[Expression of kidney injury molecule-1 in renal ischemic postconditioning and its protective effect against renal ischemia-reperfusion injury in rats]

Xiang Ji, Lu-lin Ma, Jian Lu, Shu-dong Zhang, Yi Huang, Xiao-fei Hou, Xin Ma
Beijing da Xue Xue Bao. Yi Xue Ban, Journal of Peking University. Health Sciences 2012 August 18, 44 (4): 511-7

OBJECTIVE: To investigate whether the protective mechanism of ischemic postconditioning (IPO) against renal ischemia reperfusion injury (IRI) is related to the expression of kidney injury molecule-1 (Kim-1), and whether Kim-1 can reflect the protective effect of ischemic postconditioning as a sensitive biomarker in rats so as to find early and effective indicators to use IPO in clinical research of urology in future.

METHODS: Eighty-five male SD rats (240-300 g) were randomly divided into three groups (IRI: n=30; IPO: n=30; sham operation group: n=25). After the right nephrectomy through median abdominal incision to make the solitary kidney model, the left renal artery was separated from the renal pedicle. In IRI group, the left renal artery was blocked for 45 min before reperfusion. In IPO group, six cycles of 10 s reperfusion-10 s reocclusion of the left kidney were performed after 45 min ischemia. The blood samples and the kidney cortex tissues were taken at the time points of 6 h, 12 h, 24 h, 48 h and 72 h after reperfusion, with 5 rats for each time point. The plasma samples were obtained for urea and creatinine detection. A modified quantitative RT-PCR was used to quantitate the Kim-1 mRNA expression of renal tissue. Five rats were chosen from groups IRI and IPO respectively to obtain the urine samples of each rat, 0 h, 6 h, 12 h, 24 h, 48 h, and 72 h after reperfusion. The Kim-1 levels of urine were detected by ELISA. Pathological examinations were performed to check the differences between the three groups.

RESULTS: Urine tests and RT-PCR showed that, in IRI and IPO groups, Kim-1 and its mRNA levels began to rise after 6 h of reperfusion and reached the peak at 24 h synchronously. Urine Kim-1 levels in IRI group were significantly higher than those of the IPO group at 6 h, 12 h, 24 h, 72 h (P<0.05). The Kim-1 mRNAs in IPO group were lower than those in IRI group at the time points of 6 h, 12 h, 24 h, and 48 h (P<0.05), and the levels decreased more rapidly after 24 h. BUN and Cr significantly increased at 12 h, which were later than the Kim-1 and Kim-1 mRNA. The BUN and Cr levels in IRI group were higher than those in IPO group after 24 h (P<0.05). The pathological examination showed that there was less epithelial injury in IPO group.

CONCLUSION: Ischemic postconditioning can attenuate the renal ischemia reperfusion injury and downregulate the expression of Kim-1 and Kim-1 mRNA. Kim-1, as a biomarker and protective factor of acute kidney injury (AKI), can sensitively reflect the renal protective effect by ischemic postconditioning.

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