The role of thromboinflammation in acute kidney injury among patients with septic coagulopathy

In flammation and coagulation are critical self-defense mechanisms for mitigating infection that can nonetheless induce tissue injury and organ dysfunction. In severe cases, like sepsis, a dysregulated thromboin flammatory response may result in multiorgan dysfunction. Sepsis-associated acute kidney injury (AKI) is a signi ficant contributor to patient morbidity and mortality. The connection between AKI and thromboin flammation is largely due to unique aspects of the renal vasculature. Speci fically, the interaction between blood cells with the endothelial, glomerular, and peritubular capillary systems during thromboin flammation reduces oxygen supply to tubular epithelial cells. Previous studies have focused on tubular epithelial cell damage due to hypoxia, oxidative stress, and nephrotoxins. Although these factors are pivotal in acute tubular injury or necrosis, recent studies have demonstrated that AKI in sepsis encompasses a mixture of tubular and glomerular damage subtypes. In cases of sepsisinduced coagulopathy, thromboin flammation within the glomerulus and peritubular capillaries is an important pathogenic mechanism for AKI. Unfortunately, and despite the use of renal replacement therapy, the development of AKI in sepsis continues to be associated with high morbidity, mortality, and clinical challenges requiring alternative approaches. This review introduces the important role of thromboin flammation in AKI pathogenesis and details innovative vascular-targeting therapeutic strategies.