Iron metabolism — a roleof hepcidin

Iron is the fourth most common element in the Earth’s crust and the most abundant transition metal in the human body. All living organisms have evolved sophisticated mechanisms to maintain appropriate iron levels in their cells and within their body. Maintaining the correct iron balance is crucial for health. Within the last few years, our understanding of iron metabolism has dramatically increased due to the discovery of hepcidin, produced by hepatocytes, modulated in response to anemia, hypoxia, or inflammation. This is a circulating antimicrobial peptide mainly synthesized in the liver, which has been recently proposed as a factor regulating the uptake of dietary iron and its mobilization from macrophages and hepatic stores. Inflammation causes an increase of production of hepcidin, which is a potent mediator of anemia of chronic diseases. Anemia in chronic kidney disease is mainly due to erythropoietin deficiency but these patients often have a chronic inflammatory state. It has been found that anemia upregulated lipocalin 2 (NGAL) in the liver and serum. The regulation of iron metabolism involves the interaction of a number of specific proteins as well as the interplay between iron absorption and iron loss. It has also been shown recently that the kidney too is involved in iron metabolism On the other hand, NGAL (neutrophil gelatinase-associated lipocalin) binds small, iron carrying molecules-siderophores. Both NGAL and hepcidin express antimicrobial properties. NGAL could be involved in both kidney function and iron metabolism similarly to hepcidin. The aim of this review is to summarize the current knowledge dealing with a possible role of hepcidin in iron metabolism and its regulation, particularly in kidney disease. In addition, current methods of determination of hepcidin are reviewed. L26.2