strategies that can be considered to optimize the benefits of treating anemia.

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          Most cited references51

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          Association between albuminuria, kidney function, and inflammatory biomarker profile in CKD in CRIC.

          Increased risk of mortality in patients with CKD has been attributed to inflammation. However, the association between kidney function, albuminuria, and biomarkers of inflammation has not been examined in a large cohort of CKD patients. This study measured the plasma levels of IL-1β, IL-1 receptor antagonist (IL-1RA), IL-6, TNF-α, TGF-β, high-sensitivity C-reactive protein (hs-CRP), fibrinogen, and serum albumin in 3939 participants enrolled in the Chronic Renal Insufficiency Cohort study between June 2003 and September 2008. An inflammation score was established based on plasma levels of IL-1β, IL-6, TNF-α, hs-CRP, and fibrinogen. Estimated GFR (eGFR) and serum cystatin C were used as measures of kidney function. Albuminuria was quantitated by urine albumin to creatinine ratio (UACR). Plasma levels of IL-1β, IL-1RA, IL-6, TNF-α, hs-CRP, and fibrinogen were higher among participants with lower levels of eGFR. Inflammation score was higher among those with lower eGFR and higher UACR. In regression analysis adjusted for multiple covariates, eGFR, cystatin C, and UACR were strongly associated with fibrinogen, serum albumin, IL-6, and TNF-α. Each unit increase in eGFR, cystatin C, and UACR was associated with a -1.2% (95% confidence interval, -1.4, -1), 64.9% (56.8, 73.3) and 0.6% (0.4, 0.8) change in IL-6, respectively (P<0.001). Biomarkers of inflammation were inversely associated with measures of kidney function and positively with albuminuria.
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            Chronic inflammation in end-stage renal disease and dialysis

            Abstract Under normal conditions, inflammation is a protective and physiological response to various harmful stimuli. However, in several chronic debilitating disorders, such as chronic kidney disease, inflammation becomes maladaptive, uncontrolled and persistent. Systemic persistent inflammation has, for almost 20 years, been recognized as a major contributor to the uraemic phenotype (such as cardiovascular disease, protein energy wasting, depression, osteoporosis and frailty), and a predictor of cardiovascular and total mortality. Since inflammation is mechanistically related to several ageing processes (inflammageing), it may be a major driver of a progeric phenotype in the uraemic milieu. Inflammation is likely the consequence of a multifactorial aetiology and interacts with a number of factors that emerge when uraemic toxins accumulate. Beside interventions aiming to decrease the production of inflammatory molecules in the uraemic milieu, novel strategies to increase the removal of large middle molecules, such as expanded haemodialysis, may be an opportunity to decrease the inflammatory allostatic load associated with retention of middle molecular weight uraemic toxins.
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              Update on Anemia in ESRD and Earlier Stages of CKD: Core Curriculum 2018

              Anemia is a frequent complication during the later stages of chronic kidney disease. When present, it may cause symptoms such as fatigue and shortness of breath. The pathogenesis of anemia in chronic kidney disease is complex, but a central feature is a relative deficit of erythropoietin. New information has elucidated the critical role of the hypoxia-sensing system in mediating erythropoietin synthesis and release. Iron deficiency is a second important factor in the anemia of chronic kidney disease. New insights into the dynamics of iron metabolism have clarified the role of chronic inflammation and hepcidin as key mediators of impaired iron utilization. In this article, we review the epidemiology, pathobiology, clinical evaluation, and treatment of anemia in chronic kidney disease.
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                Author and article information

                Journal
                Int J Nephrol Renovasc Dis
                Int J Nephrol Renovasc Dis
                ijnrd
                ijnrd
                International Journal of Nephrology and Renovascular Disease
                Dove
                1178-7058
                08 October 2020
                2020
                : 13
                : 231-237
                Affiliations
                [1 ]University Hospital of the Federal University of Maranhão , São Luís, Brazil
                [2 ]Federal University of Maranhão , São Luís, Brazil
                Author notes
                Correspondence: Elton Jonh Freitas Santos University Hospital of the Federal University of Maranhão , Rua Barão de Itapary – 227, Centro, São LuísCEP 65020-070, MA, BrazilTel +98 2109.1089/2109.1024 Email eltonfreitas86@yahoo.com.br
                Author information
                http://orcid.org/0000-0002-1743-9103
                http://orcid.org/0000-0003-1851-9495
                http://orcid.org/0000-0003-3027-2763
                http://orcid.org/0000-0003-4105-2010
                http://orcid.org/0000-0001-9711-0182
                Article
                239151
                10.2147/IJNRD.S239151
                7549651
                33116754
                52dcd3f2-bd85-461d-8370-3bb049f2027f
                © 2020 Santos et al.

                This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms ( https://www.dovepress.com/terms.php).

                History
                : 23 June 2020
                : 22 September 2020
                Page count
                Figures: 0, Tables: 1, References: 51, Pages: 7
                Categories
                Review

                Nephrology
                anemia,chronic kidney disease,erythropoietin,drug resistance
                Nephrology
                anemia, chronic kidney disease, erythropoietin, drug resistance

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