Additional file 3: of Hyaluronic acid is associated with organ dysfunction in acute respiratory distress syndrome

Circulating and alveolar hyaluronic acid (HA) levels are positively correlated within 48 hours of diagnosis (A) of acute respiratory distress syndrome (ARDS) but not at days 4 ± 1 (B) or 8 ± 1 (C). This figure provides the reader with graphical representation and corresponding statistical analysis of the correlation between HA levels at various sample collection times during the study. As discussed in the text, there is weak correlation at day 0 and no correlation at days 4 and 8, which, per our hypothesis, supports independent compartmentalized effects or processing of HA. (DOCX 262 kb

Additional file 2: of Hyaluronic acid is associated with organ dysfunction in acute respiratory distress syndrome

Sequential organ failure assessment score. Description: This table provides the reader with information regarding what components contribute to and how to calculate the composite lung injury score. (DOCX 102 kb

Le Courrier

19 avril 18501850/04/19 (N109)

Additional file 1: Table S1. of Associations between single nucleotide polymorphisms in the FAS pathway and acute kidney injury

Genes (n = 45) in the Fas/Fas ligand (FasL) pathway characterized using tag single nucleotide polymorphisms (tagSNPs). Table S2. TagSNPs genotyped using Illumina GoldenGate genotyping assays. Table S3a. Outcomes by acute kidney injury (AKI) stage in Caucasians. Table S3b. Outcomes by AKI stage in African-Americans. Table S4. Characteristics of African-Americans in the Fluid and Catheter Treatment Trial (FACTT) with genotype data (n = 88). Table S5a. Odds ratios for AKI associated with individual SNPs among Caucasians (comparing no AKI vs. stage 1–3 AKI). Table S5b. Odds ratios for AKI associated with individual SNPs among Caucasians (comparing no AKI vs. stage 2–3 AKI). Table S6a. Odds ratios for AKI associated with individual SNPs among African-Americans (comparing no AKI vs. stage 1–3 AKI). Table S6b. Odds ratios for AKI associated with individual SNPs among African-Americans (comparing no AKI vs. stage 2–3 AKI). Table S7a. Fas/FasL pathway polymorphisms in the FACTT associated (p <0.05) with AKI susceptibility in African-American subjects from the FACTT. Table S7b. Fas/FasL pathway polymorphisms in the FACTT associated (p <0.05) with AKI (stage 2–3 vs. stage 0) in African-Americans (Stage 1 excluded). (XML 972 bytes

Additional file 1: of Association of markers of endothelial dysregulation Ang1 and Ang2 with acute kidney injury in critically ill patients

Pairwise correlation matrix of endothelial and inflammatory biomarkers. Pearson’s correlation coefficient (ρ) was used to estimate the magnitude of the linear correlation between log-transformed biomarker concentrations. (DOCX 15 kb

Additional file 2: of Association of markers of endothelial dysregulation Ang1 and Ang2 with acute kidney injury in critically ill patients

Associations of biomarkers with AKI (Stage 2–3 versus no AKI). For associations of biomarkers with the risk of AKI, we examined associations of biomarkers with severe AKI, to increase specificity of the outcome definition. (DOCX 15 kb

Additional file 1: of Circulating levels of soluble Fas (sCD95) are associated with risk for development of a nonresolving acute kidney injury subphenotype

Supplemental data file that includes supplementary tables referenced in the text. (DOCX 32 kb

Additional file 1: Table S1. of Acute kidney injury subphenotypes based on creatinine trajectory identifies patients at increased risk of death

Definitions of AKI subphenotypes and unadjusted relative risk of trajectory with hospital mortality in group 1 (trauma). Table S2. Patient characteristics in group 1 (trauma) by AKI subphenotypes. Table S3. Patient characteristics in group 2 (mixed medical and surgical) by AKI subphenotypes. Table S4. Patient characteristics with a resolving AKI subphenotype in group 2. Figure S1. Flowchart of patient inclusion. (DOCX 46 kb