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Introduction: Stem cell transplantation (SCT) involves a great risk of acute kidney injury (AKI), which is largely committed to fatality derived from SCT. Liver-type fatty acid-binding protein (L-FABP) is a 15kDa protein expressed in human renal proximal tubular cells, and is shed into urine in response to renal tissue ischemia or oxidative stress. Urinary L-FABP (uL-FABP) has been reported to be not only a sensitive biomarker to detect incipient AKI but also a potential marker for something more than a measure of renal insult. This study addressed utility of uL-FABP, as it has not been fully understood on the clinical platform of SCT. Patients and Methods: A prospective cohort study was conducted in 81 patients who received allogeneic SCT in our hospital from April 2009 to March 2012 (median age, 49 years; median [range] follow-up period, 771 [2-1923] days). All had hematological malignancies, and were recipients of the first SCT. Associations of increased uL-FABP before executing conditioning therapy (at baseline) and clinical outcomes including incidence of AKI, non-relapse mortality (NRM), and overall survival (OS) were investigated. AKI was defined, based on the creatinine (Cr) criteria of the 2013 Kidney Disease Global Outcomes. AKI that developed within the first 30 days after SCT was considered in this study. The recipients were stratified into an elevated and a normal uL-FABP group at baseline, according to the reference value for healthy adult individuals (8.5µg/gCr). Hazard ratio (HR) with its 95% confidence interval (CI) of uL-FABP elevation was calculated for OS using the Cox proportional hazard model and for NRM using the Fine-Gray proportional hazards model, adjusted for confounders which had P -values ≤ 0.2 in univariate analyses. Results: Patients had been diagnosed with acute myeloid leukemia (n = 36), acute lymphoid leukemia (n = 23), myelodysplastic syndrome (n = 17), and myeloproliferative neoplasm (n = 5). The elevated and normal uL-FABP groups included 17 (21%) and 64 (79%) patients, respectively. The proportion of high disease risk was significantly greater in the elevated than in the normal uL-FAB P group (70.6 % vs. 31.3%, P = 0.005). There were no significant differences in age, serum Cr level, and the proportion of gender, hematopoietic cell transplantation comorbidity index (HCT-CI) ≥3, myeloablative conditioning regimen, stem-cell sources (bone marrow, peripheral blood, cord blood), related donor type and matched human leukocyte antigen compatibility. AKI emerged in 28 recipients (34.6%) at day 30? following SCT (median [range], 14 [0-30] days). The cumulative incidence [95% CI] of AKI was significantly greater in the elevated than in the normal uL-FABP group (64.7% [36-83.1 %] vs. 26.6% [16.4-37.8 %], P Conclusions: uL-FABP is a simple and non-invasive measurement to target patients at increased risk of AKI, NRM and OS following allogeneic SCT. The presence of antecedent subclinical renal injury, which can be detected by uL-FABP elevation at baseline, may provide prognostic information beyond renal outcome after allogeneic SCT. Disclosures No relevant conflicts of interest to declare.

Abstract 1998 Background: Microalbuminuria is a risk factor for the development of chronic kidney disease (CKD), cardiovascular disease and mortality in the general population. We studied if the incidence of microalbuminuria following hematopoietic stem cell transplantation (SCT) could be a warning sign of the future CKD and all-cause mortality. Method: A 1-year prospective cohort study was conducted in 29 patients (46.3±12.5 years) receiving allogeneic myeloablative SCT. Patients with prevalent CKD and those who died by 1 month after SCT were excluded from the cohort. Albumin to creatinine ratio (ACR) in a morning urine sample was consecutively measured before conditioning therapy (baseline), at the time of SCT, days 7 and 14, and 1 month after SCT. Microalbuminuria was defined as ACR ≥30mg/girl. CKD was defined as a decrease in estimated glomerular filtration rate (eGFR) less than 60 ml/min/1.73m2, sustained at least for 3 months. Cumulative incidence of CKD or mortality or both was assessed by the Kaplan-Meier method. Multivariate Cox regression analysis was used to calculate the hazard ratio (HR) of developing these outcomes within 1 year, adjusted for covariates with clinical and statistical significance. Results: The prevalence of microalbuminuria was 6.9% at baseline, and increased to 62.1% at the day of SCT. It varied among the time points; 62.1% on day 7, 48.3% on day 14 and 51.7% on 1 month, respectively. Mortality within 1 year was 27.6%. Cumulative incidence of CKD or mortality or both was significantly higher in the group with □emicroalbuminuria on 1 month' than in the opposite. [figure1] In addition, the presence of □emicroalbuminuria on 1 month' was significantly associated with each outcome: for CKD, HR 14.5, 95% confidence interval (CI) 2.88 to 121, P=0.0006; for death, HR 11.7, 95% CI 1.58 to 252, P=0.0138; for either CKD or death, HR 16.6, 95% CI 3.79 to 151, P=0.0001, respectively. Conclusion: The incidence of microalbuminuria following SCT is a promising predictor of the development of CKD and short-term mortality. Disclosures: No relevant conflicts of interest to declare.