Relevant bibliographies by topics / Dietary iron overload

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Academic literature on the topic 'Dietary iron overload'

Author: Grafiati
Published: 4 June 2021
Last updated: 10 March 2023

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Journal articles on the topic "Dietary iron overload"

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Kincaid, Anne L., and Michael K. Stoskopf. "Passerine dietary iron overload syndrome." Zoo Biology 6, no. 1 (1987): 79–88. http://dx.doi.org/10.1002/zoo.1430060109.

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Omara, Felix O., Barry R. Blakley, and Lusimbo S. Wanjala. "Hepatotoxicity Associated with Dietary Iron Overload in Mice." Human & Experimental Toxicology 12, no. 6 (November 1993): 463–67. http://dx.doi.org/10.1177/096032719301200603.

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1 Weanling male CD-1 mice were fed 120 (control), 5000 and 8000 mg of iron kg-1 for seven weeks. The haematocrit ( P=0.265), water consumption ( P=0.170) and percentage body weight ratios of kidney, spleen and heart were not affected by iron supplementation. 2 Iron supplementation reduced weight gain ( P=0.023), increased weight of liver ( P=0.0001), the iron deposition index and concentration of iron in the liver ( P<0.01). A strong correlation between liver iron concentration and level of iron in the diet ( r=0.989) was observed. Histologically, the deposition of iron was restricted to the hepatocytes, Kupffer cells and splenic macrophages. 3 Consumption of 5000 and 8000 mg of iron kg-1 resulted in hepatic damage, as judged by elevated serum alkaline phosphatase and alanine aminotransferase activities ( P<0.05). 4 This study indicates that prolonged feeding of excess dietary iron has the potential to cause hepatic accumulation of iron with resultant liver toxicity, and that mice may be a suitable model to study the mechanisms of dietary iron overload.
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Sobotka, T. J., P. Whittaker, J. M. Sobotka, R. E. Brodie, D. Y. Wander, M. Robl, M. Bryant, and C. N. Barton. "Neurobehavioral dysfunctions associated with dietary iron overload." Physiology & Behavior 59, no. 2 (February 1996): 213–19. http://dx.doi.org/10.1016/0031-9384(95)02030-6.

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Mori, Mutsuki, Takeshi Izawa, Yohei Inai, Sho Fujiwara, Ryo Aikawa, Mitsuru Kuwamura, and Jyoji Yamate. "Dietary Iron Overload Differentially Modulates Chemically-Induced Liver Injury in Rats." Nutrients 12, no. 9 (September 11, 2020): 2784. http://dx.doi.org/10.3390/nu12092784.

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Hepatic iron overload is well known as an important risk factor for progression of liver diseases; however, it is unknown whether it can alter the susceptibility to drug-induced hepatotoxicity. Here we investigate the pathological roles of iron overload in two single-dose models of chemically-induced liver injury. Rats were fed a high-iron (Fe) or standard diet (Cont) for four weeks and were then administered with allyl alcohol (AA) or carbon tetrachloride (CCl4). Twenty-four hours after administration mild mononuclear cell infiltration was seen in the periportal/portal area (Zone 1) in Cont-AA group, whereas extensive hepatocellular necrosis was seen in Fe-AA group. Centrilobular (Zone 3) hepatocellular necrosis was prominent in Cont-CCl4 group, which was attenuated in Fe-CCl4 group. Hepatic lipid peroxidation and hepatocellular DNA damage increased in Fe-AA group compared with Cont-AA group. Hepatic caspase-3 cleavage increased in Cont-CCl4 group, which was suppressed in Fe-CCl4 group. Our results showed that dietary iron overload exacerbates AA-induced Zone-1 liver injury via enhanced oxidative stress while it attenuates CCl4-induced Zone-3 liver injury, partly via the suppression of apoptosis pathway. This study suggested that susceptibility to drugs or chemical compounds can be differentially altered in iron-overloaded livers.
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Lesjak, Marija, and Surjit K. S. Srai. "Role of Dietary Flavonoids in Iron Homeostasis." Pharmaceuticals 12, no. 3 (August 8, 2019): 119. http://dx.doi.org/10.3390/ph12030119.

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Balancing systemic iron levels within narrow limits is critical for human health, as both iron deficiency and overload lead to serious disorders. There are no known physiologically controlled pathways to eliminate iron from the body and therefore iron homeostasis is maintained by modifying dietary iron absorption. Several dietary factors, such as flavonoids, are known to greatly affect iron absorption. Recent evidence suggests that flavonoids can affect iron status by regulating expression and activity of proteins involved the systemic regulation of iron metabolism and iron absorption. We provide an overview of the links between different dietary flavonoids and iron homeostasis together with the mechanism of flavonoids effect on iron metabolism. In addition, we also discuss the clinical relevance of state-of-the-art knowledge regarding therapeutic potential that flavonoids may have for conditions that are low in iron such as anaemia or iron overload diseases.
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Asare, George A., Michael C. Kew, Kensese S. Mossanda, Alan C. Paterson, Kwanele Siziba, and Christiana P. Kahler-Venter. "Effects of Exogenous Antioxidants on Dietary Iron Overload." Journal of Clinical Biochemistry and Nutrition 44, no. 1 (2009): 85–94. http://dx.doi.org/10.3164/jcbn.08-184.

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Whittaker, Paul, Virginia C. Dunkel, Thomas J. Bucci, Donna F. Kusewitt, J. Dale Thurman, Alan Warbritton, and George L. Wolff. "Genome-Linked Toxic Responses to Dietary Iron Overload." Toxicologic Pathology 25, no. 6 (November 1997): 556–64. http://dx.doi.org/10.1177/019262339702500604.

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McNamara, Lynette, Vanessa R. Panz, Frederick J. Raal, Janice Paiker, Barry I. Joffe, Victor R. Gordeuk, and A. Patrick MacPhail. "Basal Endocrine Status in African Dietary Iron Overload." Endocrine 21, no. 3 (2003): 241–44. http://dx.doi.org/10.1385/endo:21:3:241.

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Volani, Chiara, Giuseppe Paglia, Sigurdur Smarason, Peter Pramstaller, Egon Demetz, Christa Pfeifhofer-Obermair, and Guenter Weiss. "Metabolic Signature of Dietary Iron Overload in a Mouse Model." Cells 7, no. 12 (December 11, 2018): 264. http://dx.doi.org/10.3390/cells7120264.

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Iron is an essential co-factor for several metabolic processes, including the Krebs cycle and mitochondrial oxidative phosphorylation. Therefore, maintaining an appropriate iron balance is essential to ensure sufficient energy production and to avoid excessive reactive oxygen species formation. Iron overload impairs mitochondrial fitness; however, little is known about the associated metabolic changes. Here we aimed to characterize the metabolic signature triggered by dietary iron overload over time in a mouse model, where mice received either a standard or a high-iron diet. Metabolic profiling was assessed in blood, plasma and liver tissue. Peripheral blood was collected by means of volumetric absorptive microsampling (VAMS). Extracted blood and tissue metabolites were analyzed by liquid chromatography combined to high resolution mass spectrometry. Upon dietary iron loading we found increased glucose, aspartic acid and 2-/3-hydroxybutyric acid levels but low lactate and malate levels in peripheral blood and plasma, pointing to a re-programming of glucose homeostasis and the Krebs cycle. Further, iron loading resulted in the stimulation of the urea cycle in the liver. In addition, oxidative stress was enhanced in circulation and coincided with increased liver glutathione and systemic cysteine synthesis. Overall, iron supplementation affected several central metabolic circuits over time. Hence, in vivo investigation of metabolic signatures represents a novel and useful tool for getting deeper insights into iron-dependent regulatory circuits and for monitoring of patients with primary and secondary iron overload, and those ones receiving iron supplementation therapy.
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Fischer, Christine, Chiara Volani, Timea Komlódi, Markus Seifert, Egon Demetz, Lara Valente de Souza, Kristina Auer, et al. "Dietary Iron Overload and Hfe−/− Related Hemochromatosis Alter Hepatic Mitochondrial Function." Antioxidants 10, no. 11 (November 16, 2021): 1818. http://dx.doi.org/10.3390/antiox10111818.

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Iron is an essential co-factor for many cellular metabolic processes, and mitochondria are main sites of utilization. Iron accumulation promotes production of reactive oxygen species (ROS) via the catalytic activity of iron species. Herein, we investigated the consequences of dietary and genetic iron overload on mitochondrial function. C57BL/6N wildtype and Hfe−/− mice, the latter a genetic hemochromatosis model, received either normal diet (ND) or high iron diet (HI) for two weeks. Liver mitochondrial respiration was measured using high-resolution respirometry along with analysis of expression of specific proteins and ROS production. HI promoted tissue iron accumulation and slightly affected mitochondrial function in wildtype mice. Hepatic mitochondrial function was impaired in Hfe−/− mice on ND and HI. Compared to wildtype mice, Hfe−/− mice on ND showed increased mitochondrial respiratory capacity. Hfe−/− mice on HI showed very high liver iron levels, decreased mitochondrial respiratory capacity and increased ROS production associated with reduced mitochondrial aconitase activity. Although Hfe−/− resulted in increased mitochondrial iron loading, the concentration of metabolically reactive cytoplasmic iron and mitochondrial density remained unchanged. Our data show multiple effects of dietary and genetic iron loading on mitochondrial function and linked metabolic pathways, providing an explanation for fatigue in iron-overloaded hemochromatosis patients, and suggests iron reduction therapy for improvement of mitochondrial function.
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Dissertations / Theses on the topic "Dietary iron overload"

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Shirase, Tomoyuki. "Suppression of SLC11A2 expression is essential to maintain duodenal integrity during dietary iron overload." Kyoto University, 2012. http://hdl.handle.net/2433/152506.

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Steffani, L. "MODELLI SPERIMENTALI DI SOVRACCARICO DIETETICO DI FERRO: EFFETTI CENTRALI E PERIFERICI SU METABOLISMO E FUNZIONE RIPRODUTTIVA." Doctoral thesis, Università degli Studi di Milano, 2014. http://hdl.handle.net/2434/232404.

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Background and Aim. Iron is an essential micronutrient, which is involved as a cofactor in fundamental biochemical activities, and it is necessary for proper brain development in the fetal and early neonatal period. However, cellular iron overload produces toxic build-up in many organs, including brain, and, under aerobic conditions, catalyses the propagation of reactive oxygen species and the generation of highly reactive radicals through Fenton Chemistry. Association between metabolic and reproductive impairment has been proved in patients affected by dysmetabolic iron overload syndrome (DIOS). In particular, iron is the most important factor afflicting the hypothalamic-pituitary axis in a dose-dependent fashion leading to hypogonadotropic hypogonadism (HH). Our previous studies in a mouse model of DIOS showed the association between dietary iron overload, visceral adipose tissue insulin resistance and hypertriglyceridemia. Aim of this thesis was to assess whether and how iron overload may affect (a) the reproductive axis (mainly at the hypothalamic-pituitary levels) in a mouse model of DIOS; (b) the migratory feature and GnRH secretory pattern in GN-11 and GT1-7 cells, in vitro models of immature/migratory and mature/GnRH-secreting neurons, respectively. Results. In male mice, dietary-iron overload (IED) led to: a) an increment in testis iron content, b) a reduction in testicular weight and length, c) no changes in hypothalamic iron content c) no changes in mRNA levels of iron-responsive genes, transferrin receptor (TfR) and ferritin H (FtH), in testes and hypothalamus d) an up-regulation of hypothalamic GnRH mRNA levels, e) no changes in hypothalamic Kiss1 and GPR54 gene expression, e) a reduction in pituitary LHβ gene expression. Moreover, the hypothalamic increment of TNFα gene expression along with the phosphorylation/activation of AMPK protein suggested the presence of an inflammatory condition. Increased hypothalamic CHOP mRNA levels also confirmed the endoplasmic reticulum stress feature. IED mice gained less weight than controls showing a reduction in VAT mass and in serum leptin levels, whereas hypothalamic NPY mRNA levels were increased and POMC gene expression was reduced. Western blot analysis showed that the pAkt/Akt ratio was up-regulated in the hypothalamus of IED mice, whereas phosphorylation of ERK1/2 (pERK) protein resulted unchanged in both groups. As far as GN-11 and GT1-7 cells are concerned, a 24-hour treatment with 200 µM Ferric Ammonium Citrate (FAC, source of ferric iron) induced an increment in the intracellular specific iron content of both cell-based models without affecting the cell viability and morphology. Gene expression analysis showed that both cell lines express TfR and FtH, whose mRNA levels were modulated by iron overload. Exposure of GN-11 cells to FAC resulted in the dose (200–1000 µM FAC for 24 hours)- and time (24-72 hours with 200 µM FAC)-dependent inhibition of FBS-induced chemomigration, as assessed by Boyden chamber assay. Pre-treatment with 200 µM deferoxamine (DFO, a specific iron chelator) reverted the above reported iron-driven effect on cell migration. Time-course experiments showed that 200 μM FAC was associated with increased pERK1/2 and pAkt protein levels and with decreased pAMPK ones. Chemomigration assays carried out with the specific inhibitors of ERK1/2, Akt and AMPK highlighted that only Akt pathway seems involved in FAC-mediated inhibition of GN-11 cell migration. In GN-11 cells, iron treatment increased IL-6 gene expression in a dose-dependent mode, whereas NF-kB nuclear translocation and activation was not affected. Up-regulated SOD2 mRNA levels confirmed a condition of activated oxidative stress. Conclusions. The present data show that dietary-iron overload impairs the reproductive axis, probably leading to HH, but further experiments are needed to understand the anatomic site mainly involved in iron-driven damage. Iron treatment negatively affects the migration of GN-11 neuronal cells by the activation of Akt signaling pathway. Hence, iron overload may impair the migration of GnRH neurons from the olfactory placode into forebrain and hypothalamus, where these neurons promote the reproductive competence.
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Asare, G. A. "Dietary iron overload. the generation of reactive oxygen species and hepatocarcinogenesis in experimental rats (Part 1)." Thesis, 2003. https://hdl.handle.net/10539/24947.

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A thesis submitted to the Faculty of Health Sciences, University of the Witwatersrand In fulfilment of the requirements for the degree of Doctor of Philosophy Johannesburg, 2003
Dietary iron (Fe) overload, originally referred to as Bantu Visceral Siderosis, is an Reloading condition that is still prevalent in rural populations of sub-Saharan Africa. The better known Fe loading disease, hereditary haemochromatosis (HFI) is frequently complicated by hepatocellular carcinoma (HCC) and, in rare instances this occurs in the absence of cirrhosis. The latter, together with recent evidence that dietary Fe overload in the Black African carries an increased risk for HCC, suggests that excessive hepatic iron may itself be carcinogenic. The aim of the study was to determine if Fe alone could induce HCC in experimental rat models and, if so, to investigate possible mechanisms of hepatocarcinogenesis. 360 Wistar albino rats (Rattus norvegicus) were divided into 6 groups. The first group, the control animals, was designated C group. Groups 2-6 were Fe-fed alone or in combination with other chemicals: group 2 Fe alone (Fe group), group 3 (Fe + V) vitamins A & E supplementation [50 mg all trans-retinol (vitamin A) and 500 mg a-tocopherol (vitamin E) per kg diet], group 4 (Fe - V) received a diet totally devoid of vitamins A & E, group 5 (Fe + ASA) received 20 mg aspirin (ASA) per day, group 6 (Fe + Cu) received 300 mg/kg diet of copper sulphate (CuS04) supplementation for 12 months followed by 3% copper hydroxide carbonate [CuC03»Cu(0H)2]
IT2018
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Cempaka, Anggun Rindang, and 安谷. "Dietary Pattern by Reduced Rank Regression Predicts Dysmetabolic Iron Overload Syndrome in Taiwanese Adults." Thesis, 2018. http://ndltd.ncl.edu.tw/handle/5sd2c7.

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Asare, G. A. "Dietary iron overload. the generation of reactive oxygen species and hepatocarcinogenesis in experimental rats models. (Part 2)." Thesis, 2003. https://hdl.handle.net/10539/24957.

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A thesis submitted to the Faculty of Health Sciences, University of the Witwatersrand In fulfilment of the requirements for the degree of Doctor of Philosophy Johannesburg, 2003
Dietary iron (Fe) overload, originally referred to as Bantu Visceral Siderosis, is an Fe- loading condition that is still prevalent in rural populations of sub-Saharan Africa. The better known Fe loading disease, hereditary haemochromatosis (HH) is frequently complicated by hepatocellular carcinoma (HCC) and, in rare instances this occurs in the absence of cirrhosis. The latter, together with recent evidence that dietary Fe overload in the Black African carries an increased risk for HCC, suggests that excessive hepatic iron may itself be carcinogenic. The aim of the study was to determine if Fe alone could induce HCC in experimental rat models and, if so, to investigate possible mechanisms of hepatocarcinogenesis. 360 Wistar albino rats (Rattus norvegicus) were divided into 6 groups. The first group, the control animals, was designated C group. Groups 2 - 6 were Fe-fed alone or in combination with other chemicals: group 2 Fe alone (Fe group), group 3 (Fe + V) vitamins A & E supplementation [50 mg all trans-retinol (vitamin A) and 500 mg a-tocopherol (vitamin E) per kg diet], group 4 (Fe - V) received a diet totally devoid of vitamins A & E, group 5 (Fe + ASA) received 20 mg aspirin (ASA) per day, group 6 (Fe + Cu) received 300 mg/kg diet of copper sulphate (CuS04) supplementation for 12 months
IT2018
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Bronze, Michelle Saltao. "Interaction between dietary iron overload and aflatoxin B1 in hepatocarcinogenesis using an experimental rat model." Thesis, 2007. http://hdl.handle.net/10539/2093.

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Student Number : 9902006N - MSc(Med) Dissertation - School of Medicine - Faculty of Health Sciences
Hepatocellular carcinoma (HCC) is the most common primary malignant tumour of the liver. Aflatoxin B1 (AFB1) is a potent hepatocarcinogen, and dietary iron overload has been shown to contribute to HCC development in black africans. Both are well studied hepatotoxins. The aim of this study was to use a Wistar rat model over a 12 month period to investigate synergy and the extent thereof between AFB1 ingestion and dietary iron overload. 25ug/day of AFB1, reconstituted in DMSO, was administered by gavaging the animals, over a period of 10 days with a 2 day interval in between. The chow diet was supplemented with 0.75% (w/w) ferrocene iron. Experimental subjects were divided into 4 groups. Group 1 was fed the normal chow diet. Group 2 was fed 0.75% (w/w) ferrocene iron alone. Group 3 was gavaged 250μg AFB1 alone. Group 4 was fed the 0.75% (w/w) ferrocene iron and gavaged 250μg AFB1. A number of assays were conducted to investigate synergy. Colorimetric assays were used to measure serum iron, total-iron binding capacity, ALT, AST, GGT, nitrite production, lipid peroxidation and hydroxyproline concentrations. ELISA’s were used to determine ferritin, 8-isoprostane and 8-hydroxyguanosine concentrations. Nontransferrin bound iron was measured using an HPLC method. A chemiluminescent assay was used to measure superoxide anion production. Cytokines were measured using a suspension array system. Mutagenicity was assessed using the Ames mutagenicity assay using salmonella typhimirium strains TA97, TA98, TA100 and TA102. Iron profiling indicated that iron overloading occurred with the ingestion of the ferrocene diet. Biomarkers of oxidative stress, as illustrated by the measurement of 8-hydroxyguanosine and lipid peroxidation, showed additive synergistic effects between the two carcinogens. The anti-inflammatory interleukin-10 was shown to be markedly elevated with the co-administration of the two carcinogens, indicating the elevated inflammatory processes. Additive synergistic effects were noted in terms of the liver disease marker ALT. The salmonella typhimirium strain TA102 used in the Ames mutagenicity test showed increased colony counts with respect to the coadministration of carcinogens (P<0.05), although no synergistic effect was noted. In a few of the presented parameters, the AFB1 group was not significantly different to the control group, although significant differences between the Fe group and the Fe + AFB1 groups were noted. The implication of which is that the presence of AFB1 is increasing the activity of Fe as a carcinogen, thereby acting as a co-carcinogen. Examples of such parameters illustrating this are presented in the results section including serum ALT, serum nitrite, liver and serum lipid peroxidation, liver and serum 8-hydroxyguanosine, some of the mutagenicity assays, and interleukin-10. The conclusion of this study suggests that AFB1 acts as a co-carcinogen in the presence of iron overloading, implying that a synergistic relationship between these two toxins exists.
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Books on the topic "Dietary iron overload"

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

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Yehuda, Shlomo, and David I. Mostofsky. Iron Deficiency and Overload. Springer, 2011.

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Hallahan, Lawrence C. Dietary iron and iron overload (hemosiderosis) illness: Index of new information. ABBE Publishers Association of Washington, D.C, 1998.

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Yehuda, Shlomo, and David I. Mostofsky. Iron Deficiency and Overload: From Basic Biology to Clinical Medicine. Humana, 2012.

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Macdougall, Iain C. Clinical aspects and overview of renal anaemia. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0123.

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Anaemia is an almost ubiquitous complication of chronic kidney disease, which has a number of implications for the patient. It is associated with adverse outcomes, an increased rate of red cell transfusions, poor quality of life, and reduced physical capacity. Severe anaemia also impacts on cardiac function, as well as on platelet function, the latter contributing to the bleeding diathesis of uraemia. Renal anaemia occurs mainly in the later stages of chronic kidney disease (stages 3B, 4, and 5), and up to 95% of patients on dialysis suffer from this condition. It is caused largely by inappropriately low erythropoietin levels, but other factors such as a shortened red cell survival also play a part. The anaemia is usually normochromic and normocytic, unless concomitant iron deficiency is present. The latter is also common in renal failure, partly due to low dietary iron intake and absorption, and partly due to increased iron losses. Prior to the 1990s, treatment options were limited, and many patients (particularly those on haemodialysis) required regular blood transfusions, resulting in iron overload and human leucocyte antigen sensitization. Correction of anaemia requires two main treatment strategies: increased stimulation of erythropoiesis, and maintenance of an adequate iron supply to the bone marrow. Ever since the introduction of recombinant human erythropoietin, it has been possible to boost erythropoietic activity, and both oral and intravenous iron products are available to provide supplemental iron. In dialysis patients, oral iron is usually poorly absorbed due to upregulation of hepcidin activity, and intravenous iron is often required. The physiological processes relevant to red cell production are described, as well as the prevalence, characteristics, pathogenesis, and physiological consequences of renal anaemia.
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