Volume 68, Issue 11 (4 2011)                   Tehran Univ Med J 2011, 68(11): 681-685 | Back to browse issues page

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R A L, S S, M L P. The relationship between pro-hepcidin and serum biochemical parameters in chronic hemodialysis patients: a study on 54 patients. Tehran Univ Med J. 2011; 68 (11) :681-685
URL: http://tumj.tums.ac.ir/article-1-297-en.html
1- , kian1380@yahoo.com
Abstract:   (3634 Views)

Background: Prohepcidin, a liver-derived peptide with antimicrobial properties, is regulated by factors such as iron load and inflammation. Hepcidin is a central player in iron homeostasis. It downregulates the iron exporter ferroportin, thereby inhibiting iron absorption, release and recycling. Thus, prohepcidin increases the possibility of iron-limited erythropoiesis and development of anemia. In end-stage renal disease (ESRD), plasma hepcidin levels are elevated, which may contribute to iron deficiency in these patients. This study was undertaken to investigate the relationship between prohepcidin and serum biochemical parameters related to anemia and inflammation in the aforesaid patients.

Methods: Fifty-four stable patients with uremia who were on chronic hemodialysis were enrolled in the study. The patients were withheld from intravenous iron two weeks prior to laboratory measurements. Later, (total) prohepcidin was measured by ELISA method as were other parameters including serum iron, TIBC, TSAT, Hct, ferritin, albumin, CRP, ESR, cholesterol and triglyceride.

Results: Serum prohepcidin levels were higher than normal values in the patients, but they were not correlated to the serum iron, TIBC, TSAT, Hct, ferritin, albumin, cholesterol and triglyceride (p>0.05). No significant association were also found with ESR (p=0.97, r= -0.005) or CRP (p=0.053, r =0.26).

Conclusion: Serum prohepcidin level was higher in chronic hemodialysis patients but it was not predictive of iron status or inflammatory conditions in these patients. Confirmation of these results may necessitate studies with larger sample sizes or measurement of the biologically active form of hepcidin.

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