Discussion
CKD, toxicity, medullary hypoxia, nephrotoxic, diabetic type 2, CM, acute coronary syndrome, diabetic, CI-AKI, CIN, diabetes
INFLAMMATORY RESPONSES, CONTRAST-INDUCED ACUTE KIDNEY INJURY, COMPLICATION, CIN, ACUTE CORONARY SYNDROME, OXIDATIVE STRESS, DIABETES
Contrast-induced acute kidney injury (CI-AKI) is a common complication of CM intravascular injection; the physiopathology is complex and not well-understood. Our randomized trial aimed to assess the impact of a reloading dose with 80 mg of atorvastatin on CIN incidence in patients who underwent coronary invasive procedures and who were pre-treated with atorvastatin. The incidence of Scr-based CIN was 10% and the incidence of CYs-based CIN was 31.8% in our trial. In previous studies, the incidence of CYs-CIN ranged between 11 and 28% [The mechanisms of CIN are not well-understood. The most recognized mechanisms are renal vasoconstriction, medullary hypoxia, direct tubular cell toxicity of CM, inflammatory mechanisms, and oxidative stress. All these factors lead to epithelial and endothelial cell apoptosis and GFR reduction [The beneficial impact of statins in CIN prevention has been largely demonstrated [Our trial suggested that reloading with high-dose atorvastatin reduces the risk of CIN in diabetic type 2 patients. This beneficial effect could be explained by a reduction in inflammatory reactions after contrast injection, as it was assessed by the significant increase of the hs-CRP level in the NR group and not in the AR group.Prophylactic treatment with high-dose atorvastatin reduced the incidence of both SCr- and CyC-based CIN in patients with ACS following PCI, which might be attributed to its properties of reducing oxidative stress and inhibiting inflammatory responses.Reloading with atorvastatin was not superior to maintaining the habitual dose in non-diabetic patients and the overall population. This finding could be explained by the population included in the study, where we already used many means of CIN prevention (chronic statin therapy, rehydration, withdrawal of nephrotoxic drugs, low osmolar contrast products), and it could be difficult to show a benefit from an additional strategy. However, the control group included patients who were already on chronic statins. We recall that in the previous statin studies, the control group included statin-naïve patients.A recent meta-analysis, including seven RCTs of 4256 participants proved that the risk of developing CIN in patients with CKD pre-treated with statins was significantly lower than that in patients pre-treated with placebo (RR = 0.57. 95%CI = 0.43–0.76. p<0.001); in the subgroup analysis, statin pre-treatment could decrease the risk of CIN in CKD patients with diabetes (RR = 0.54. 95% CI = 0.39–0.76. p<0.001), but not in CKD patients without DM (RR = 0.84. 95% CI = 0.44–1.60. p = 0.606) [Paradoxically, Naikuan et al who compared the efficacy of high-dose atorvastatin (40 mg) to conventional-dose atorvastatin (10 mg) on the prevention of CIN in patients with acute coronary syndrome undergoing percutaneous intervention didn’t find a beneficial impact in diabetic groups and they attributed this finding to the low proportion of high-risk patients or lower dose of atorvastatin compared to the studies mentioned above [