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Chemotherapy-induced Cardiotoxicity and Mitigation / Acute Kidney Injury Research · Journal article
Frontiers in Cardiovascular Medicine · September 9, 2026
Encouraging direction, but not yet definitive.
This retrospective study reports that a combined panel of three biomarkers (CRP, procalcitonin, microalbuminuria) achieved an AUC of 0.856 for predicting contrast-induced nephropathy after PCI, substantially exceeding individual markers and the Mehran score. The authors explicitly note that cancer patients on active systemic therapy were excluded and only a minority had cancer history, so the proposed cardio-oncology application remains mechanistically motivated hypothesis rather than demonstrated fact.
Retrospective cohort study. Consecutive patients undergoing elective or urgent PCI. Patients on active systemic anticancer therapy were excluded; cancer history comprised only a minority of the cohort.. Intervention: Combined pre-procedural assessment of CRP, PCT, and MAU with calculation of additive biomarker score (0–3).. Compared with: Individual biomarkers, Mehran risk score.. n = 486. Single centre; specific location not stated in source..
CIN developed in 92 patients (18.9%) of 486 total CRP >10 mg/L predicted CIN independently with OR = 3.15 (p < 0.001) PCT >0.05 ng/mL predicted CIN independently with OR = 2.87 (p < 0.001)
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The three-biomarker panel offers a simple additive scoring approach (0–3) for pre-procedural risk stratification in general PCI populations, outperforming traditional clinical scores and potentially guiding preventive strategies. However, the exclusion of active cancer patients and predominance of non-cancer patients mean the cardio-oncology application—the stated motivation—requires dedicated prospective study before implementation in that setting.
A retrospective single-centre study of 486 patients demonstrating that a three-biomarker panel outperforms existing risk scores for a surrogate endpoint (serum creatinine change), with clear effect sizes but requiring prospective validation and generalization to cardio-oncology populations.
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Quoted from the source exactly as published.
The three-biomarker panel offers a simple additive scoring approach (0–3) for pre-procedural risk stratification in general PCI populations, outperforming traditional clinical scores and potentially guiding preventive strategies. However, the exclusion of active cancer patients and predominance of non-cancer patients mean the cardio-oncology application—the stated motivation—requires dedicated prospective study before implementation in that setting.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
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.
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