Neutrophil gelatinase-associated lipocalin (NGAL) for the prediction of acute kidney injury in chronic kidney disease patients treated with primary percutaneous coronary intervention. (February 2021)

• Record Type: Journal Article
• Authors: Banai, Ariel; Rozenfeld, Keren-Lee; Levit, Dana; Merdler, Ilan; Loewenstein, Itamar; Banai, Shmuel; Shacham, Yacov
• Is Part Of: IJC heart & vasculature. Volume 32(2021)
• Publication Date: 2021-02
• Subjects: NGAL -- AKI -- STEMI -- PCI; Cardiovascular system -- Diseases -- Periodicals; Cardiovascular system -- Pathophysiology -- Periodicals; 616.1005
• DOI: 10.1016/j.ijcha.2020.100695
• Languages: English
• ISSNs: 2352-9067

Abstract

Highlights: Chronic kidney disease (CKD) patients may demonstrate elevated NGAL levels reflecting chronic impairment condition. We evaluated plasma NGAL level for identification of AKI superimposed on CKD vs. "de novo" AKI among (STEMI) patients undergoing primary PCI. NGAL is a useful tool for the identification of patients with CKD in high risk for AKI following primary PCI. However, Different cutoff values of plasma NGAL for "de novo" AKI and AKI superimposed on CKD may be necessary for Table 1, 2 and 3 diagnosis. Abstract: Introduction: Elevated plasma levels of neutrophil gelatinase-associated lipocalin (NGAL) is a marker of tubular damage and aid in the early identification of acute kidney injury (AKI). We evaluated NGAL levels for identification of AKI superimposed on chronic kidney disease (CKD) vs. "de novo" AKI among ST elevation myocardial infarction (STEMI) patients undergoing primary coronary intervention (PCI). Methods: 217 STEMI patients treated with PCI were prospectively included, 34 (16%) had baseline CKD. Plasma NGAL levels were drawn 24 h following PCI. Receiver-operator characteristic (ROC) methods were used to identify optimal sensitivity and specificity for the observed NGAL range in AKI patients with and without CKD. Results: Overall AKI incidence was 13%. NGAL levels were significantly higher for patients with AKI compared to no-AKI, irrespective of CKD. Different optimal cutoff value for NGAL to predict AKI were found for patients with CKD (133 ng/ml, sensitivity of 73% and specificity of 75%; AUC: 0.837, p < 0.001) and for non-CKD (104 ng/ml with sensitivity of 79% and specificity of 82%; AUC: 0.844, p < 0.001). In a multivariate logistic regression model, NGAL levels were independently associated with AKI in patients with and without CKD (HR 1.04, 95% CI: 1.01–1.08; p = 0.024; and HR 1.03, 95% CI: 1.01–1.04; p = 0.001), respectively. Conclusions: Elevated plasma NGAL levels identify patients who are at high-risk to develop AKI following primary PCI. Determining different cutoff values of plasma NGAL for de novo AKI and AKI superimposed on CKD may be necessary for accurate AKI diagnosis and risk stratification.