Discussion
intravascular coronary, CM, necrosis, AKI, acute kidney injury
DEGENERATION, OXIDATIVE STRESS, INFLAMMATION, DNA DAMAGE, TUMOR NECROSIS, NECROSIS, PATHOGENESIS, INFLAMMATORY RESPONSE
Post-contrast acute kidney injury (PC-AKI) should be defined as ≥ 1.5–1.9 times baseline increase in serum creatinine or increase in serum creatinine of ≥ 0.3mg/dl (The KDIGO definition of AKI) in the 48–72 h following CM administration  [Published literature about post-contrast acute kidney injury (PC-AKI) mainly focuses on cardiac intervention as intravascular coronary angiography and rarely focuses on patients undergoing urological elective contrast-enhanced computed tomography. In a comparative study, PC-AKI was noted in 8.3% and 29.8% in urology and cardiology patients, respectively [Although the pathogenesis of PC-AKI is not fully understood, Contrast agents have direct cytotoxic effects on vascular endothelial cells, or renal tubular epithelial cells resulting in inflammation, necrosis, and apoptosis [Atorvastatin (statin) reduces the PC-AKI inflammatory response and apoptosis of renal tubular epithelial cells. Treatment with atorvastatin also decreases the serum expression levels of Interleukins-1b, I Interleukins-6, Interleukins-8 and Tumor necrosis factor alpha. Atorvastatin might ameliorate PC-AKI through anti-apoptosis pathway associated with the Bcl-2/caspase-3 [Oxidative stress shares some role in the pathogenesis of PC-AKI. Intracellular ROS are produced when the nephrons are exposed to contrast medium. When intracellular ROS synthesis rate overcomes the rate of their excretion, leads to oxidative-antioxidant imbalance, causing lipid peroxidation of biofilm, intracellular protein degeneration, and DNA damage [Vitamin C, an antioxidant, attenuates the oxidative damage caused by CM and might effectively prevent PC-AKI. It has been reported that vitamin C effectively countered oxidative damage by reducing and scavenging reactive oxygen species that damage macromolecules such as lipids, proteins, and DNA [The PRATO-ACS trial showed that the incidence of PC-AKI was significantly lower in the statin group (6.7%) than in controls (15.1%) with significant In Tepel et al., RCT, prophylactic oral In our RCT, the mean ± SD serum creatinine rise in both groups, from 0.80 ± 0.22 mg/dl to 0.82 ± 0.24 mg/dl (Also, the mean ± SD estimated GFR decreased significantly in both groups with better significance in the statin plus ascorbic acid group (We found that PC-AKI occurred in 9.8% and 3% in placebo and statin plus ascorbic acid group, respectively, according to new KDIGO criteria (serum creatinine ≥ 0.3 mg/dl), while using pre-procedure intravenous fluid. In Weibord study, 3.5% demonstrated a rise in serum creatinine ≥ 0.5 mg/dl. Although only 6% of outpatients received pre- and post-procedure intravenous fluid [Our trial has some limitations, we exclude patients with serum creatinine > 1.4 mg/dl. We choose serum creatinine as it is the most commonly used laboratory value as a screening test before CECT [