Renal Anemia of Inflammation: The Name Is Self-Explanatory

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dc.contributor.authorYilmaz, Mahmut Ilker
dc.contributor.authorSolak, Yalcin
dc.contributor.authorCovic, Adrian
dc.contributor.authorGoldsmith, David
dc.contributor.authorKanbay, Mehmet
dc.date.accessioned2020-03-26T18:15:58Z
dc.date.available2020-03-26T18:15:58Z
dc.date.issued2011
dc.departmentSelçuk Üniversitesien_US
dc.description.abstractBackground: Anemia is inevitable as chronic kidney disease (CKD) advances. With the advent of erythropoietin-stimulating agents (ESAs), considerable improvement has been achieved in the management of anemia. However, some patients show a reduced response to ESAs. Methods: Many factors affect the response to ESA treatment. CKD is now considered as an inflammatory disorder and this understanding led to the recognition of the central role of inflammation in ESA resistance. Inflammation is related to untoward outcomes, including atherosclerosis and anemia, in the CKD population. Furthermore, recognition of deleterious effects of proinflammatory markers at different levels of erythropoiesis led to a change in the name of 'anemia of chronic disease' to anemia of inflammation. Results: The discovery of hepcidin as the major controller of iron metabolism in anemia of inflammation answered many questions regarding the interaction of erythropoietin, iron and bone marrow. Hepcidin production in the liver is driven by three major factors: inflammation, iron overload and anemia/hypoxia. Hepcidin levels are increased in patients with CKD due to the interaction of many factors; a comprehensive understanding of these pathways is thus critical in the effort to alleviate anemia of inflammation and ESA resistance. Conclusion: In this review, we discussed the epidemiology, determinants and consequences of anemia of inflammation in CKD patients with special emphasis on the central role of hepcidin along with molecular pathways driving its production. Copyright (C) 2011 S. Karger AG, Baselen_US
dc.identifier.doi10.1159/000328037en_US
dc.identifier.endpage225en_US
dc.identifier.issn0253-5068en_US
dc.identifier.issn1421-9735en_US
dc.identifier.issue3en_US
dc.identifier.pmid21829013en_US
dc.identifier.scopusqualityQ1en_US
dc.identifier.startpage220en_US
dc.identifier.urihttps://dx.doi.org/10.1159/000328037
dc.identifier.urihttps://hdl.handle.net/20.500.12395/26787
dc.identifier.volume32en_US
dc.identifier.wosWOS:000293831400011en_US
dc.identifier.wosqualityQ2en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherKARGERen_US
dc.relation.ispartofBLOOD PURIFICATIONen_US
dc.relation.publicationcategoryDiğeren_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.selcuk20240510_oaigen_US
dc.subjectAnemiaen_US
dc.subjectInflammationen_US
dc.subjectChronic kidney diseaseen_US
dc.titleRenal Anemia of Inflammation: The Name Is Self-Explanatoryen_US
dc.typeReviewen_US

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