Neutrophil Gelatinase Associated Liocalin in Predicting AKI in Coronary Artery Disease

Overview

The aim of this work is to assess the clinical significance of serum levels of neutrophil gelatinase-associated lipocalin (NGAL) to predict AKI in patients exposed to PCI.

ST-elevated myocardial infarction(STEMI) patients are at a particularly high risk of acute kidney injury (AKI) because of the complexity of hemodynamic disorders and adverse effects associated with the use of radiopaque diagnostic and treatment methods (Smirnov AV.et al.,2009) With wide application of percutaneous coronary intervention (PCI) technology in patients with coronary artery disease (CAD), contrast-induced acute kidney injury (CI-AKI) has become a serious complication and is the third leading cause of AKI in hospitalized patients.(Gleeson.et al. 2004) To date,AKI diagnosis has been limited to observation of increasing levels of serum creatinine,decrease in urine output,and alterations in urinary chemistry (Bellomo.et al.2004;Mehta.et al. 2007) Nevertheless,serum creatinine levels do not increase significantly until renal function has decreased to 50% in addition,the level of serum creatinine may be affected by the patient's muscle mass,catabolic state,protein intake,weight,sex and tubular secretion of creatinine.Therefore,applying serum creatinine as a biomarker for diagnosing AKI may result in the loss of valuable time (Mishra.et al.2005;Sirota.et al.2011) Neutrophil Gelatinase-associated lipocalin(NGAL) belongs to the lipocalin family and is produced predominantly by the liver and white blood cells(Hvidberg.et al.,2005). A small polypeptide, neutrophil gelatinase-associated lipocalin (NGAL), is one of the most promising and best-studied AKI biomarkers (Mishra.et al.,2003; Devarajan.et al 2003) The expression of NGAL was predominantly in proliferating and regenerating tubular epithelial cells, which suggested a role in repair. (Mori.et al.2005) The majority of NGAL, secreted by injured renal tubule epithelial cells, is in a 25kDa monomeric form. In contrast, neutrophils have been claimed to release NGAL primarily as a 45kDa homodimer, i.e. two NGAL monomers linked by a disulfide bridge. It also exists as a 135-kDa heterodimer, covalently conjugated with gelatinase (Cai.et al.2010) NGAL is easily detected in blood and urine due to its small size and resistance to degradation. It can be measured non-invasively using routine laboratory analysers as well as some point of care devices. Furthermore, NGAL concentration in both urine and plasma rises rapidly in a dose-dependent manner that is proportional to the degree of acute kidney damage (Haase-Fielitz.et al.2009) NGAL has previously been termed the 'troponin-like' biomarker to detect subclinical AKI even in the absence of diagnostic increases in SCr (Devarajan.,2010;Haase,et al.2011) Additionally, NGAL has been reported to be predictive 48 h prior to the actual time of injury; therefore, renal replacement therapy can be planned earlier(Cruz,et al.2010)

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