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Updated: May 30, 2026
A Large Animal Model for Acute Kidney Injury by Temporary Bilateral Renal Artery Occlusion
Published on: February 2, 2021
The distant organ effects of acute kidney injury
1Department of Medicine, Johns Hopkins School of Medicine, Baltimore, Maryland, USA.
Abstract:
Despite the availability of renal replacement therapy, acute kidney injury (AKI) is associated with high mortality and morbidity. In humans, it is difficult to determine whether AKI is a cause or consequence of excess morbidity. In animal models, however, it is increasingly clear that AKI induces distant organ dysfunction. Identified pathways include inflammatory cascades, apoptosis, the induction of remote oxidative stress, and differential molecular expression. Specifically, growing evidence implicates renal injury as an instigator and multiplier of pulmonary, cardiac, hepatic, and neurologic dysfunction. Accurate identification of these pathways will be critical in developing targeted therapies to improve outcomes in AKI. The purpose of this review is to summarize both clinical and preclinical studies of AKI and its role in distant organ injury.
Insights
Acute kidney injury (AKI) causes organ damage beyond the kidneys. Understanding these pathways is key to developing new treatments for this serious condition.
Area of Science:
- Nephrology
- Pathophysiology
- Translational Medicine
Background:
- Acute kidney injury (AKI) presents significant mortality and morbidity challenges.
- Distinguishing AKI as a cause versus consequence of illness in humans is complex.
- Animal models demonstrate AKI's role in inducing dysfunction in distant organs.
Purpose of the Study:
- To review clinical and preclinical research on AKI.
- To elucidate AKI's role in distant organ injury.
Main Methods:
- Literature review of clinical studies.
- Literature review of preclinical (animal model) studies.
Main Results:
- AKI is increasingly recognized as a cause of distant organ dysfunction.
- Identified pathways include inflammation, apoptosis, oxidative stress, and molecular expression changes.
- Renal injury is implicated in pulmonary, cardiac, hepatic, and neurologic dysfunction.
Conclusions:
- AKI can instigate and exacerbate dysfunction in multiple organs.
- Identifying specific molecular pathways is crucial for targeted AKI therapies.
- Further research is needed to improve patient outcomes in AKI.
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