02; 95% CI 1.50–12.0; P = 0.0051). As compared with the group without early AKI, the urinary L-FABP level in early AKI group was significantly higher not only on the day of SCT

but also at the baseline. Then, ROC analysis demonstrated the urinary L-FABP level at baseline had good discriminative ability for the early AKI. Conclusion: One-quarter of allogeneic Kinase Inhibitor Library SCT recipients developed the early AKI, which was linked with increased risk of their short-term mortality. Antecedent kidney damage, which can be identified by urinary L-FABP concentration, may portend the emergence of early-onset AKI. YAMASHITA TETSUSHI1, DOI KENT2, TSUKAMOTO MAKI1, NANGAKU MASAOMI1, YAHAGI NAOKI2, NOIRI EISEI3 1Department of Nephrology and Endocrinology, Graduate school of Medicine, The University of Tokyo; selleck chemicals llc 2Department of Critical Care Medicine, The University of Tokyo Hospital; 3Department of Hemodialysis and Apheresis, The University of Tokyo Hospital Introduction: Tissue inhibitor of metalloproteinases-2 (TIMP-2) has recently been reported to detect severe AKI better than new AKI biomarkers that have recently introduced to the clinical such as NGAL. Methods: This study enrolled 98 patients who were admitted to the adult mixed ICU of The University of Tokyo Hospital from July 2011 to October 2011 by consecutive sampling. Urine TIMP-2 and NAG, and plasma NGAL and IL-6 were measured

on ICU admission. This Tryptophan synthase study was aimed to evaluate whether these biomarkers

could predict AKI and its severity, and mortality by ROC analysis. Results: AKI occurred in 42 (42.9%) patients including 27 (27.6%) severe AKI (KDIGO stage 2 or 3). The area under the ROC curve for each marker was shown in Table. Forty one (41.8%) patients was complicated with sepsis, including 19 (19.4%) severe AKI. In accordance with previous reports, plasma NGAL and IL-6 were increased by sepsis, however urine TIMP-2 and NAG was increased not by sepsis but by the presence of severe AKI (Figure). In-hospital mortality was 15.3% in this cohort and urine TIMP-2 and NAG, and plasma NGAL were significantly higher in the non-survivors than the survivors, whereas plasma IL-6 was not significantly associated with mortality. Conclusion: A new urine biomarker of TIMP-2 is increased especially in severe AKI and associated with mortality. Sepsis appeared to have a smaller impact on urine TIMP-2 and NAG compared with plasma NGAL and IL-6. This distinct feature of biomarkers will enable to evaluate the contribution of sepsis to the development of AKI. TANAKA YUKI1, KUME SHINJI1, MAEDA SHIRO2, OSHIMA ITSUKI3, ARAKI HISAZUMI1, ISSHIKI KEIJI1, ARAKI SHIN-ICHI1, UZU TAKASHI1, MAEGAWA HIROSHI1 1Department of Medicine, Shiga University of Medical Science, Japan; 2Laboratory for Endocrinology, Metabolism and Kidney diseases, RIKEN Center for Integrative Medical Science, Japan; 3Discovery Research Laboratories, Shionogi & Co., Ltd.