The influence of the pleiotropic action of erythropoietin and its derivatives on nephroprotection

Erythropoietin (EPO) is traditionally described as a hematopoietic cytokine or growth hormone regulating proliferation, differentiation, and survival of erythroid progenitors. The use of EPO in patients with chronic kidney disease (CKD) was a milestone achievement in the treatment of anemia. However...

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Bibliographic Details
Published in:Medical science monitor 2013-07, Vol.19, p.599-605
Main Authors: Bartnicki, Piotr, Kowalczyk, Mariusz, Rysz, Jacek
Format: Article
Language:English
Subjects:
Apoptosis - drug effects
Erythropoietin - pharmacology
Erythropoietin - therapeutic use
Humans
Inflammation - drug therapy
Kidney - drug effects
Kidney - pathology
Oxidative Stress - drug effects
Protective Agents - pharmacology
Protective Agents - therapeutic use
Review
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Summary:Erythropoietin (EPO) is traditionally described as a hematopoietic cytokine or growth hormone regulating proliferation, differentiation, and survival of erythroid progenitors. The use of EPO in patients with chronic kidney disease (CKD) was a milestone achievement in the treatment of anemia. However, EPO involves some degree of risk, which increases with increasing hemoglobin levels. A growing number of studies have assessed the renoprotective effects of EPO in acute kidney injury (AKI) or CKD. Analysis of the biological effects of erythropoietin and pathophysiology of CKD in these studies suggests that treatment with erythropoiesis-stimulating agents (ESAs) may exert renoprotection by pleiotropic actions on several targets and directly or indirectly slow the progression of CKD. By reducing ischemia and oxidative stress or strengthening anti-apoptotic processes, EPO may prevent the development of interstitial fibrosis and the destruction of tubular cells. Furthermore, it could have a direct protective impact on the integrity of the interstitial capillary network through its effects on endothelial cells and promotion of vascular repair, or modulate inflammation response. Thus, it is biologically plausible to suggest that correcting anemia with ESAs could slow the progression of CKD.                         The aim of this article is to discuss these possible renoprotection mechanisms and provide a comprehensive overview of erythropoietin and its derivatives.
ISSN:1643-3750
1234-1010
1643-3750
DOI:10.12659/MSM.889023