Fax +41 61 306 12 34 E-Mail karger@karger.ch www.karger.com Review Kidney Blood Press Res 2010;33:157–165 DOI: 10.1159/000315436 Neutrophil Gelatinase-Associated Lipocalin and Hepcidin: What Do They Have in Common and Is There a Potential Interaction? Jolanta Malyszko   a Vladimir Tesar   b Iain C. Macdougall   c   a  Department of Nephrology and Transplantology, Medical University, Bialystok, Poland; b  Department of Nephrology, 1st School of Medicine, Charles University, Prague, Czech Republic; c  Department of Renal Medicine, King’s College Hospital, London, UK seem to be independently related. Taking into account the antimicrobial moieties of NGAL, further studies are needed to address the role of NGAL in iron metabolism and inflam- mation in renal failure. Copyright © 2010 S. Karger AG, Basel Iron is the fourth most common element in the Earth’s crust and the most abundant transition metal in the hu- man body. It is a paradoxical element in that it is required by all aerobic organisms, as it is essential for growth and survival. It is essential primarily to ensure transport of oxygen or to catalyze reactions of electron transfer, nitro- gen fixation or DNA synthesis. On the other hand, it is also toxic due to its capacity to react with oxygen and to catalyze the production of reactive oxygen species. Iron is virtually insoluble under conditions occurring in our cells and body fluids, and maintaining the correct iron balance is crucial for health. All living organisms have evolved sophisticated mechanisms to maintain appropri- ate iron levels in their cells and within their body [1]. Over the last few years, our understanding of iron metabolism has dramatically increased due to the discovery of hepci- din. The regulation of iron metabolism involves the in- Key Words Iron  Neutrophil gelatinase-associated lipocalin  Hepcidin Abstract Iron is the fourth most common element in the Earth’s crust and is crucial for life. Over the last few years, our understand- ing of iron metabolism has dramatically increased due to the discovery of hepcidin, which is produced by hepatocytes and modulated in response to anemia, hypoxia and inflam- mation. It has been found that anemia upregulates lipocalin 2 (NGAL; neutrophil gelatinase-associated lipocalin) in the liver and serum. The aim of this review is to summarize the current knowledge dealing with a possible role of hepcidin and NGAL in iron metabolism and its regulation, particularly in kidney disease. Elevated NGAL a few days after insult is a possible preventive or protective mechanism limiting renal injury. NGAL is an innate antibacterial factor as well as hep- cidin. NGAL binds siderophores, thereby preventing iron uptake by bacteria. Hepcidin, an antibacterial defensin, pre- vents iron absorption from the gut and iron release from macrophages, leading to hypoferremia and anemia. Both proteins sequester iron, but by different mechanisms. How- ever, these proteins involved in iron metabolism do not Published online: May 26, 2010 Prof. Jolanta Malyszko, FASN Department of Nephrology and Transplantology Medical University, Zurawia 14 PL–15-540 Bialystok (Poland) Tel. +48 857 409 464, Fax +48 857 434 586, E-Mail jolmal  @  poczta.onet.pl © 2010 S. Karger AG, Basel 1420–4096/10/0332–0157$26.00/0 Accessible online at: www.karger.com/kbr