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Hepsidin: Peranannya dalam Patogenesis dan Implikasinya terhadap Tata Laksana Anemia pada Penyakit Ginjal Kronis (Hepcidin: Role in the Pathogenesis and Implications for Management of Anemia in Chronic Kidney Disease)
ABSTRACT:
Anemia is prevalent in chronic kidney disease (CKD) patients and associated with increased morbidity and mortality. Current management of anemia in CKD resolves around iron supplementation, erythropoiesis-stimulating agents (ESA), and red cell transfusion. Hepcidin is a peptide produced in liver and is a key regulator of systemic iron homeostasis to prevent iron overload by iron sequestration in macrophages and decreasing enteral iron absorption. The production is increased by inflammation and iron supplementation; attenuated by hypoxia, anemia, iron deficiency, increased erythropoiesis activity and ESA. Studies have shown that hepcidin serum level in patients with CKD is increased. High hepcidin serum level contributes to anemia in CKD by mediating iron-restricted erythropoiesis, inhibiting erythroid colony formation, and impairing red blood cell survival. Its implication is that hepcidin has the potential to be an important biomarker of iron status, a guide to predict and monitor iron therapy response, and a predictor of ESA response and resistance. Also, hepcidin has the potential to become a therapeutic target for hepcidin antagonist agent which could lead to effective treatment of anemia in CKD.
Key words: anemia, chronic kidney disease, hepcidin
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