Bupropion Cannot Reduce Acute Kidney Injury Due to Ischemia-Reperfusion

Guzmán-de la Garza FJ, Cabello-García AJ, Ibarra-Hernandez JM, Martini-Antonio MT, Alarcón-Galván G, Cámara-Lemaroy CR, Vargas-Villarreal J, Hernández SG, Garza JC, Muzquiz-Vidales R, Cordero-Perez P, Garza NEF and Salinas-Martinez AM

Bupropion can limit the increase of TNF-alpha, reducing the inflammatory response and injury due to Ischemia- Reperfusion (I/R) on tissues such as the bowel. Our objective was to evaluate bupropion as a preconditioning agent for ischemic acute kidney injury.

Experiments were performed on female Wistar rats. Bupropion groups received 25 mg/kg 60 min before the maneuver. As a first step, 30 rats with a right nephrectomy were divided into 6 groups (n=5): sham 24, sham 48, bupropion 24, bupropion 48, ischemia-reperfusion 24 and ischemia-reperfusion 48. After 60 min of ischemia (except sham groups) 24 or 48 h of reperfusion was allowed. During a second step, 30 rats, with both kidneys conserved, were divided into 6 groups (n=5): sham 3, sham 72, bupropion 3, bupropion 72, ischemia-reperfusion 3, and ischemia-reperfusion 72 (IR72). Ischemia in these groups (except sham groups) was performed for 60 min only on the left kidney, and 3 or 72 h of reperfusion were allowed. Serum and histologic evaluations were done.

After 48 h of reperfusion, all mono-renal rats that received bupropion died. Bupropion cannot avoid histological damage nor does it impact creatinine clearance, BUN, TNF-α or KIM-1 serum levels secondary to I/R. In conclusion: The pharmacologic preconditioning with Bupropion cannot improve the AKI evolution in rats with renal ischemiareperfusion injury.