Introduction: Acute tubular necrosis (ATN) is the most common cause of intrinsic acute kidney injury (IAKI) (80%).kidney biopsy is usually not performed in intrinsic renal AKI. It is reserved when clinical assessement and or laboratory investigations oe evolutive data are suggestive of other causes of IAKI. The evolution of ATN is generally favorable with restitution ad integrum after regeneration of the tubules and parallel functional recovery in a few days to a few weeks. The aim of this study is to document the evolutionary features of biopsy proven ATN in our population. Methods: A retrospective cohort study including 58 patients with biopsy proven ATN during 2000-2019. Clinical-biological parameters and renal functions outcome were collected. Patients were classified in three groups regarding renal function evolution at 3 months : G1 : total renal function recovery, G2 : partial renal function recovery and G3 : ESRD (end stage renal disease).Results: This study included 58 patients (29 women and 29 men). Average age was 46,3 yearsAE 19 years. 32,8% of patients were hypertensive, 13,8% diabetic, 5,2% dyslipidemic, 3,4% had heart disease, 3,4% had neoplasia and 3,4% had a pre-exsiting chronic kidney disease. 74,1% have a preserved diuresis while 25,9% were oligoanuric. Regarding the causes of ATN, 20,6% were of ischemic origin and 61,8% were toxic or drug origin. During the acute phase of ATN, 74,1% of patients required a few hemodialysis sessions. Monitoring of renal function showed total improvement in 17,2% , partial improvement in 41,4% and no recovery in 27,6%, 3,4% died in the acute phase. We looked at the group that required long term dialysis GFR was significantly lower (p=0,02). Among the co-morbidities studied, a significant association was found only on hypertensive patients (p=0.034). Concerning the histological features, a significant association was noted with intertitial fibrosis. Conclusions: The evolution of ATN seems to be favorable in most cases, involving clinical, biological and histological factors. The prevention of this complication is essentially based on the identification of patients at risk, the avoidance of nephrotoxic factors and the rapid and early correction of triggering factors.