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      Plasma Prohepcidin Positively Correlates with Hematocrit in Chronic Hemodialysis Patients

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          Background/Aims: Experimental studies have demonstrated interleukin-6 and iron load induce expression of hepcidin (an iron regulatory peptide), whereas anemia and erythropoietin (EPO) suppress its expression. We are the first to explore the relationships of plasma prohepcidin (the pro-hormone of hepcidin) in patients undergoing chronic hemodialysis (HD). Methods: We enrolled 71 chronic HD patients. During the preceding 3 months before enrollment, they all had steady weekly levels of haematocrit (Hct) and fixed subcutaneous doses of recombinant human EPO. Plasma levels of prohepcidin, proinflammatory cytokines, and EPO were determined by ELISA kits. Results: Of the patients, prohepcidin levels correlated positively with Hct, and negatively with interleukin-6 and EPO. Examined by a multivariate lineal regression method, we found Hct was the only significant predictor of plasma prohepcidin level. However, prohepcidin had no significant correlation with iron profiles. Conclusion: Our findings suggest prohepcidin expression in chronic HD patients might be positively regulated by Hct.

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          Most cited references 5

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          Pro-hepcidin: expression and cell specific localisation in the liver and its regulation in hereditary haemochromatosis, chronic renal insufficiency, and renal anaemia.

          The hepatic peptide hormone hepcidin, which has recently been isolated from human plasma and urine, is thought to be a central regulator of iron homeostasis. We investigated the presence and cellular localisation of hepcidin in the liver and developed a non-invasive assay to analyse its regulation in patients with hereditary haemochromatosis (HH), chronic renal insufficiency (CRI), and renal anaemia (RA). Expression and localisation of hepcidin was shown by reverse transcription-polymerase chain reaction, western blot, immunocytochemistry, and immunofluorescence in human and guinea pig liver. Serum concentrations were determined in various groups of patients using a sensitive enzyme linked immunosorbent assay (ELISA). Western blot analysis with region specific antibodies identified a approximately 10 kDa peptide corresponding to the apparent molecular mass of pro-hepcidin. Localisation studies revealed that pro-hepcidin is expressed at the basolateral membrane domain of hepatocytes and is also present in blood. We developed a stable sensitive ELISA for detection and determination of pro-hepcidin in human serum. Mean pro-hepcidin level in human serum of healthy volunteers was 106.2 ng/ml. Enhanced levels of pro-hepcidin (148.1 ng/ml) were found in patients with CRI but normal haemoglobin values, indicating that the kidneys may metabolise and/or eliminate the circulating hormone. In contrast, concentrations of pro-hepcidin were significantly decreased in patients with HH (70.2 ng/ml) and also in patients with RA (115.0 ng/ml) compared with the CRI group. From the detection of pro-hepcidin in human serum, we conclude that the prohormone may be involved in the regulation of iron metabolism in HH. Decreased pro-hepcidin levels could play an important role in the pathogenesis of HH.
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            High C-reactive protein is a strong predictor of resistance to erythropoietin in hemodialysis patients.

            Inflammation is one of the major causes of resistance to erythropoietin (EPO) treatment. In the present study, the relationship between serum C-reactive protein (s-CRP) and the dose of recombinant human EPO required to maintain hemoglobin levels at approximately 12 g/dL was analyzed in 30 hemodialysis patients. The weekly EPO dose in patients with s-CRP > or = 20 mg/L was, on average, 80% higher than in patients with s-CRP less than 20 mg/L. The EPO doses and s-CRP were both inversely correlated to the levels of serum albumin and serum iron, suggesting that the principal mechanism by which inflammatory cytokines inhibit erythropoiesis is coupled to iron metabolism, ie, functional iron deficiency. Our results demonstrate the usefulness of s-CRP as a predictor of resistance to EPO treatment.
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              Prohepcidin accumulates in renal insufficiency.

              The understanding of iron metabolism has increased substantially during the last decade. Several new transporters and iron regulating molecules have been described. Hepcidin, a small hepatic peptide has recently been proposed as a central mediator of dietary iron absorption. We have investigated the relationship between prohepcidin, the prohormone of hepcidin, and renal function and iron status. Forty six patients, referred for 51Cr-EDTA clearance were included in this study. Renal function was assessed by determination of serum creatinine, creatinine clearance, serum cystatin C and serum beta-trace protein. Iron status was evaluated by determination of serum iron, transferrin, transferrin saturation and serum ferritin. All determinations were performed using commercial reagents (Roche Diagnostics, Dade Behring). Serum prohepcidin was determined using an ELISA kit. Serum prohepcidin was found to correlate with 51Cr-EDTA clearance (r = -0.44; p = 0.005), creatinine clearance, serum creatinine, beta-trace protein and cystatin C. No significant relationship was observed between serum prohepcidin concentrations and red cell count, hemoglobin concentration or hematocrit. No significant correlation was found in this population between prohepcidin concentrations and iron status. Increased serum prohepcidin concentrations were observed with declining kidney function. We observed no relationship between red cell indices or iron status and serum prohepcidin concentrations.

                Author and article information

                Blood Purif
                Blood Purification
                S. Karger AG
                April 2006
                27 April 2006
                : 24
                : 3
                : 311-316
                aDepartment of Internal Medicine, Far Eastern Memorial Hospital, and Departments of bInternal Medicine and cClinical Research, National Taiwan University Hospital, Taipei, Taiwan
                91453 Blood Purif 2006;24:311–316
                © 2006 S. Karger AG, Basel

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                Tables: 4, References: 16, Pages: 6
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