Can we expect something from prohepcidin measurement in hemodialysis patients?

HD patients, or its accumulation due to renal failure, logically inhibits the iron release by macrophages, limiting its availability for erythropoiesis [4] . In accordance with the negative correlation between prohepcidin and hematocrit are the findings of Dallalio et al. [5] , who in a recent in vitro study detected that hepcidin can contribute to anemia not only through an effect on iron metabolism, but also through inhibition of erythroid progenitor proliferation and survival. What then is the explanation for the discrepancy among the three studies regarding the correlation of prohepcidin with hematocrit? Why was no relation detected between prohepcidin and markers of iron metabolism? The same kit was used for accessing prohepcidin levels in HD patients and its mean value was similar in all three studies (200–250 ng/ml). Is prohepcidin measurement useless for understanding better the anemia in HD and consequently as a marker of erythropoietin resistance in the future? In our opinion, at the present time we are not able to answer the above question due to the complex interrelations among the various factors involved in the regulation of hepcidin expression. For example, serum iron and transferrin saturation are markers of iron metabolism but are also influenced by inflammation, which decreases their levels. Ferritin is a marker of iron stores and an acute phase reactant. Inflammation increases CRP as well as hepSir, We read the article by Hsu et al. [1] that was recently published in your journal. The authors evaluated the effect of plasma prohepcidin on iron metabolism and erythropoiesis – in relation to inflammation as well – in hemodialysis (HD) patients. Their results were unexpected, since they detected a positive correlation between prohepcidin and hematocrit, no correlation with iron metabolism markers and CRP, and a negative correlation with IL-6. These results are very disappointing regarding the role of hepcidin in anemia of chronic disease and the resistance in recombinant erythropoietin therapy in HD patients. Our team performed a similar study, which is going to be published in a future issue of Acta Haematologica [2] . It has already been presented in abstrcat from in the XLIII ERA–EDTA Congress. We also failed to detect a correlation of serum prohepcidin with various serum iron metabolism markers and CRP. However, multiple linear regression analysis considering age, inflammation, iron adequacy, erythropoietin dose and prohepcidin levels revealed that prohepcidin was the major determinant of hematocrit, but in a negative way. Malyszco et al. [3] also showed, in a univariate analysis, that prohepcidin correlated negatively with hematocrit. The negative correlation of prohepcidin with hematocrit seems reasonable, since the prohepcidin hyperproduction due to microinflammation usually encountered in Published online: November 16, 2006