Key result
Residual inflammatory risk is linked to ~14% higher post-CABG acute kidney injury risk.
Why the study?
Do residual cholesterol and inflammation risks increase postoperative acute kidney injury and long-term mortality in patients undergoing coronary artery bypass grafting?
Cohort (n=35,788)
Do residual cholesterol and inflammation risks increase postoperative acute kidney injury and long-term mortality in patients undergoing coronary artery bypass grafting?
Residual inflammatory and cholesterol risks increase the likelihood of postoperative AKI and mortality after CABG, suggesting a role for risk-stratified perioperative statin therapy.
Background Acute kidney injury (AKI) is a common complication after coronary artery bypass grafting (CABG), and is associated with increased mortality. Randomized controlled trials demonstrated that residual cholesterol and inflammation risks remained in patients with cardiovascular disease. However, few studies have investigated the impact of residual risk profiles on AKI in patients after CABG. Purpose This study aims to assess the impact of residual risk profiles on postoperative AKI and long-term mortality in patients undergoing CABG, while also investigating their potential role in guiding personalized perioperative statin therapy decisions. Methods A total of 35,788 consecutive patients undergoing CABG were enrolled between 1 January, 2013 and 1 October, 2022. Participants were categorized into four groups based on the levels of remnant cholesterol and hypersensitive C-reactive protein: no residual risk, residual inflammatory risk (RIR), residual cholesterol risk (RCR), and combined residual cholesterol and inflammatory risk (RCIR). The study outcomes included postoperative AKI, as defined by the Kidney Disease: Improving Global Outcomes (KDIGO) criteria, and 5-year mortality. Logistic regression and Cox proportional hazard models were used to evaluate the association between residual risk profiles and adverse outcomes. Additional analyses investigated the heterogeneity in the effects of statin treatment on severe AKI across residual risk profiles. Results Compared to patients with no residual risk, those with RIR exhibited an increased risk of developing AKI after multiple adjustments. Specifically, RIR was associated with a 14% higher risk of any AKI (OR: 1.14, 95% CI: 1.08-1.21) and a 61% increased risk for severe AKI (KDIGO stages 2/3) (OR: 1.61, 95% CI: 1.41-1.84). In contrast, RCR was significantly related to severe AKI only in patients with diabetes (OR: 1.39, 95% CI: 1.04-1.83). Moreover, the combination of both residual risks further exacerbated the risk of severe AKI (OR: 1.77, 95% CI: 1.38-2.23), with diabetic patients experiencing a higher risk (OR: 1.90, 95% CI: 1.38-2.56) compared to non-diabetic patients (OR: 1.58, 95% CI: 1.06-2.28). Regarding therapeutic implications, perioperative statin therapy increased the risk of severe AKI in patients with no residual risk (OR: 1.27, 95% CI: 1.04-1.53), but conferred significant protection against AKI in those with RCR (OR: 0.58, 95% CI: 0.34-0.96). For long-term outcomes, patients with RIR exhibited a 34% higher 5-year mortality risk (HR 1.34, 95% CI 1.19-1.52). Conclusions Residual inflammation significantly increased the risk of postoperative AKI and long-term mortality after CABG, whereas residual cholesterol was associated with severe AKI only in diabetic patients. The combination of both residual risks exhibited a more pronounced effect on severe AKI. Residual risk profiles may guide personalized statin use to improve kidney outcomes after CABG.
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Chen et al. (2025) conducted a cohort in Coronary artery bypass grafting (CABG) (n=35,788). Residual inflammatory risk (RIR) vs. No residual risk was evaluated on Postoperative acute kidney injury (any AKI) (OR 1.14, 95% CI 1.08-1.21). Compared to no residual risk, residual inflammatory risk was associated with a 14% higher risk of any acute kidney injury after CABG (OR 1.14; 95% CI 1.08-1.21).
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