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  [3]. Two large meta-analyses of 19,000 patients who had received IV CM showed PC-AKI incidences of 5.0–6.4% [3].

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 [10]. In Weisbord et al. trial, patients with eGFRs < 60 ml/min underwent non-emergent CECT in the inpatient and outpatient, about 3.5% of them manifested an increase in serum creatinine ≥ 0.5 mg/dl [14].

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 [15]. The official guidelines published by the ESUR and the American College of Radiology and both recommend prophylactic hydration (1.0–1.5 mL/kg/h) in patients at risk for AKI at least 6 h before and after CM administration [2].

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 [16].

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 [17].

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 [18, 19].

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 p = 0.003. Vitamin C plus saline administration is effective to reduce the risk of CI-AKI by 25% [20]. In our trial, PC-AKI occurred in 11 patients (9.8%) in placebo group and in 3 patients (3%) statin plus ascorbic acid group (p = 0.04).

In Tepel et al., RCT, prophylactic oral N-acetylcysteine for CKD patient with GFR < 50 ml/minute who underwent elective contrast-enhanced computed tomography prevents the reduction in renal function. In the control and N-acetylcysteine group, the mean serum creatinine concentration increased from 2.4 ± 1.3 to 2.6 ± 1.5 mg/dl (p = 0.18) and decrease from 2.5 ± 1.3 to 2.1 ± 1.3 mg/dl (p < 0.001), respectively [8].

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 (p = 0.11) and from 0.80 ± 0.21 mg/dl to 0.81 ± 0.23 mg/dl (p = 0.14), in placebo and statin plus ascorbic acid groups, respectively.

Also, the mean ± SD estimated GFR decreased significantly in both groups with better significance in the statin plus ascorbic acid group (p < 0.001) versus (p = 0.003). In placebo group, mean ± SD estimated GFR decreased significantly from 100.45 ± 24.60 to 92.85 ± 24.78 ml/min (p < 0.001). The same occurred in the statin plus ascorbic acid group, the mean ± SD estimated GFR decreased significantly from 102.27 ± 34.47 to 96.17 ± 24.31 ml/min (p = 0.003). The difference may be attributed to difference in baseline characteristics, our patients were normal serum creatinine, however, in Tepel et al. the patients were CKD patients.

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 [14]. We think that may be attributed the difference in PC-AKI definition.

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 [11]. The incidence of PC-AKI increases dramatically after a threshold serum creatinine of 1.2–1.5 mg/dl is reached. So, randomised trials with large patient numbers for this category are warranted. Also, we calculate GFR using MDRD in patients without apparent basal renal disease, not the renal scintigraphy.