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Abstract
Recently, a complex regulatory network that governs iron traffic has emerged, and points to hepcidin as a major evolutionary conserved regulator of iron distribution. We conducted this study to evaluate the role of hepcidin in anemia of chronic renal failure patients and to evaluate the relation between hepcidin and other indices in those patients. Analytical cross sectional cohort control study was carried out on chronic renal failure patients attending Nephrology Unit of Pediatric department at Zagazig university Hospital. Our results can be summarized as follow: There was significant decline in hemoglobin and hematocrit levels in the studied diseased groups with significant rise in serum urea and creatinine levels. A significant rise in serum ferritin was detected while there was no significant difference between TIBC and serum iron levels between the diseased groups and the normal control group. There was a significant rise in iPTH levels in the diseased group (Ι) in comparison to the normal control group. A significant rise in serum cholesterol and triglycerides was detected while there was a significant decline in the level of albumin in our patients. Our study demonstrated a significant rise in serum Hepcidin levels in the diseased groups . A significant positive correlation was demonstrated between serum hepcidin levels and serum ferritin while a significant negative correlation was revealed between serum hepcidin and hemoglobin , Hematocrit and TIBC. Also we didn`t find a significant correlation between serum hepcidin and C.R.P as an inflammatory marker in our patients. No significant difference was detected in hepcidin levels in the patients whom were on iron chelation therapy neither on intravenous iron therapy in comparison to whom were not.