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

Toshiaki Iba, Julie Helms, Cheryl L. Maier, Marcel Levi, Ecaterina Scarlatescu, Jerrold H. Levy

Research output: Contribution to journalReview articleAcademicpeer-review

2 Citations (Scopus)


Inflammation 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 thromboinflammatory response may result in multiorgan dysfunction. Sepsis-associated acute kidney injury (AKI) is a significant contributor to patient morbidity and mortality. The connection between AKI and thromboinflammation is largely due to unique aspects of the renal vasculature. Specifically, the interaction between blood cells with the endothelial, glomerular, and peritubular capillary systems during thromboinflammation 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 sepsis-induced coagulopathy, thromboinflammation 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 thromboinflammation in AKI pathogenesis and details innovative vascular-targeting therapeutic strategies.
Original languageEnglish
Pages (from-to)1530-1540
Number of pages11
JournalJournal of thrombosis and haemostasis
Issue number6
Early online date2024
Publication statusPublished - Jun 2024


  • acute kidney injury
  • anticoagulation
  • coagulopathy
  • inflammation
  • sepsis
  • thromboinflammation

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