Abstract. Leptospirosis is a common disease in tropical countries, and the kidney is one of the main target organs. Membrane proteins of Leptospira are capable of causing endothelial damage in vitro, but there have been no studies in humans evaluating endothelial glycocalyx damage and its correlation with acute kidney injury (AKI). We performed a cohort study in an outbreak of leptospirosis among military personnel. AKI was diagnosed in 14 of 46 (30.4%) patients. Leptospirosis was associated with higher levels of intercellular adhesion molecule-1 (ICAM-1; 483.1 ± 31.7 versus 234.9 ± 24.4 mg/L, P 0.001) and syndecan-1 (73.7 ± 15.9 versus 21.2 ± 7.9 ng/mL, P 0.001) compared with exposed controls. Patients with leptospirosis-associated AKI had increased level of syndecan-1 (112.1 ± 45.4 versus 41.5 ± 11.7 ng/mL, P = 0.021) and ICAM-1 (576.9 ± 70.4 versus 434.9 ± 35.3, P = 0.034) compared with leptospirosis patients with no AKI. Association was verified between syndecan-1 and ICAM-1 with serum creatinine elevation and neutrophil gelatinaseassociated lipocalin (NGAL) levels. This association remained even after multivariate analysis including other AKIassociated characteristics. Endothelial injury biomarkers are associated with leptospirosis-associated renal damage.

Background Acute kidney injury (AKI) is a significant complication in patients with cancer, and nephrotoxic drugs are among the most common causes of AKI. To date, there is no study evaluating the potential role of renal biomarkers in children receiving nephrotoxic chemotherapy. Methods A prospective study was conducted in children receiving methotrexate (MTX) or platinum-based treatment. Urinary kidney injury molecule-1 (KIM-1) was measured 24 h after the initiation of the chemotherapy infusion, and serum creatinine (sCr) was measured prior to drug infusion and at 24, 48, 72, and 96 h, 1 and 2 weeks, and 3 months postinitiation of treatment. Results A total of 64 children were evaluated, of whom 21 (32.8 %) developed AKI. The majority had AKI stage 1 (n= 12, 57.1 %) and only one developed AKI stage 3. Median values of urinary KIM-1 were higher in patients with AKI than in those without AKI [10.7, interquartile range (IQR) 1.6-17.9 vs. 4.3 (IQR 1.3-6.1) ng/mg creatinine; p<0.01]. Urinary KIM-1 showed good discrimination for AKI in patients receiving nephrotoxic chemotherapy, with an area under the receiver operator characteristic curve for AKI up to 1 week later of 0.82 (95% confidence interval 0.66-0.95). Even when measured only 24 h after drug infusion, urinary KIM-1 still showed good discrimination to predict persistent renal impairment three months later. Conclusion Urinary KIM-1 measured 24 h after the start of drug infusion has the potential to detect early AKI in pediatric patients treated with MTX or platinum-class drugs.