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

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. 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. 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]. 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

N-acetylcysteine prevents kidney and lung disturbances in renal ischemia/ reperfusion injury in rat

One of the most common causes of acute kidney injury [AKI] is kidney ischemia/reperfusion injury [IRI]. The distant organ injury such as acute lung injury is one of the side effects of AKI or kidney IRI. In this study, we performed bilateral renal IRI in rats and the protective role of N acetylcysteine [NAC] in kidney and lung was investigated. Rats [n = 30] were randomly assigned to four experiment groups. The group 1 was assigned as sham operated group. Before kidney IRI performance, the others groups were treated with saline [group 2], 150 mg/kg [group 3] or 500 mg/kg [group 4] of NAC, and the treatment were continued daily after IRI for next 3 days. At day 3, the all groups' animals were subjected for the measurements. The serum level of blood urea nitrogen [BUN] and creatinine [Cr] in the control group increased significantly [P < 0.05], and administration of NAC [150 mg/kg] decreased the serum levels of Cr and BUN. However, only the serum level of Cr decreased significantly [P < 0.05]. NAC did not improve kidney weight and damage; however, its low dose [150 mg/kg] attenuated the lung injury score [P < 0.05] when compared with the control group. No significant differences were observed in lung water content and endothelial permeability, serum levels of malondialdehyde and nitrite between the groups. Low dose of NAC as a protectant agent may protect the kidney function and lung tissue damage after kidney IRI