Cardiac surgery with cardiopulmonary bypass (CPB) is the most frequent major surgical procedure worldwide. Acute kidney injury (AKI) is a common and serious complication encountered in 30–40% after CPB. Once AKI is established, there is no effective treatment for human AKI, and dialysis merely provides supportive care. There in lies the Achilles’ heel of AKI management; the paucity of early biomarkers has lead to an unacceptable delay in initiating therapy in humans. Serum creatinine is insensitive for the early detection of AKI. KIM-1 is one of the most highly induced proteins in the kidney after AKI in animal models, and a proteolytically processed domain of KIM-1 is easily detected in the urine soon after AKI. In a small human cross-sectional study, KIM-1 expression was markedly induced in proximal tubules in kidney biopsies from patients with established AKI (primarily ischemic), and urinary KIM-1 measured by ELISA distinguished ischemic AKI from prerenal azotemia and chronic renal disease. In a case-control study of children undergoing CPB, urinary KIM-1 levels were markedly enhanced in subjects who subsequently developed AKI. Thus, KIM-1 represents a promising candidate for inclusion in the urinary “AKI Biomarker Panel”, with NGAL being most sensitive at the earliest time points and KIM-1 potentially adding specificity at slightly later time points. One advantage of KIM-1 as a urinary biomarker is the fact that its expression seems to be limited to the injured or diseased kidney, and no systemic source of KIM-1 has been described.Perioperative administration of alpha2-adrenergic agonist dexmedetomidine, has been shown to reduce anesthetic requirements, enhance hemodynamic stability and provide sedation during postoperative recovery following coronary artery bypass. Dexmedetomidine-induced sympatholysis might attenuate harmful hemodynamic events resulting in prevention of AKI. In fact, alpha2-adrenoceptor activation does produce some potentially renal protective effects including inhibition of renin release,increased glomerular filtration and increased secretion of sodium and water . Moreover, pretreatment with clonidine, the archetype of alpha2-adrenergic agonists, has shown beneficial renal effects after cardiac surgery .In an earlier study it was found that urine output tended to be greater in patients receiving dexmedetomidine than in those receiving placebo in post-coronary artery bypass grafting (CABG) patients. To date, no single pharmacological regimen has conclusively proved its efficacy in preventing AKI and any potential means to decrease the number of cardiac surgery patients encountering this deleterious adverse effect should be sought. The present study is directed to examine the renal protection of dexmedetomidine as tested by KIM-1 , and the study included 72 pediatric patients of average age 6 months -8 years and average weight of 6-20 kilograms. Different elective pediatric cardiac surgeries of average duration 3-5 hours were undergone for these patients under general anesthesia. The patients were randomly assigned and divided into 2 groups namely Dexmedetomidine group (n=36) and Control group (n=36).There was no significant rise in level of KIM-1 between both groups , but there was significant difference indicating AKI in control group in patients with prolonged bypass .There was significant rise in level of KIM -1 between the baseline sample and 24 hour sample within the same group .In prolonged bypass only ,the number of patients diagnosed with AKI in control group was double the number of patients with AKI in group Dex . Data obtained in this study showed that dexmedetomidine has renal protective value by decreasing AKI in patients with prolonged by pass more than 90 minutes . KIM-1 is more sensitive than serum creatinine in diagnosing AKI