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Background: Anemia 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. Aim of the work: to assess hepcidin level in non dialysis patients (CKD stage 4 &5) treated from Hepatitis C virus and its relation to iron parameters. Patients and Methods: This study was conducted on 20 CKD patients (stage 4 and 5) treated from hepatitis C virus. All candi- dates included in this study subjected to careful history taking, full clinical examination and investigations (including complete blood count, renal chemistry, HCVAb, serum iron, total iron binding capacity, TSAT%, ferritin and hsCRP. Serum hepcidin was analyzed by ELISA technique. Results: Serum hepcidin was 26.3567.26; 40% in stage III, 37.8% in stage IV and 22.2% in stage V. There was statistically significant difference between GFR stages according to Hb., Drug intake ACE inhibitor/ARB, Plt., Creatinine, BUN, Iron, TIBC, Ferritin, T SAT%, CRP and Serum Hepcidin. We showed significant correlations between serum hepcidin and TIC, Iron, TIBC, Ferritin and TSAT%. Conclusion: Median hepcidin value is elevated in nondialysis CKD patients due to increased inflammation and decreased clearance of hepcidin. Furthermore, iron status modifies serum hepcidin level and its association with Hb. Increased hepcidin level leads to iron-restricted erythropoiesis and recombinant human EPO (rhEPO) resistance by inhibiting iron absorption from gut and iron recycling from macrophages. Hence, elevated hepcidin can predict need for parenteral iron to overcome hepcidin-mediated iron-restricted erythropoiesis and need for relatively higher rhEPO doses to suppress hepcidin. [ABSTRACT FROM AUTHOR]

Background: The etiology of anemia in End Stage Renal Disease is multifactorial. Importantly, ESRD patients also have several abnormalities in systemic homeostasis of iron, an essential component in the production of red blood cells. Aim of the Work: to assess hepcidin level in negative virology End Stage Renal Disease patients & its relation to iron level and erythropoiesis. Patients and Methods: This study was conducted on 45 patients who are stage V chronic kidney disease on regular haemodialysis. Ten age and sex matched controls were included in the study. The study included 29 (64.4%) males and 16 (35.6%) females; their mean age was 53.40611.56 years. The prevalence of diabetes among the studied cases was 17.8%, while that of hypertensive was 42.2%. Mean of serum iron level was 64.23619.53. Mean of TIBC was 409.96667.85. Mean of Ferritin level 394.556139.23 and mean of Hepcidin level was 218.516127. Results: Significant negative correlation between Hepcidin level and the Hemoglobin level, and highly significant positive correlation between Hepcidin level and serum Ferritin. Hepcidin up-regulation in the setting of CKD, with subsequent increased serum levels, results in impaired iron absorption from the intestine and decreased iron release from body storage sites. Ultimately, in the setting of such elevated levels, a state of functional iron deficiency may develop and lead to anemia due to iron-restricted erythropoiesis. Conclusion: Based on current evidence, it seems likely that hep- cidin represents a potentially modifiable mediator of anemia of CKD and is thus a potential target for future anemia therapy. [ABSTRACT FROM AUTHOR]

Background: Anemia is a severe complication of chronic kidney disease (CKD) that is seen in more than 80% of patients with impaired renal function. Hepcidin, an acute phase reactant protein produced in the liver, is a key regulator of iron homeostasis. Aim of the Work: to assess hepcidin level in 45 non-dialysis patients (CKD stage IV and V with negative virology) and its relation to iron parameters. Patients and Methods: A cross sectional study was conducted at Nasser Institute for Treatment and Research on 45 patients with chronic kidney disease stage IV and V. All patients included in this study were subjected to the following: Careful history taking, full clinical examination and proper laboratory investigations. Results: A statistically significant difference was found between CKD stage 4 and stage 5 according to Hb., iron, TIBC, Frerretin, serum and CRP. Also, there was a significant positive correlation of serum hepcidin with serum ferretin and hsCRP, while Hb and iron were significantly negatively correlated with hepcidin. We found statistically significant decrease in Hb level, serum Iron level, and TIBC in CKD stage 5 less than stage 4. We found statistically significant increase in Hepcidin level, serum ferritin, and hsCRP in CKD stage 5 more than stage 4. We found statistically significant Positive correlation between serum hepcidin with serum ferretin among patients with CKD stage 4 and 5. We found statistically significant Positive correlation between serum hepcidin with hsCRP among patients with CKD stage 4 and 5. We found statistically significant negative correlation between serum hepcidin with Hb among patients with CKD stage 4 and 5. A statistically significant Positive correlation between serum hepcidin with serum Iron among patients with CKD stage 4 and 5. Also we reported a statistically non-significant negative correlation between serum hepcidin and TIBC. Conclusion: Elevated hepcidin can predict the need for parenteral iron to overcome hepcidin-mediated iron-restricted erythropoiesis and need for relatively higher rhEPO doses to suppress hepcidin in CKD patients with negative viral markers. [ABSTRACT FROM AUTHOR]