الفهرس 
Anemia in chronic Kidney Disease
Regulation of IL-6 synthesis:Only 14 pages are availabe for public view
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Abstract
CKD is a worldwide public health problem. CKD is more prevalent in the elderly population. However, while younger patients with CKD typically experience progressive loss of kidney function, 30% of patients over 65 years of age with CKD have stable disease(1). According to the KDIGO guidelines, anemia in adults and children<15 years with CKD when the Hb concentration is >13.0 g/dl in males and 12.0 g/dl in females(2). Many CKD patients have functional iron deficiency, characterized by impaired iron release from body stores which is unable to meet the demand for erythropoiesis(3). Shortened red blood cell survival also contributes to development of anemia, as demonstrated by radioisotope labeling studies. Although the etiology is not clear, metabolic and mechanical factors have been proposed(4). Many data suggest that hepcidin excess may account for the impaired dietary iron absorption and reticuloendothelial cell iron blockade which present in many CKD patients(3). Interleukin-6 (IL-6) also issues a warning signal in the event of tissue damage. Damage-associated molecular patterns (DAMPs), that are released from damaged or dying cells in noninfectious inflammations as burn or trauma, directly or indirectly promote inflammation(5). IL-6 is also involved in the regulation of serum iron and zinc levels via control of their transporters. As for serum iron, IL-6 induces hepcidin production, that blocks the action of iron transporter ferroportin 1 on gut and thus, decreases serum iron levels. This means that the IL-6-hepcidin axis is responsible for hypoferremia and anemia associated with chronic inflammation.