Biomarkers of oxidative stress and inflammation in contrast-associated acute kidney injury

Abstract

Iodinated contrast-induced acute kidney injury (CI-AKI) is a common cause of renal failure, especially in patients with risk factors. This study analyses different renal biomarkers in patients undergoing computed tomography scans with iodinated contrast to identify the molecular and cellular mechanisms involved in the pathogenesis of CI-AKI. Prospective study that included patients with high risk of renal disease who received iodinated contrast (iohexol) for the computed tomography scans. Functional biomarkers (creatinine and cystatin C), inflammatory and oxidative stress markers (neutrophil gelatinase-associated lipocalin [NGAL], interleukin-8 [IL-8], superoxide dismutase [SOD], F2-isoprostanes, and cardiotrophin-1), and cell cycle biomarkers (Nephrocheck®) were analysed before the iodinated contrast and 4, 12, 24, and 48 hours post-contrast, in relation to the incidence of IC-AKI. IC-AKI was observed in 30.6% of the 62 study participants and in 57.1% of the patients with diabetes and renal dysfunction. Factors associated with IC-AKI were a higher mean age (74.4 vs 64.9 years), pre-existing renal dysfunction (60 vs 16.7%), and higher adjusted mean volume of iohexol (42.9 vs 32.1%). As for non-functional biomarkers. No differences were found between patients with and without CI-AKI. The use of iodinated contrast was associated with a decrease in SOD antioxidant activity at 4 hours and an increase in IL-8 at 12 hours post-administration of the iodinated contrast. Administration of iohexol in computed tomography scans in patients with high risk of renal disease results in an elevated percentage of CI-AKI, attributable to ischemia/reperfusion injury and/or direct toxicity of the iodinated contrast.