Beschreibung:
<jats:p>Acute kidney injury (AKI) is a syndrome that may be caused by a number of different diseases. The existence of renal biomarkers that work for many kinds of AKI indicate that there may be an underlying common molecular pathway by which AKI causes progression of chronic kidney disease (CKD). By comparing six high‐quality microarray studies of renal gene expression after AKI in models of different diseases (gram negative sepsis, gram positive sepsis, ischemia‐reperfusion, malignant hypertension, rhabdomyolysis and cisplatin toxicity) a total of 5254 genes were differentially expressed in at least one of the AKI models. 66% we only found in one of the models showing that there are unique features to AKI depending on the precipitating disease. There were in‐common features in the form of four genes that were differentially expressed in all six models, 49 in at least five, and 215 were in‐common between at least four models. The in‐common genes included many of the known biomarkers and damage associated molecular patterns (DAMPs) indicating that these are an integral part of the molecular response to AKI of any etiology. The most connected gene in the network was MYC, which suggests that it may be a central regulator of renal gene expression in AKI. The outlining of this molecular network may be useful for understanding the progression from AKI to chronic kidney disease, but also for identifying new potential biomarkers.</jats:p><jats:p><jats:bold>Support or Funding Information</jats:bold></jats:p><jats:p>The study was supported by grants from the Swedish Heart and Lung Foundation, and the Swedish Society for Medical Research.</jats:p><jats:p>This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in <jats:italic>The FASEB Journal</jats:italic>.</jats:p>