Abstract
ObjectivesEnhanced reactive oxygen species formation within the kidney following the administration of contrast media may play a key role in the development of contrast-induced nephropathy (CIN). Bilirubin has emerged as an important endogenous antioxidant molecule. This study was undertaken to determine whether bilirubin is associated with CIN and future cardiovascular events in patients undergoing coronary intervention.MethodsTotally, 544 consecutive patients received coronary intervention were enrolled. All patients were followed up for at least 3 years or until the occurrence of a major event. The primary endpoint was CIN, defined as a rise in serum creatinine (SCr) of 0.5 mg/dl or a 25% increase from the baseline value within 48 hours after the procedure. The secondary endpoint was the combined occurrence of major adverse cardiovascular events (MACE), including death, nonfatal myocardial infarction, and ischemic stroke.ResultsOverall, CIN occurred in 85 (15.6%) patients. All patients were stratified into 3 groups (low/normal/high) according to the serum bilirubin levels. In a multivariate logistic analysis, the odds ratio for CIN with low-bilirubin levels relative to high-bilirubin levels was 11.82 (95% CI, 3.25–43.03). By Cox regression analysis, serum bilirubin levels was an independent predictor of MACE in patients undergoing coronary intervention (low vs. high hazard ratio 2.26; 95% CI, 1.05–4.90).ConclusionsCIN is a serious complication of coronary intervention. Higher serum bilirubin concentrations were associated with lower risk of CIN and fewer cardiovascular events. The development of interventions that promote bilirubin levels may be a potential target to reduce CIN and future MACE in patients undergoing coronary intervention.
Highlights
Contrast-induced nephropathy (CIN) remains a serious clinical problem in the use of iodinated contrast media, which accounts for a significant number of cases of hospital-acquired acute kidney injury [1,2,3]
Enhanced reactive oxygen species (ROS) generation in clinical conditions predisposing to CIN and the evidence for enhanced ROS formation following exposure to contrast media, highlight the possibility that oxidative stress may play an important role in the pathogenesis of CIN
No significant differences were found between the patients with or without CIN with respect to smoking status, serum levels of lipid profiles and liver enzymes, and underlying diseases such as hypercholesterolemia and previous MI
Summary
Contrast-induced nephropathy (CIN) remains a serious clinical problem in the use of iodinated contrast media, which accounts for a significant number of cases of hospital-acquired acute kidney injury [1,2,3]. CIN is a possible complication of coronary diagnostic and interventional procedures. Its development has been associated with increased in-hospital and long-term morbidity and mortality, prolonged hospitalization, and long-term renal impairment [5,6,7]. Proposed pathophysiologic mechanisms through which contrast administration may potentiate renal injury include oxidative stress, free radical damage, and endothelial dysfunction [8], [9]. Enhanced reactive oxygen species (ROS) generation in clinical conditions predisposing to CIN and the evidence for enhanced ROS formation following exposure to contrast media, highlight the possibility that oxidative stress may play an important role in the pathogenesis of CIN
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