XueChao Yuan, ZeXiang Xu, Xin Guo
Combined pre-procedural assessment of CRP, PCT, and MAU provided excellent discriminatory ability (AUC=0.856) for CIN prediction, substantially superior to individual biomarkers and traditional clinical risk factors. These complementary markers-capturing systemic inflammation, acute inflammatory stress, and baseline renal endothelial integrity, respectively-offer a clinically practical framework for biomarker-guided risk stratification in a general PCI population. As patients on active systemic anticancer therapy were excluded and patients with a cancer history comprised only a minority of the cohort, the potential extension of this panel to cardio-oncology practice is proposed as a mechanistically motivated hypothesis that requires dedicated validation rather than as a demonstrated application.
BACKGROUND: Cancer patients with cardiovascular comorbidities requiring contrast-based cardiac procedures face substantially amplified risk for contrast-induced nephropathy (CIN), driven by anticancer therapy-related systemic inflammation, nephrotoxicity, and endothelial dysfunction. Validated biomarker-based risk stratification tools that capture these distinct pathophysiologic mechanisms are urgently needed in cancer cardiology practice. This study evaluated the combined predictive value of C-reactive protein (CRP), procalcitonin (PCT), and microalbuminuria (MAU) for CIN development following percutaneous coronary intervention (PCI), with direct implications for cardio-oncology risk stratification.
METHODS: We retrospectively analyzed 486 consecutive patients undergoing elective or urgent PCI between March 2021 and November 2024. Baseline CRP, PCT, and MAU were measured within 24 h pre-procedure. CIN was defined as serum creatinine increase ≥0.5 mg/dL or ≥25% from baseline within 48-72 h post-contrast.
RESULTS: CIN developed in 92 patients (18.9%). All three biomarkers independently predicted CIN in multivariable analysis: CRP >10 mg/L (OR = 3.15, p < 0.001), PCT >0.05 ng/mL (OR = 2.87, p < 0.001), and MAU ≥30 mg/24 h (OR = 3.42, p < 0.001). The combined three-biomarker panel demonstrated superior discrimination (AUC = 0.856, 95% CI: 0.818-0.894) compared to individual markers (AUC 0.682-0.728) and the Mehran score (AUC = 0.714). An additive biomarker score (0-3) stratified CIN risk from 5.8% (score 0) to 50.0% (score 3), representing an approximately8.6-fold gradient.
CONCLUSION: Combined pre-procedural assessment of CRP, PCT, and MAU provided excellent discriminatory ability (AUC=0.856) for CIN prediction, substantially superior to individual biomarkers and traditional clinical risk factors. These complementary markers-capturing systemic inflammation, acute inflammatory stress, and baseline renal endothelial integrity, respectively-offer a clinically practical framework for biomarker-guided risk stratification in a general PCI population. As patients on active systemic anticancer therapy were excluded and patients with a cancer history comprised only a minority of the cohort, the potential extension of this panel to cardio-oncology practice is proposed as a mechanistically motivated hypothesis that requires dedicated validation rather than as a demonstrated application.