Inflammation plays a critical role not only in development and progression of atherosclerosis but also in pathogenesis of the destabilization of atherosclerotic plaque that leads to ACS [1, 26] . Activation and degranulation of polymorphonuclear neutrophils and probably an underestimated critical components of an acute coronary inflammation event. Infiltrating macrophages and neutrophils participate in the transformation of stable coronary artery plaques to unstable lesions with a thin fibrous cap [27] . It has been repeatedly reported that thrombosed plaques were densely infiltrated by neutrophils and macrophages [28, 29] . Macrophages and neutrophils and some other types of leukocytes produce various proteolytic enzymes which facilitate the rupture of plaques by thinning and weakening their normally thick and firm cap [30, 31] . NGAL is one protein, that is, produced not only by the distressed kidney but also by activated neutrophils and by the vascular wall cells. Recent studies have shown that neutrophils are the main source of NGAL in blood [32, 33] .