In the present study, a LPS-induced model of endotoxemia was utilized in wild-type (WT), PAI-1 deficient (PAI-1−/−) mice, and mice expressing a mutant PAI-1 with significantly diminished Vn binding capacity (PAI-1R101A/Q123K) [21] in order to gain insights into the role of PAI-1-Vn interaction in response to septic AKI. Here, VTN is linked to serum lipopolysaccharide activity.