Webinar: Iron therapy in CKD- certainties and controversies

This ISN webinar will help participants understand the role of iron in physiology and pathology, iron deficiency and iron overload, safety of iron formulations and drawbacks of iron therapy (infections, oxydative stress). 

Description of the Webinar

Anemia has been remained one of the most characteristic and visible manifestations of chronic renal failure for over 150 years. The pathogenesis of anemia of chronic kidney disease is multifactorial with inadequate production of erythropoietin and iron deficiency being the leading factor. Iron is the fourth most common element in the Earth’s crust and the most abundant transition metal in the human body. Iron is an essential element required for growth and survival. Iron is essential for multiple cellular processes mitochondrial respiration, haem biosynthesis, lipid and glucose metabolism, neuroendocrine hormone synthesis, replication, immune function. Iron homeostasis relies mainly on the control of iron efflux from duodenal enterocytes and from macrophages after the phagocytosis and degradation of senescent red blood cells and heme catabolism. Iron deficiency negatively affects mitochondrial metabolism, oxidative phosphorylation and cellular survival (impaired ISC/haem containing enzyme formation) , lipid and glucose metabolism, neurotransmitter synthesis and results in anaemia. On the other hand, iron overload can cause increased radical formation and subsequent cellular damage, mitochondrial dysfunction, shift in glucose/lipid homeostasis, reduced pro-inflammatory but increased anti-inflammatory immune activity, favour growth of microbes.

Our understanding of the molecular control of iron metabolism has increased dramatically over the past 15 years due to the discovery of hepcidin. 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 recycling by macrophages and its mobilization form hepatic stores. Hepcidin as a key regulator of iron availability is a potential future therapeutic target for managing anaemia in CKD. On the other hand, we have to bear in mind that modulation of hepcidin activity may be associated with some risks: inhibition of hepcidin may increase the risks of infection/inflammation, as well as tumor growth, stabilization of HIF in some studies enhances tumor growth, interruption of BMP (particularly BMP-6) may result in calcification of tissues (including peritoneum) and interruption of the binding of hepcidin to ferroportin may enhance iron absorption and mobilization. However, on the everyday basis iron therapy in CKD is a matter of debate whether oral or intravenous iron preparation are most suitable for patients not yet on dialyses. In hemodialyzed patients intravenous preparations are used routinely. As many iron preparations are widely available currently there is insufficient evidence to take a position in recommending one iron preparation over another in particular with respect to their potential for inducing oxidative stress. The hot issue is the relation between iron administration and infections. Most epidemiological studies are observational in nature and there are limited data available on the cumulative iron doses to establish the association between iron usage and risks of infections.

Intravenous iron is has a good safety profile and serious adverse events are vanishingly rare. Current available data cannot detect different differences in safety profiles of different formulations. If premedication and interventions for minor infusion reactions are avoided, SAEs are not seen. It is possible that the overwhelming number of SAEs ostensibly attributed to IV iron are iatrogenic. There are no effective tests to diagnose iron overload. Iron overload and its effects on other organ systems (liver, heart, pancreas, kidney) are generally rare and are very different from haemochromatosis. We know that there is a widespread variability in IV iron usage worldwide. Certainly, iron enhances the erythropoietic response to ESA therapy by increased Hb response and reduced ESA doses (economic, safety). However, there are very limited robust clinical data on safety, iron overload, oxidative stress / cardiovascular toxicity, infections and hypersensitivity reactions.

Webinar Webcast: 

This webinar will took place on Friday, Dec 4th, 2015. Those who missed out on the live webinar session are invited to watch the webcast below. You can alternatively download the webinar presentation in pdf format at the bottom of this page. 


 Post-webinar Quiz: 


About the Facilitator


Professor Jolanta Malyszko – 

Jolanta Malyszko studied medicine at the Medical University of Bialystok, Poland and graduated with diploma with distinction for the highest notes in 1989. Focused on nephrology and transplantation, she is a board-certified specialist in internal medicine (1995), nephrology (1998), clinical transplantation (2004), hypertension (2006) and diabetology (2010) in Poland. From 2002 she is a Professor at her Alma Mater. Her clinical training was performed in the Intensive Care Unit with Toxicology Center, Nephrology Department, Centre Hospitaliser Universitaire Rouen, France (1992), Department of Nephrology and Rheumatology, Heinrich-Heine University, Dusseldorf, Germany (EDTA-ERA scholarship, 1997), King’s College of London (2010), Ichilov Hospital, Tel Aviv (2011).

Currently she is a Member of the Executive Council of the Polish Society of Nephrology and member of the Executive Council of the Polish Society of Transplantation. Previously she served as secretary general of the Polish Society of Nephrology (2004-2007). Member of ERA-EDTA from 1996. Also served as Professor Associe Universite du Quebec a Trois Rivieres, Canada (2008-2011). Currently chairman of the 2nd Department of Nephrology, Medical University of Bialystok, Poland from 2013 and a member of the Executive Council of ERA-EDTA (2015-2018). Her research interests are iron metabolism and anemia in CKD as well as cardiovascular complications in CKD. She is author and co-author of over 300 original papers in peer-reviewed journals, over 100 review papers and 27 book chapters (IF over 480, citations over 3500 and h-index-28). 



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Last modified on Wednesday, 20 January 2016 10:59

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