Molecular mechanisms of trauma-induced acute kidney injury: Inflammatory and metabolic insights from animal models

David M. Burmeister, Belinda I. Gómez, Michael A. Dubick*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

33 Scopus citations

Abstract

Trauma-induced acute kidney injury (AKI), such as after hemorrhagic shock (HS) or burn, remains a significant problem in the intensive care unit and is associated with increased mortality. The pathophysiology that drives AKI post-trauma is multi-factorial, and includes both inflammatory and metabolic alterations. Identifying the systemic profile that contributes to AKI is crucial not only for early diagnosis, but also for identifying treatments that improve kidney function and maintaining long-term patient health. In an effort to elucidate this molecular pathophysiology researchers have utilized a variety of animal models including chemically-induced (i.e., cisplatin), blocking renal perfusion (i.e., arterial clamping) and inducing burn or HS. As the latter burn and HS models are unequivocally applicable to studying AKI in the context of traumatic injury, this review will summarize the inflammatory and metabolic insights associated with AKI gained with these animal models. Moreover, novel therapeutic strategies brought forth with these models will be discussed.

Original languageEnglish
Pages (from-to)2661-2671
Number of pages11
JournalBiochimica et Biophysica Acta - Molecular Basis of Disease
Volume1863
Issue number10
DOIs
StatePublished - Oct 2017
Externally publishedYes

Keywords

  • Acute kidney injury
  • Animal models
  • Burn
  • Hemorrhage
  • Inflammation
  • Oxidative stress

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