In the present study, we demonstrated that rats submitted to renal ischaemia for 45 min develop AKI that becomes pronounced by 48 h after IRI, at which point we observed a peak in plasma urea, a drop in the glomerular filtration rate (i.e. creatinine clearance) and acute tubular necrosis, leading to increases in the urinary flow rate and FENa, as well as urinary concentrating defects, mainly due to decreased protein expression of AQP2. This evidence concerns the gene AQP2 and acute kidney injury.