Association of Serum Lipocalin-2 (LCN2) with Thoracic Aortic Calcification in CKD Stage 5: A Cross-Sectional Study

Background: This study explores the association between serum neutrophil gelatinase-associated lipocalin (LCN2) and thoracic aortic calcification (TAC) in stage 5 chronic kidney disease (CKD) patients, while evaluating LCN2’s potential as a predictive biomarker for TAC in this population. Methods: This cross-sectional study included 160 patients with CKD5 from three hospitals between May 2023 and 2025. TAC volume was quantified via dual-source spiral CT, and serum LCN2 levels were measured by ELISA. Bivariate/multivariate regression identified vascular calcification predictors. ROC curves evaluated LCN2's predictive value alone or combined with biomarkers, with model comparisons via DeLong’s test. A predictive model was validated by DCA for clinical benefit. Results: Group Comparison Analysis Patients with TAC had significantly higher serum LCN2, total cholesterol, albumin, alkaline phosphatase (ALP) , and parathyroid hormone (PTH) levels, and were older than those without calcification. Correlation Analysis Spearman’s analysis revealed a positive correlation between serum LCN2 levels and TAC volume in CKD5 patients (r = 0.569, P < 0.001). Multivariate Logistic Regression and Model Performance Multivariate logistic regression identified serum LCN2, ferritin, ALP, and PTH as independent predictors of vascular calcification in CKD (CKD-VC). Serum LCN2 alone yielded an AUC of 0.802 (95% CI: 0.705–0.898) for vascular calcification prediction, with a cutoff of 1007.405 ng/L (sensitivity 60.4%, specificity 88.9%). Model 1 (ferritin, ALP, PTH) had an AUC of 0.820 (95% CI: 0.719–0.897). Model 2, incorporating LCN2, improved AUC to 0.899 (95% CI: 0.812–0.955). DeLong’s test confirmed significant AUC improvement of Model 2 over Model 1 (Z = 1.986, P = 0.047), validating LCN2’s independent contribution to CKD-VC. Clinical Utility of the Prediction Model DCA demonstrated that the prediction model incorporating serum LCN2 provided a higher net clinical benefit compared to models excluding this biomarker. Conclusion: Previous research shows that LCN2 promotes CKD-VC by aggravating vascular smooth muscle cell ferroptosis via NCOA4/FTH1-mediated ferritinophagy. Inhibiting LCN2 has therapeutic potential. This study suggests that LCN2 combined with clinical parameters improves calcification prediction accuracy, emphasizing its diagnostic and therapeutic potential.