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Updated: May 24, 2026

Technical Refinement of a Bilateral Renal Ischemia-Reperfusion Mouse Model for Acute Kidney Injury Research
Published on: November 3, 2023
Immunotherapy for acute kidney injury
Miriam Berry1, Menna R Clatworthy
1Division of Renal Medicine, Department of Medicine, University of Cambridge, Cambridge, UK.
Acute kidney injury (AKI), often caused by acute tubular necrosis (ATN), involves inflammation. Targeting NLRP3 inflammasome activation and IL-1β-mediated neutrophil recruitment may offer new immunotherapy for ATN.
Area of Science:
- Immunology
- Nephrology
- Pathophysiology
Background:
- Acute kidney injury (AKI) is a common clinical problem, frequently resulting from acute tubular necrosis (ATN).
- ATN often stems from reduced blood flow, seen in sepsis or renal transplantation.
- Current treatments for ATN are limited, highlighting the need for novel therapeutic strategies.
Purpose of the Study:
- To review recent advancements in understanding the immune system's response to cell death.
- To explore the relevance of these immune responses to the pathophysiology of ATN.
- To identify potential novel therapeutic targets for immunotherapy in ATN.
Main Methods:
- Review of current literature on immune responses in ATN.
- Analysis of the role of inflammasomes and inflammatory mediators.
- Focus on cell death pathways and their contribution to kidney injury.
Main Results:
- Inflammatory responses significantly impact ATN severity and patient outcomes.
- NLRP3 inflammasome activation is implicated in ATN pathogenesis.
- IL-1β-mediated neutrophil recruitment plays a crucial role in ATN.
Conclusions:
- Understanding immune system responses to cell death offers insights into ATN.
- NLRP3 inflammasome and IL-1β-driven neutrophil recruitment are key players in ATN.
- Targeting these inflammatory pathways presents promising avenues for ATN immunotherapy.
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