Renal allograft dysfunction could be due to hypovolumia, renal vessel thrombosis, rejection, acute tubular necrosis (ATN), cyclosporine toxicity and post renal obstruction. Segmental infarct is a poorly characterized complication of renal allograft. It is due to disruption or thrombosis in one of renal artery branches. We report here a case of renal allograft dysfunction that occurred after allograft segmental infarction. We propose that infarct material could induce ATN and renal allograft dysfunction Patient was a 30- year-old man who received a living unrelated renal transplantation. He was started on immuno­suppressive therapy with the Basiliximab, steroid, mycophenolate mofetil and cyclosporine. Allograft had a good function and produced more than 10 liter urine in first 24 of transplantation. Urine output decreased visibly thereafter and reached less than 0.5 liter at fifth day of transplantation. Doppler ultrasound study revealed a lack of perfusion in the lower pole of the renal allograft that was supplied by a polar artery and it was damaged during engraftment. Patient’s blood pressure rose to 180/120 mmHg on the second day of transplantation. By fifth day of transplantation serum creatinine levels were 6 mg/dl, serum lactic dehydrogenase (LDH):1730IU/L (250-500), Alanin aminotransferase (ALT):120IU/L(5-40) and Asparate Aminotransferase (AST) was:160IU/L (5-40), White blood cell count: 11000/ml, Platelets: 256000/ ml , Hemoglubine: 9.5 mg/dl. Hemodialysis was started and with a clinical diagnosis of acute rejection he received antithymocyte globuline (ATG) therapy. Light microscopic study of the allograft biopsy that was taken on 8th day of transplantation disclosed tubular cells necrosis without interstitial inflammation or tabulates. Glomerulus’s and vessels were normal. Immuno­flurescence staining for peri-tubular capillaries for C4d deposition was negative. We have speculated that substances such as TNF-α heat shock proteins (HSP70 and HSP60) that are released from the necrotic area could spread thought the renal cortex and act as endogenous tubular toxins and trigger intense tissue damage.