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1

Crichton, Robert. Iron Metabolism. Chichester, UK: John Wiley & Sons, Ltd, 2016. http://dx.doi.org/10.1002/9781118925645.

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2

Mark, Worwood, ed. Iron metabolism. London: Baillière Tindall, 2002.

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3

Wick, Manfred, Wulf Pinggera, and Paul Lehmann. Ferritin in Iron Metabolism. Vienna: Springer Vienna, 1995. http://dx.doi.org/10.1007/978-3-7091-4421-3.

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4

Wick, Manfred, Wulf Pinggera, and Paul Lehmann. Ferritin in Iron Metabolism. Vienna: Springer Vienna, 1991. http://dx.doi.org/10.1007/978-3-7091-4435-0.

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5

Testa, Ugo. Proteins of iron metabolism. Boca Raton, Fla: CRC Press, 2002.

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6

1938-, Lönnerdal Bo, ed. Iron metabolism in infants. Boca Raton, Fla: CRC Press, 1990.

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7

Crichton, Robert R. Inorganic biochemistry of iron metabolism. New York: E. Horwood, 1991.

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8

C, Hershko, ed. Clinical disorders of iron metabolism. London: Baillière Tindall, 1994.

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9

C, Ferreira Glória, Moura José J. G, and Franco Ricardo, eds. Iron metabolism: Inorganic biochemistry and regulatory mechanisms. Weinheim: Wiley-VCH, 1999.

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10

Chang, Yan-Zhong, ed. Brain Iron Metabolism and CNS Diseases. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-13-9589-5.

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11

Wick, Manfred, Wulf Pinggera, and Paul Lehmann. Iron Metabolism, Anemias. Diagnosis and Therapy. Vienna: Springer Vienna, 2000. http://dx.doi.org/10.1007/978-3-7091-3909-7.

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12

Finn, Hugh Michael D. Iron (III)-citrate metabolism and iron homeostasis in Pseudomonas fluorescens. Sudbury, Ont: Laurentian University, School of Graduate Studies, 2001.

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13

Dincer, Yildiz. Iron deficiency and its complications. Hauppauge, N.Y: Nova Science Publishers, 2011.

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14

Wick, Manfred, Paul Lehmann, and Wulf Pinggera. Clinical Aspects and Laboratory Iron Metabolism, Anemias. Vienna: Springer Vienna, 2003. http://dx.doi.org/10.1007/978-3-7091-3719-2.

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15

Wick, Manfred, Wulf Pinggera, and Paul Lehmann. Clinical Aspects and Laboratory — Iron Metabolism, Anemias. Vienna: Springer Vienna, 2011. http://dx.doi.org/10.1007/978-3-7091-0087-5.

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16

Fahmy, Magdy. Cytokine-mediated modulation of cellular iron metabolism. Birmingham: University of Birmingham, 1991.

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17

M, Loehr Thomas, ed. Iron carriers and iron proteins. New York: VCH, 1989.

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18

Yehuda, Shlomo. Iron deficiency and overload: From basic biology to clinical medicine. New York, N.Y: Humana Press, 2010.

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19

Astrid, Sigel, and Sigel Helmut, eds. Iron transport and storage in microorganisms, plants, and animals. New York: Marcel Dekker, 1998.

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20

C, Barton James, ed. Handbook of iron overload disorders. Cambridge: Cambridge University Press, 2010.

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21

Ferreira, Glória C., José J. G. Moura, and Ricardo Franco, eds. Iron Metabolism. Wiley, 1999. http://dx.doi.org/10.1002/9783527613700.

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22

Bernat, Ivan. Iron Metabolism. Springer, 2013.

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23

Iron metabolism. London: Baillière Tindall, 2002.

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24

Porter, Ruth, and David W. FitzSimons. Iron Metabolism. Wiley & Sons, Incorporated, John, 2009.

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25

Crichton, Robert. Iron Metabolism. Wiley & Sons, Incorporated, John, 2009.

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26

Bernat, Ivan. Iron Metabolism. Springer London, Limited, 2012.

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27

Bernat, Ivan. Iron Metabolism. Springer, 2013.

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28

Iron Metabolism: Hepcidin. Elsevier, 2019. http://dx.doi.org/10.1016/s0083-6729(19)x0002-3.

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29

Litwack, Gerald. Iron Metabolism: Hepcidin. Elsevier Science & Technology Books, 2019.

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30

Litwack, Gerald. Iron Metabolism - Hepcidin. Elsevier Science & Technology, 2019.

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31

Vydyborets, S., and International Science Group. Iron Metabolism and Iron Deficiency Conditions. Primedia eLaunch LLC, 2022.

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32

Glória C. Ferreira (Editor), José João G. Moura (Editor), and Ricardo Franco (Editor), eds. Iron Metabolism - Inorganic Biochemistry and Regulatory Metabolism. Wiley-VCH, 1999.

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33

Testa, Ugo. Proteins of Iron Metabolism. Taylor & Francis Group, 2001.

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34

Testa, Ugo. Proteins of Iron Metabolism. Taylor & Francis Group, 2001.

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35

Lonnerdal, Bo. Iron Metabolism in Infants. Taylor & Francis Group, 2020.

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36

Lönnerdal, Bo. Iron Metabolism in Infants. Taylor & Francis Group, 2020.

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37

Pinggera, W., P. Lehmann, and Manfred Wick. Ferritin in Iron Metabolism. 2nd ed. Springer-Verlag, Austria, 1995.

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38

Lonnerdal, Bo. Iron Metabolism in Infants. Edited by Bo Lönnerdal. CRC Press, 2020. http://dx.doi.org/10.1201/9781003068365.

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39

Testa, Ugo. Proteins of Iron Metabolism. Taylor & Francis Group, 2019.

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40

Lonnerdal, Bo. Iron Metabolism in Infants. Taylor & Francis Group, 2020.

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41

Testa, Ugo. Proteins of Iron Metabolism. Informa Healthcare, 2001.

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42

Lonnerdal, Bo. Iron Metabolism in Infants. Taylor & Francis Group, 2020.

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43

Lonnerdal, Bo. Iron Metabolism in Infants. Taylor & Francis Group, 2020.

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44

Joshi, Ricky S. Cellular Iron Metabolism - The IRP. INTECH Open Access Publisher, 2012.

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45

Iron metabolism and disease 2008. Trivandrum: Research Signpost, 2008.

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46

Crichton, R., and Robert Crichton. Inorganic Biochemistry of Iron Metabolism. Wiley & Sons, Incorporated, John, 2003.

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47

Naegeli, S. R., H. D. Philips, and Franz Gross. Iron Metabolism: An International Symposium. Springer, 2012.

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48

Vydyborets, S., Y. Derpak, and International Science Group. Blood Donation and Iron Metabolism. Primedia eLaunch LLC, 2022.

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49

Malyszko, Jolanta, and Iain C. Macdougall. Iron metabolism in chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0125.

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Abstract:
While whole-body (‘absolute’) iron deficiency is common and probably increased in frequency in chronic kidney disease (CKD), functional iron deficiency is a particular problem in CKD. Absolute iron deficiency is likely to be present in advanced CKD when the ferritin falls below 100 ng/mL and the TSAT falls below 20%. Functional iron deficiency is characterized by the presence of adequate iron stores (as defined by conventional criteria), but with an inability to mobilize this iron rapidly enough to adequately support erythropoiesis with the administration of erythropoietin. Among such patients, the serum ferritin level is either normal or elevated (usually between 100 and 800 ng/mL), with a TSAT typically ≤20%. Hepcidin, a novel peptide discovered at the turn of the twenty-first century, is an iron gatekeeper that plays a key role in functional iron deficiency, and the ‘anaemia of chronic disease’. The main function of hepcidin is homeostatic regulation of iron metabolism and mediation of host defence and inflammation. Hepcidin is the predominant negative regulator of iron absorption in the small intestine, iron transport across the placenta, and iron release from the macrophages. Novel strategies that modulate hepcidin and its target ferroportin for the treatment of anaemia of chronic diseases are currently undergoing extensive research.
50

Hershko, Chaim. Iron Chelation Therapy. Springer, 2002.

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