Indexed Neutrophil Gelatinase-Associated Lipocalin: Improving Prediction and Ruling Out of Contrast-Induced Nephropathy.

BACKGROUND

The risk for contrast-induced acute kidney injury (CI-AKI) following cardiac procedures involving contrast administration is particularly high among chronic kidney disease (CKD) patients. Neutrophil gelatinase-associated lipocalin (NGAL) has been widely studied as an early marker for renal injury. However, CKD could impact NGAL levels and alter their predictive performance. This study aimed to evaluate a novel baseline "indexed NGAL" (I-NGAL), calculated by adjusting NGAL to the estimated glomerular filtration rate (eGFR), for the prediction of CI-AKI in CKD patients undergoing elective transcatheter aortic valve replacement (TAVR).

METHODS

A total of 134 CKD patients undergoing elective TAVR were included. Serum NGAL levels were drawn at hospital admission. Patients were followed for the occurrence of CI-AKI. Receiver-operator characteristic methods were used to identify optimal sensitivity and specificity for I-NGAL. Univariate and multivariate binary logistic regression models were used to assess I-NGAL predictive performance.

RESULTS

Overall, 35/134 patients (26%) developed CI-AKI following TAVR; both NGAL and I-NGAL were significantly higher among patients having CI-AKI. I-NGAL results had a higher predictive ability than unindexed NGAL results (AUC of 0.83 vs. 0.78, p < 0.001). The optimal I-NGAL cutoff for prediction of CI-AKI was 4, with a sensitivity of 71%, a specificity of 77%, and a negative predictive value of 88%. In a multivariate logistic regression model, I-NGAL was independently associated with CI-AKI (OR 1.22, 95% CI: 1.05-1.41; p = 0.007). I-NGAL level >4 was also independently associated with CI-AKI (OR 8.13, 95% CI 3-21.8, p < 0.001).

CONCLUSION

Among CKD patients undergoing elective TAVR, adjusting baseline NGAL values according to eGFR yields an I-NGAL that serves as an improved tool for predicting and ruling out CI-AKI, regardless of baseline renal function.