الفهرس 
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Abstract
Inflammation and oxidative stress are two faces of one coin in end stage renal disease patients (ESRD) on maintenance hemodialysis. Their interconnection induces anemia complicated with erythropoietin hyporesponsiveness. The biochemical basis behind the resistance to erythropoietin therapy with frequent hemoglobinemia, oxidative stress and iron status have not been fully recovered. Two equal groups (40 patients each) of responders and non-responders to recombinant human erythropoietin therapy (higher than 300 IU /kg/wk of epoetin) were used in the study. Hematological and biochemical analysis of collecting blood and serum samples were performed along with serum electrophoretic protein foot printing. The leukocytes DNA fragmentation was used to evaluate the degree of oxidative insult. Erythropoietin (EPO) good responders showed lower erythrocyte malondialdehyde (E-MDA) level; less pronounced DNA fragmentation of circulating leukocytes than poor responder with elevated hemoglobin, albumin, A/G ratio, total iron, and ferritin levels. Contrariwise, lower erythrocyte superoxide dismutase (E-SOD) and catalase activities in EPO poor responder group than good responder one. Other serum constituents and electrophoretic protein pattern showed a no significant difference between the two groups. There were higher levels of inflammatory markers, interleukin-6 (IL-6) and C- reactive protein (CRP) in EPO poor responder than good responder. The present data showed negative correlations between Hb with both IL-6 and CRP levels, indicating a positive correlation between inflammatory markers and severity of anemia. A direct correlation between Hb and antioxidant enzymes (E-SOD and catalase) was noticed, while the inverse correlation with E-MDA was recorded.