Rodent models of AKI and AKI-CKD transition: an update in 2024

Research output: Contribution to journalReview articlepeer-review

Abstract

Despite known drawbacks, rodent models are essential tools in the research of renal development, physiology, and pathogenesis. In the past decade, rodent models have been developed and used to mimic different etiologies of acute kidney injury (AKI), AKI to chronic kidney disease (CKD) transition or progression, and AKI with comorbidities. These models have been applied for both mechanistic research and preclinical drug development. However, current rodent models have their limitations, especially since they often do not fully recapitulate the pathophysiology of AKI in human patients, and thus need further refinement. Here, we discuss the present status of these rodent models, including the pathophysiologic compatibility, clinical translational significance, key factors affecting model consistency, and their main limitations. Future efforts should focus on establishing robust models that simulate the major clinical and molecular phenotypes of human AKI and its progression.

Original languageEnglish (US)
Pages (from-to)F563-F583
JournalAmerican Journal of Physiology - Renal Physiology
Volume326
Issue number4
DOIs
StatePublished - Apr 2024

Keywords

  • cisplatin nephrotoxicity
  • renal ischemia-reperfusion
  • rhabdomyolysis
  • rodent model
  • sepsis

ASJC Scopus subject areas

  • Physiology
  • Urology

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