Gene expression profiling of sepsis-associated acute kidney injury

Sepsis accounts for more than 50% of all acute kidney injury (AKI) cases, and the combination of sepsis and AKI increases the risk of mortality from sepsis alone. However, to the best of our knowledge, the specific mechanism by which sepsis causes AKI has not yet been fully elucidated, and there is no targeted therapy for sepsis-associated AKI (SA-AKI). The present study investigated gene expression profiles using RNA sequencing (RNA-Seq) and bioinformatics analyses to assess the function of differentially expressed genes (DEGs) and the molecular mechanisms relevant to the prognosis of SA-AKI. From the bioinformatics analysis, 2,256 downregulated and 3,146 upregulated genes were identified (false discovery rate <0.1 and fold-change >2). Gene Ontology analysis revealed that the genes were enriched in cellular metabolic processes, cell death and apoptosis. The enriched transcription factors were v-rel reticuloendotheliosis viral oncogene homolog A and signaling transducer and activator of transcription 3. The enriched microRNAs (miRNAs or miRs) among the DEGs were miR-30e, miR-181a, miR-340, miR-466d and miR-466l. Furthermore, the enriched pathways included toll-like receptor signaling, nod-like receptor signaling and the Janus kinase/STAT signaling pathway. In conclusion, the present study identified certain prognosis-related genes, transcription factors, miRNAs and pathways by analyzing gene expression profiles of SA-AKI using RNA-Seq, which provides some basis for future experimental studies.