Abstract
Acute kidney injury (AKI) is defined as an abrupt or rapid decline in renal filtration function. Erythropoietin (EPO) as a hematopoietic and multifunctional hormone is produced primarily by kidney. Many investigations have shown that EPO as an antioxidant agent has shown several effects such as anti-apoptotic, antioxidant, and anti-inflammatory and also angiogenic activities. The biological activities of EPO are mediated by binding to its receptor (EPOR). The potential role of EPO in kidney is related to the presence of functional EPOR in renal mesangial cells, tubular epithelial cells and the glomerulus. Antioxidants and reactive oxygen species (ROS) scavengers such as EPO, can protect the kidneys against conditions that induce nephrotoxicity. Most studies in the field of renoprotective effects of EPO have focused on AKI models. In this paper we sought to review the ameliorative effects of EPO against various agents or conditions that induce nephrotoxicity including ischemia/reperfusion injury (IRI), cisplatin, gentamicin, rhabdomyolysis, amikacin and vancomycin.
Highlights
Erythropoietin (EPO) is a glycoprotein and cytoprotective multifunctional hormone
The activities of EPO are mediated by binding to EPO-receptor and the positive role of EPO in the kidney is related to presence of functional EPO-receptor in renal mesangial cells and renal tubular epithelial cells. These findings revealed an association between administration of EPO and reduction of renal injuries, induced by cisplatin, gentamicin, rhabdomyolysis, vancomycin and amikacin in rats and renal ischemia/reperfusion injury (IRI) as one of the most common causes of acute kidney injury
Previous studies and this review showed the encouraging results on potential therapeutic impact of EPO in acute kidney injury
Summary
Erythropoietin (EPO) is a glycoprotein and cytoprotective multifunctional hormone. Numerous studies have shown several effects of EPO including anti-apoptotic, antioxidant, and antiinflammatory and angiogenic activities [1]. Acute kidney injury (AKI) is characterized by a rapid decline in renal function, electrolyte and fluid imbalance and generally classified as pre-renal, intrinsic, and postrenal dysfunction. It develops rapidly over a few hours or a few days [3]. Numerous experimental investigations have attempted to explain the ameliorative
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