Remote ischemic per-conditioning did not modulate kidney Klotho expression in acute kidney injury induced by renal ischemia/reperfusion injury.

BACKGROUND: Renal ischemia-reperfusion injury (I/RI) is a major medical problem related to high mortality and morbidity. Klotho plays a critical role in the kidney pathogenesis of I/RI. The current study aimed to investigate the effect of cyclic remote ischemic perconditioning (RIPerC) on renal downregulation of the Klotho protein in bilateral ischemic reperfusion (BIR). MATERIAL AND METHOD: Twenty-four Sprague-Dawley rats were divided into (I) sham group which was subjected to abdominal mid-line incision without ischemia; (II) BIR group which was exposed to 60 min ischemia followed by 24 h of reperfusion; and (III) The BIR + RIPerC group which was subjected to the same renal BIR and occlusion of the left femoral artery (cyclic 4*5'/5'). After 24-h, the blood and kidney samples were collected. Plasma creatinine (Cr) levels and blood urea nitrogen (BUN) were determined. Total antioxidant capacity (TAC); total oxidant status (TOS); oxidative stress index (OSI); mRNA levels of IL-6, TNF-α, NF-kβ, IL-10, and klotho; and pathological changes were evaluated in the renal tissues. RESULTS: BIR resulted in renal dysfunction, as confirmed by higher plasma levels of Cr and BUN and structural changes. This was accompanied by increased TOS levels, OSI index, and decreased TAC levels. IL-6, TNF-α and NF-kβ upregulated, and klotho and IL-10 downregulated after renal ischemia. In the BIR + RIPerC group, RIPerC attenuated the destructive effects of BIR. RIPerC was effective in decreasing oxidative stress and inflammation. However, this procedure cannot upregulate the Klotho gene. CONCLUSION: Remote ischemic per-conditioning provides protection against renal ischemic reperfusion injury without the klotho pathway.