Circulation Journal Official Journal of the Japanese Circulation Society http://www. j-circ.or.jp ncreasingly in high-risk patients for renal failure, such as those who are aged or have diabetes mellitus or hypertension, acute kidney injury (AKI) often complicates cardiac surgery. The prevalence of AKI has been reported as up to 30% in the postoperative period 1 and thus associated with an increase in short-term mortality, regardless of the severity of AKI. 2 AKI is also associated with long-term mortality. 3 Therefore, preventing the development of AKI in such patients who undergo cardiac surgery has been a big challenge for us.
Article p 213AKI has been diagnosed by consensus-based classification and criteria such as RIFLE (Risk, Injury, Failure, Loss, and End stage) and AKIN (Acute Kidney Injury Network). These use incremental changes in the maximum serum creatinine level from baseline or hourly urine output for the diagnosis. However, an increase in serum creatinine merely reflects "the result" of decreased glomerular filtration rate (GFR) and can take several days to reach the steady state. Once AKI becomes established, we could give only limited treatment. Because the decline in GFR begins before the elevation in serum creatinine, earlier diagnosis of developing AKI has been a critical issue.The main mechanisms of AKI after cardiac surgery involve hemodynamic, atheroembolic, nephrotoxic, and inflammatory factors. Among them, AKI is largely attributed to acute ischemic tubular necrosis. In the peri-operative period, hemodynamic insults such as hypotension frequently precede the development of AKI. Acute ischemic damage of the tubular cells is followed by their detachment, which causes obstruction of the tubular lumen and subsequent decrease in the GFR. Classical markers of AKI, such as serum creatine, only detect the last stage of this process. There has been recent development of biomarkers that allow us to detect AKI in the early phase. These biomarkers, which include neutrophil gelatinase-associated lipocalin (N-GAL), kidney injury molecule-1, liver-type free fatty acid-binding protein (L-FABP) and interleukin-18, have shown potential benefit for early detection of AKI. 4 The biomarkers are classified into 3 types: (1) inflammatory, (2) renal tubular proteins that are excreted in to the tubular lumen after exposure to insult, and (3) surrogate markers of tubular injury. 5 These biomarkers could uncover the ongoing process of tubular damage that leads to decreased GFR (Figure).L-FABP is a 14-kDa cytoplasmic protein in the proximal tubules and it plays a physiological role in the cell through binding free fatty acid and might have a renoprotective action by reducing lipid peroxidation under ischemic conditions. 6 L-FABP might have potential benefit as a biomarker for early detection of AKI, because it reflects deteriorating renal microcirculation and is elevated in urine by secretion from the proximal tubular cells soon after ischemic insults. 7 In this issue of the Journal, Matsui et al 8 report the usefu...