Ischaemia-reperfusion injury in renal transplantation: the role of nitric oxide in an experimental rat model

OBJECTIVE To investigate the role of nitric oxide (NO) in ischaemia-reperfusion (I/R) injury in a renal transplant rat model, as I/R injury is a common consequence of renal transplantation and NO has many protective properties that might protect the kidney after I/R injury. MATERIALS AND METHODS In all, 30 male Sprague-Dawley rats weighing 350-400 g and aged 4-6 months underwent renal transplantation and received FK506 (an immunosuppressant) to overcome early acute rejection episodes. The rats were divided randomly into three groups (10 rats each): Group I, treated with FK506 (2 mg/kg body weight {[}bw], once daily), served as the control group; Group II, treated with FK506 2 mg/kg bw and L-arginine 300 mg/kg bw; and Group III, treated with FK506 (2 mg/kg bw) and, n-omega-nitro-l-arginine methyl ester (L-NAME; 50 mg/kg bw). Urine and blood samples were taken at 0 (before operation), 2, 7, and 14 days after transplantation for estimation of urine sodium, creatinine, fractional excretion of sodium, serum creatinine, sodium, and blood urea nitrogen (BUN). Kidney specimens were taken for histological examination by light microscopy. RESULTS Serum creatinine and BUN levels significantly decreased in the L-arginine-treated group (both P < 0.001) while they were significantly increased in the L-NAME-treated group (P < 0.005 and P < 0.001, respectively) compared with the control group at all time intervals. Light microscopic examination of the renal biopsies in the control group showed acute tubular necrosis, which was minimal in kidneys transplanted and treated with L-arginine and more markedly with L-NAME. CONCLUSION I/R injury impaired graft function during the first week after transplantation. Injection of L-arginine before ischaemia antagonized graft deterioration and improved morphological appearance.