Role of hepcidin as a biomarker for iron status and its effect on anemia management in patients with chronic kidney disease (stage II-Iv) after HCV treatment

Abstract

nemia is a severe complication of chronic kidney disease (CKD) that is seen in more than 80% of patients with impaired renal function. Although there are many mechanisms involved in the pathogenesis of anemia of renal disease, the primary cause is the inadequate production of erythropoietin by the damaged kidneys. Erythropoietin is produced in the peritubular cells of the kidney and is the major hormone involved in erythropoiesis. When erythropoietin levels are low, an inadequate number of oxygen-carrying red blood cells are produced. Adequate iron stores are essential for achieving maximum benefit from erythropoietic agents, such as recombinant human erythropoietin (rhEPO) or darbepoetinalfa. Decreased iron stores or decreased availability of iron are the most common reasons for resistance to the effect of these agents. Recombinant erythropoietin (rhEPO) has transformed anemia therapy in patients with chronic kidney disease (CKD). However, rhEPO resistance, often associated with iron deficiency and inflammation, remains a challenging problem. Current available iron indices do not reliably identify iron-restricted erythropoiesis, often a sequel of inflammation, or those patients who would likely benefit from parenteral iron therapy.