scholarly journals More than a simple biomarker: the role of NGAL in cardiovascular and renal diseases

2018 ◽  
Vol 132 (9) ◽  
pp. 909-923 ◽  
Author(s):  
Mathieu Buonafine ◽  
Ernesto Martinez-Martinez ◽  
Frédéric Jaisser

Neutrophil gelatinase-associated lipocalin (NGAL) is a small circulating protein that is highly modulated in a wide variety of pathological situations, making it a useful biomarker of various disease states. It is one of the best markers of acute kidney injury, as it is rapidly released after tubular damage. However, a growing body of evidence highlights an important role for NGAL beyond that of a biomarker of renal dysfunction. Indeed, numerous studies have demonstrated a role for NGAL in both cardiovascular and renal diseases. In the present review, we summarize current knowledge concerning the involvement of NGAL in cardiovascular and renal diseases and discuss the various mechanisms underlying its pathological implications.

Author(s):  
OmPrakash Kalra ◽  
Sonal Pruthi ◽  
Scienthia Sanjeevani ◽  
Ashish Goel ◽  
Sarathi Kalra

2021 ◽  
pp. 1-11
Author(s):  
Katrien Leyssens ◽  
Niels Van Regenmortel ◽  
Ella Roelant ◽  
Khadija Guerti ◽  
Marie Madeleine Couttenye ◽  
...  

<b><i>Introduction:</i></b> Acute kidney injury (AKI) is a frequent complication among patients in the intensive care unit (ICU). The limitations of serum Cr (sCr) in timely detecting AKI are well known. Beta-trace protein (BTP) is emerging as a novel endogenous glomerular filtration rate marker. The aim of this study was to explore the role of BTP as a marker of AKI. <b><i>Methods:</i></b> Patients admitted to the ICU undergoing surgery were included. BTP, sCr, Cystatin C (CysC), and neutrophil gelatinase-associated lipocalin (NGAL) were measured preoperatively, postoperatively (post-op), and at the first (D1) and second (D2) post-op day. AKI was defined as an increase of sCr to ≥1.5-fold from baseline within 2 days after surgery. <b><i>Results:</i></b> Of the 52 patients studied, 10 patients (19%) developed AKI. Patients with AKI were older (69.6 ± 10.7 vs. 58.1 ± 16.7 years, <i>p</i> = 0.043) and had a longer length of ICU stay (13 [IQR 6–49] vs. 6 [IQR 5–8] days, <i>p</i> = 0.032). Between the 2 groups, the evolution of BTP, sCr, CysC, and NGAL over time differed significantly, with overall higher values in the AKI group. ROC analysis for the detection of AKI within 2 days after surgery showed a great accuracy for BTP. The area under the curve (AUC) for BTP post-op; D1; and D2 was, respectively, 0.869 ± 0.049; 0.938 ± 0.035; and 0.943 ± 0.032. The discriminative power of a BTP measurement on D1 was superior in detecting AKI compared to NGAL (adjusted <i>p</i> value = 0.027). We could not detect a significant difference between the AUCs of other biomarkers (NGAL, sCr, and CysC). <b><i>Conclusion:</i></b> Serum BTP is a promising marker for diagnosing AKI in ICU patients undergoing surgery.


2019 ◽  
Vol 13 (2) ◽  
pp. 128-132
Author(s):  
Greg D Guthrie ◽  
Samira Bell

Abstract There is a growing body of evidence for the role of deprivation in a broad spectrum of diseases including renal disease. Deprivation has been demonstrated to be associated with poorer outcomes across a range of renal diseases including acute kidney injury (AKI), chronic kidney disease and transplantation. In this issue of Clinical Kidney Journal, Hounkpatin et al. describe the association of socioeconomic deprivation with incidence, mortality and resolution of AKI in a large UK cohort. Investigating deprivation as a factor influencing either incidence or outcome of disease is challenging due to variations in measures of deprivation used and other confounding factors that may be contributing to the observed differences. In this editorial, we review the current literature examining the role of deprivation in renal disease.


2020 ◽  
Vol 10 (3) ◽  
pp. 154-161
Author(s):  
Ilan Merdler ◽  
Keren-Lee Rozenfeld ◽  
David Zahler ◽  
Moshe Shtark ◽  
Ilana Goldiner ◽  
...  

Introduction and Objective: Neutrophil gelatinase-associated lipocalin (NGAL), a glycoprotein released by renal tubular cells, can be used as a marker of early tubular damage. We evaluated plasma NGAL level utilization for the identification of acute kidney injury (AKI) among ST-elevation myocardial infarction (STEMI) patients undergoing primary coronary intervention (PCI). Methods: 131 STEMI patients treated with PCI were prospectively included. Plasma NGAL levels were drawn prior to PCI (0 h) and 24 h afterwards. AKI was defined per KDIGO criteria of serum creatinine increase. Receiver-operating characteristic (ROC) methods were used to identify optimal sensitivity and specificity for the observed NGAL range. Results: Overall AKI incidence was 14%. NGAL levels were significantly higher for patients with AKI at both 0 h (164 ± 42 vs. 95 ± 30; p < 0.001) and 24 h (142 ± 41 vs. 93 ± 36; p < 0.001). Per ROC curve analysis, an optimal cutoff value of NGAL (>120 ng/mL) predicted AKI with 80% sensitivity and specificity (AUC 0.881, 95%, CI 0.801–0.961, p < 0.001). In a multivariate logistic regression model, NGAL levels were independently associated with AKI at 0 h (OR 1.044, 95% CI 1.013–1.076; p = 0.005) and 24 h (OR 1.018, 95% CI 1.001–1.036; p = 0.04). Conclusions: Elevated NGAL levels, suggesting renal tubular damage, are independently associated with AKI in STEMI patients undergoing primary PCI.


2015 ◽  
Vol 129 (10) ◽  
pp. 851-862 ◽  
Author(s):  
Yee Kwan Chan ◽  
Hye Kyoung Sung ◽  
Gary Sweeney

Neutrophil gelatinase-associated lipocalin (NGAL) has recently become established as an important contributor to the pathophysiology of cardiovascular disease. Accordingly, it is now viewed as an attractive candidate as a biomarker for various disease states, and in particular has recently become regarded as one of the best diagnostic biomarkers available for acute kidney injury. Nevertheless, the precise physiological effects of NGAL on the heart and the significance of their alterations during the development of heart failure are only now beginning to be characterized. Furthermore, the mechanisms via which NGAL mediates its effects are unclear because there is no conventional receptor signalling pathway. Instead, previous work suggests that regulation of iron metabolism could represent an important mechanism of NGAL action, with wide-ranging consequences spanning metabolic and cardiovascular diseases to host defence against bacterial infection. In the present review, we summarize rapidly emerging evidence for the role of NGAL in regulating heart failure. In particular, we focus on iron transport as a mechanism of NGAL action and discuss this in the context of the existing strong associations between iron overload and iron deficiency with cardiomyopathy.


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