Treatment of renal anemia: Erythropoiesis stimulating agents and beyond
Anemia, complicating the course of chronic kidney disease, is a significant parameter, whether interpreted as subjective impairment or an objective prognostic marker. Renal anemia is predominantly due to relative erythropoietin (EPO) deficiency. EPO inhibits apoptosis of erythrocyte precursors. Stud...
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Format: | Article |
Language: | English |
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The Korean Society of Nephrology
2017-09-01
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Series: | Kidney Research and Clinical Practice |
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Online Access: | https://doi.org/10.23876/j.krcp.2017.36.3.209 |
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author | Patrick Biggar Gheun-Ho Kim |
author_facet | Patrick Biggar Gheun-Ho Kim |
author_sort | Patrick Biggar |
collection | DOAJ |
description | Anemia, complicating the course of chronic kidney disease, is a significant parameter, whether interpreted as subjective impairment or an objective prognostic marker. Renal anemia is predominantly due to relative erythropoietin (EPO) deficiency. EPO inhibits apoptosis of erythrocyte precursors. Studies using EPO substitution have shown that increasing hemoglobin (Hb) levels up to 10-11 g/dL is associated with clinical improvement. However, it has not been unequivocally proven that further intensification of erythropoiesis stimulating agent (ESA) therapy actually leads to a comprehensive benefit for the patient, especially as ESAs are potentially associated with increased cerebro-cardiovascular events. Recently, new developments offer interesting options not only via stimulating erythropoeisis but also by employing additional mechanisms. The inhibition of activin, a member of the transforming growth factor superfamily, has the potential to correct anemia by stimulating liberation of mature erythrocyte forms and also to mitigate disturbed mineral and bone metabolism as well. Hypoxia-inducible factor prolyl hydroxylase inhibitors also show pleiotropic effects, which are at the focus of present research and have the potential of reducing mortality. However, conventional ESAs offer an extensive body of safety evidence, against which the newer substances should be measured. Carbamylated EPO is devoid of Hb augmenting effects whilst exerting promising tissue protective properties. Additionally, the role of hepcidin antagonists is discussed. An innovative new hemodialysis blood tube system, reducing blood contact with air, conveys a totally different and innocuous option to improve renal anemia by reducing mechanical hemolysis. |
first_indexed | 2024-12-10T16:19:51Z |
format | Article |
id | doaj.art-04001655bfc34f769ed23d1e23616119 |
institution | Directory Open Access Journal |
issn | 2211-9132 |
language | English |
last_indexed | 2024-12-10T16:19:51Z |
publishDate | 2017-09-01 |
publisher | The Korean Society of Nephrology |
record_format | Article |
series | Kidney Research and Clinical Practice |
spelling | doaj.art-04001655bfc34f769ed23d1e236161192022-12-22T01:41:51ZengThe Korean Society of NephrologyKidney Research and Clinical Practice2211-91322017-09-0136320922310.23876/j.krcp.2017.36.3.209j.krcp.2017.36.3.209Treatment of renal anemia: Erythropoiesis stimulating agents and beyondPatrick Biggar0Gheun-Ho Kim1Department of Nephrology, Klinikum Coburg, GmbH, Coburg, GermanyDepartment of Internal Medicine, Hanyang University College of Medicine, Seoul, KoreaAnemia, complicating the course of chronic kidney disease, is a significant parameter, whether interpreted as subjective impairment or an objective prognostic marker. Renal anemia is predominantly due to relative erythropoietin (EPO) deficiency. EPO inhibits apoptosis of erythrocyte precursors. Studies using EPO substitution have shown that increasing hemoglobin (Hb) levels up to 10-11 g/dL is associated with clinical improvement. However, it has not been unequivocally proven that further intensification of erythropoiesis stimulating agent (ESA) therapy actually leads to a comprehensive benefit for the patient, especially as ESAs are potentially associated with increased cerebro-cardiovascular events. Recently, new developments offer interesting options not only via stimulating erythropoeisis but also by employing additional mechanisms. The inhibition of activin, a member of the transforming growth factor superfamily, has the potential to correct anemia by stimulating liberation of mature erythrocyte forms and also to mitigate disturbed mineral and bone metabolism as well. Hypoxia-inducible factor prolyl hydroxylase inhibitors also show pleiotropic effects, which are at the focus of present research and have the potential of reducing mortality. However, conventional ESAs offer an extensive body of safety evidence, against which the newer substances should be measured. Carbamylated EPO is devoid of Hb augmenting effects whilst exerting promising tissue protective properties. Additionally, the role of hepcidin antagonists is discussed. An innovative new hemodialysis blood tube system, reducing blood contact with air, conveys a totally different and innocuous option to improve renal anemia by reducing mechanical hemolysis.https://doi.org/10.23876/j.krcp.2017.36.3.209ActivinAnemiaErythropoiesis stimulating agentHepcidinHypoxia inducible transcription factor |
spellingShingle | Patrick Biggar Gheun-Ho Kim Treatment of renal anemia: Erythropoiesis stimulating agents and beyond Kidney Research and Clinical Practice Activin Anemia Erythropoiesis stimulating agent Hepcidin Hypoxia inducible transcription factor |
title | Treatment of renal anemia: Erythropoiesis stimulating agents and beyond |
title_full | Treatment of renal anemia: Erythropoiesis stimulating agents and beyond |
title_fullStr | Treatment of renal anemia: Erythropoiesis stimulating agents and beyond |
title_full_unstemmed | Treatment of renal anemia: Erythropoiesis stimulating agents and beyond |
title_short | Treatment of renal anemia: Erythropoiesis stimulating agents and beyond |
title_sort | treatment of renal anemia erythropoiesis stimulating agents and beyond |
topic | Activin Anemia Erythropoiesis stimulating agent Hepcidin Hypoxia inducible transcription factor |
url | https://doi.org/10.23876/j.krcp.2017.36.3.209 |
work_keys_str_mv | AT patrickbiggar treatmentofrenalanemiaerythropoiesisstimulatingagentsandbeyond AT gheunhokim treatmentofrenalanemiaerythropoiesisstimulatingagentsandbeyond |