Objective: Uremia is a state of heightened inflammatory activation. This might have an impact on several parameters including those used in the management of anemia as ferritin, serum iron, transferrin saturation, C-reactive protein (CRP) and hepcidin levels. In spite of this complexity the existing data indicate that hepcidin has an advantage over ferritin in guiding treatment of anemia in patients with chronic kidney disease (CKD) as it directly reflects iron availability and the status of iron homeostasis. Aim of the study: was to determine serum hepcidin levels in maintenance haemodialysis (HD) patients and to investigate its relation to ferritin and markers of inflammation as C-reactive protein. Subjects and methods: This study was conducted on 40 maintenance haemodialysis patients and 20 agematched apparently healthy controls from October 2015 till February 2016 at the Haemodialysis Departement, National Institute of Urology and Nephrology (NIUN). Creatinine, albumin, hemoglobin, leucocytic count, CRP, hepcidin and ferritin were measured. Results: Serum ferritin and hepcidin levels were significantly higher in HD patients compared with controls (825.67 ± 956.52 ng/ml and 9.2 ± 4.2 ng/ml vs 85.1± 63.35 ng/ml and 0.75 ± 0.39 ng/ml respectively) (p< 0.001).There was significant difference in CRP in HD patients compared with controls (4.28 ± 3.7mg/L vs 1.35±1.04mg/L respectively)(p<0.05).There were insignificant positive weak correlations between serum levels of hepcidin and ferritin (r = 0.05, P = 0.74). Conclusion: Serum hepcidin levels are increased in HD patients and, hence, could be used in the evaluation of anemia in such patients. Serum hepcidin provides useful information about the level and availability of iron during inflammation as compared with traditional markers of iron status. Availability of the ELISA assay for serum hepcidin will facilitate the routine measurement of hepcidin in clinical practice.

Tumour necosis factor alpha (TNF-o:) is known to be involved in pathogenesis of acute renal allograft rejection. However, measurement of cytokine serum levels alone are not a reliable index of acute rejection episodes. TNF-o: induces the release of soluble receptors (TNF-SR55 and TNF-SR75) that have an inhibitory activity and catabolized by the kidney. Twenty nine transplant recepients were studied and compared to ten healthy controls. TNF-o:, TNF-SR55 and TNF-SR75 were measured before and after renal transplantation. The mean pre-transplantation values were 26.3 ± 9.7 pg/ml, 28.2 ± 8.3 and 42.5 ± 11.1 ng/ml respectively. According to post-transplant course patients were divided into 3 groups. Group I (stable transplant group: no= 17): The mean level of TNF-o: value was 7.5 ± 4.6 pg/ml, TNF-SR55 6.4 ± 4.7 and TNF-SR75 12.5 ± 8 ng/ml (p NS). Group Il (acute allograft rejection group: no = 8): The mean values were 37.2 ± 16.2 pg/ml, 16.9 ± 9.6 and 30.9 ± 13.4 ng/ml respectively (p< 0.05). Group III cyclosporine (CS) nephrotoxicity group: no= 4): The mean level of TNF-o: was 9.9 ± 2.1 pg/ml with a highly significant increase in its receptor values (9.4 ± 1.0 & 21.2 ± 6.8 ng/ml; vs 5.5 ± 1.2 & 12.4 ± 4.8 ng/ml respectively (P< 0.0 I). To improve the predictive value of this cytokine and its receptors,we calculated the ratios of TNF-o: to both receptors (SR55-SR75). During acute rejection episode, the ratio values to control were 2.4 ± 0.6 vs 1.4 ± 0.7 and 1.3 ± 0.5 vs 0.7 ± 0.4 respectively (P