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10.1016/j.semnephrol.2016.02.001 http://scihub22266oqcxt.onion/10.1016/j.semnephrol.2016.02.001 C4884601!4884601!27236128     free     free     free Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Semin+Nephrol 2016 ; 36 (2): 87-93 Nephropedia Template TP {{tp|p=27236128|t=2016. Iron Balance and the Role of Hepcidin in Chronic Kidney Disease |pdf=|usr=}}{{27236128}} gab.com Text Iron Balance and the Role of Hepcidin in Chronic Kidney Disease JO: Semin Nephrol http://www.kidney.de/pget.php?&tw=1&pmid=27236128 #FOAvip The hepatic iron-regulatory hormone hepcidin and its receptor, the cellular iron exporter ferroportin, constitute a feedback-regulated mechanism that maintains adequate plasma concentrations of iron-transferrin for erythropoiesis and other functions, ensures sufficient iron stores, and avoids iron toxicity and iron-dependent microbial pathogenesis. In chronic kidney disease, inflammation and impaired renal clearance increase plasma hepcidin, inhibiting duodenal iron absorption and sequestering iron in macrophages. These effects of hepcidin can cause systemic iron deficiency, decreased availability of iron for erythropoiesis, and resistance to endogenous and exogenous erythropoietin. Together with impaired renal production of erythropoietin, hepcidin-mediated iron restriction contributes to anemia of chronic kidney disease. Twit Text FOAVip Iron Balance and the Role of Hepcidin in Chronic Kidney Disease ????Semin Nephrol http://www.kidney.de/pget.php?&tw=1&pmid=27236128 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27236128 #FOAvip English Wikipedia <ref>{{Cite pmid|27236128}}</ref> Iron Balance and the Role of Hepcidin in Chronic Kidney Disease #MMPMID27236128 Ganz T; Nemeth E Semin Nephrol 2016[Mar]; 36 (2): 87-93 PMID27236128show ga The hepatic iron-regulatory hormone hepcidin and its receptor, the cellular iron exporter ferroportin, constitute a feedback-regulated mechanism that maintains adequate plasma concentrations of iron-transferrin for erythropoiesis and other functions, ensures sufficient iron stores, and avoids iron toxicity and iron-dependent microbial pathogenesis. In chronic kidney disease, inflammation and impaired renal clearance increase plasma hepcidin, inhibiting duodenal iron absorption and sequestering iron in macrophages. These effects of hepcidin can cause systemic iron deficiency, decreased availability of iron for erythropoiesis, and resistance to endogenous and exogenous erythropoietin. Together with impaired renal production of erythropoietin, hepcidin-mediated iron restriction contributes to anemia of chronic kidney disease. äIron Balance and the Role of Hepcidin in Chronic Kidney Disease (epmc).pdf DeepDyve Pubget Overpricing