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Cellular and Molecular Mechanisms of AKI

Anupam Agarwal1, Zheng Dong2, Raymond Harris3

  • 1Division of Nephrology, and Nephrology Research and Training Center, Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama; Agarwal@uab.edu.

Journal of the American Society of Nephrology : JASN
|February 11, 2016
PubMed

Insights

This review examines acute kidney injury (AKI) mechanisms, emphasizing epithelial cell damage and interactions. Improved animal models and clinical trial designs are crucial for developing effective AKI treatments.

Area of Science:

  • Nephrology
  • Cellular Biology
  • Molecular Medicine

Background:

  • Acute kidney injury (AKI) involves complex cellular and molecular processes, particularly affecting kidney epithelial cells.
  • Ischemic AKI serves as a key model for studying these mechanisms and cell-cell interactions.

Purpose of the Study:

  • To review current evidence on cellular and molecular mechanisms of AKI.
  • To assess the clinical relevance of targets investigated in experimental AKI models.
  • To identify improvements needed for AKI animal models and translational clinical trials.

Main Methods:

  • Review of existing scientific literature on AKI.
  • Analysis of cellular and molecular pathobiology in ischemic AKI models.
  • Evaluation of preclinical models and translational strategies for AKI therapeutics.

Main Results:

  • Epithelial cell pathobiology and cell-cell interactions are central to AKI.
  • Current experimental models require enhancement for better clinical translation.
  • Comorbidities like diabetes, aging, obesity, cancer, and CKD significantly impact AKI susceptibility.

Conclusions:

  • Development of context-specific animal models is essential for human AKI research.
  • Harmonization between academia and industry is needed for effective preclinical testing.
  • Optimized translational clinical trial design is critical for AKI intervention development.
Keywords:
acute renal failurekidneypathophysiology of renal disease and progression

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