To further elucidate the pathophysiological consequences of high blood suPAR levels on kidney function, tissue damage, and kidney tissue inflammation, we established an experimental polymicrobial sepsis model, comparing C57BL/6 WT, uPAR-knockout (uPAR-KO, deficient in suPAR), and a transgenic mouse strain artificially overexpressing full-length suPAR in blood (msuPAR1-OE). This evidence concerns the gene PLAUR and Sepsis.