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. 2013 Jun;4(6):648-55.

Protective role of recombinant human erythropoietin in kidney and lung injury following renal bilateral ischemia-reperfusion in rat model

Maryam Moeini  1 , Mehdi Nematbakhsh, Mohammad Fazilati, Ardeshir Talebi, Ali Asghar Pilehvarian, Fariba Azarkish, Fatemeh Eshraghi-Jazi, Zahra Pezeshki
Affiliations

Protective role of recombinant human erythropoietin in kidney and lung injury following renal bilateral ischemia-reperfusion in rat model

Maryam Moeini et al. Int J Prev Med. 2013 Jun.

Abstract

Background: Acute kidney injury (AKI) has been recognized as one of the most complex clinical complications in modern medicine, and ischemia/reperfusion (I/R) injury is well-known as a main reason of AKI. In addition, AKI leads to important systemic consequences such as acute lung injury. This study was designed to investigate the role of erythropoietin (EPO) on kidney function makers and tissue damage; and lung endothelial permeability and lung water content (LWC) in bilateral renal I/R injury model in rats.

Methods: Male Wistar rats were randomly divided into three groups of sham, I/R, and I/R treated with EPO (I/R + EPO) groups. The I/R and I/R + EPO groups were subjected to bilateral renal I/R injury; however, only the I/R + EPO group received EPO (500 IU/kg, i.p.) 2 h before ischemia surgery, and the same dose was continued once a day for 3 days after ischemia. The sham group underwent a surgical procedure without ischemia process.

Results: The blood urea nitrogen (BUN) and serum creatinine (Cr) levels, kidney tissue damage score (KTDS), and kidney weight (KW) per 100 g body weight significantly increased in I/R group (P < 0.05). EPO administration decreased levels of BUN and Cr significantly (P < 0.05), and KTDS and KW insignificantly (P = 0.1). No significant differences in kidney and serum levels of malondialdehyde, and lung vascular permeability and LWC were observed between the groups. The serum and kidney levels of nitrite were not significantly different between I/R and sham groups; however, administration of EPO increased the renal level of nitrite (P < 0.05).

Conclusions: EPO protected the kidney against I/R injury; however, it may not protect the lung tissue from the damage induced by renal I/R injury in rats.

Keywords: Erythropoietin; lung endothelial permeability; lung water content; rat.

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Conflict of interest statement

Conflict of Interest: None declared

Figures

Figure 1
Figure 1
Serum creatinine and blood urea nitrogen levels, total kidney weight per 100 g body weight, and kidney tissue damage score in the sham, ischemia/reperfusion (I/R), and I/R treated with erythropoietin groups
Figure 2
Figure 2
Kidney (k) and lung (l) tissue images (magnification ×100). K1-K3 and L1-L3 demonstrate the kidney and lung tissues image of groups 1-3. More tissue damages were observed in group 2 (K2 and L2). Erythropoietin indicates less kidney tissue damage (K3). However, it may promote the lung tissue damage (L3)
Figure 3
Figure 3
Lung endothelial permeability, lung water content, and lung tissue damage score in the sham, ischemia/reperfusion (I/R), and I/R treated with erythropoietin groups
See this image and copyright information in PMC

References

    1. Bonventre JV, Yang L. Cellular pathophysiology of ischemic acute kidney injury. J Clin Invest. 2011;121:4210–21. - PMC - PubMed
    1. Munshi R, Hsu C, Himmelfarb J. Advances in understanding ischemic acute kidney injury. BMC Med. 2011;9:11. - PMC - PubMed
    1. Sharfuddin AA, Molitoris BA. Pathophysiology of ischemic acute kidney injury. Nat Rev Nephrol. 2011;7:189–200. - PubMed
    1. Sheridan AM, Bonventre JV. Cell biology and molecular mechanisms of injury in ischemic acute renal failure. Curr Opin Nephrol Hypertens. 2000;9:427–34. - PubMed
    1. Kribben A, Edelstein CL, Schrier RW. Pathophysiology of acute renal failure. J Nephrol. 1999;12:S142–51. - PubMed

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