Kidney Ischemia Model
Kidney Ischemia Model - Related Videos
09:09
Ischemia-reperfusion Model of Acute Kidney Injury and Post Injury Fibrosis in Mice
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Cited by 141 •
2013
We describe models of moderate and severe ischemia-reperfusion-induced kidney injury in which the mice undergo unilateral renal pedicle clamping followed by simultaneous or delayed contralateral nephrectomy, respectively. These models consistently give rise to renal dysfunction and post-injury fibrosis, but injury severity and survival are dependent on mouse background, age and surgical equipment.
02:34
Modeling Preservation Injury in Porcine Donor Kidney: A Procedure to Induce Graft Dysfunction by Subjecting Kidney to Prolonged Cold Ischemia
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2025
In this video, we describe a technique to induce preservation injury via the prolonged cold ischemic storage time in porcine donor kidney.
12:51
Murine Model of Hindlimb Ischemia
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Cited by 201 •
2009
The surgical procedure for induction of unilateral hindlimb ischemia is demonstrated, with confirmation of ischemia by laser Doppler perfusion imaging.
05:36
Kidney Procurement in a Preclinical Large Animal Model
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2025
Here, we present a protocol that details a surgical model for kidney procurement in a preclinical swine model for subsequent machine perfusion or transplantation.
09:24
An Anoxia-starvation Model for Ischemia/Reperfusion in C. elegans
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Cited by 4 •
2014
A protocol is described that uses anoxia/starvation in C. elegans to model ischemia/reperfusion. Functional outcomes include increased mortality, visible abnormalities in GFP-labeled neuronal processes, and impaired behavioral responses that require neuronal function.
FAQs
Reduced oxygen availability limits cellular respiration and lowers ATP production, leaving renal cells unable to sustain energy-dependent functions. The resulting energy deficit disrupts tubular activity and vascular regulation, allowing investigators to connect impaired oxygen delivery with tissue damage. These observations help clarify how early metabolic failure contributes to acute kidney injury before later inflammatory and vascular effects develop.
Restoring blood flow can intensify injury rather than simply reverse ischemic damage. Reperfusion is associated with oxidative stress, inflammation, and endothelial dysfunction, creating additional mechanisms of tissue injury after oxygen delivery returns. Separating ischemia from reperfusion in the experimental design helps researchers evaluate which responses arise during oxygen deprivation and which emerge during recovery of perfusion.
The model captures injury in both renal tubules and the vascular system. Tubular dysfunction reflects the consequences of oxygen and ATP loss, while vascular impairment can further disturb perfusion and limit effective recovery. Endothelial dysfunction is especially relevant during reperfusion because it links altered vessel behavior with inflammation and oxidative stress, broadening the analysis beyond damage to individual tubular cells.
An experimental setup can reproduce reduced or interrupted renal blood flow under controlled conditions and then examine the tissue response, including effects after reperfusion. Investigators may compare the consequences of oxygen deprivation with subsequent recovery-related injury, using the model to track functional disruption, tissue damage, and biological responses. The controlled framework supports consistent testing of mechanisms and interventions.
Researchers can use the system to examine biological signals associated with ischemia-reperfusion injury and identify potential biomarkers of acute kidney injury. The same framework permits evaluation of protective treatments or recovery strategies by comparing renal responses under controlled injury conditions. Results can indicate whether an intervention limits tissue damage, reduces harmful responses, or improves recovery after impaired perfusion.
Findings from the model provide context for renal injury associated with transplantation, surgery, shock, and other conditions that compromise kidney perfusion. Its value lies in reproducing a controlled version of the oxygen-delivery problem while allowing detailed study of tissue responses. This connection helps investigators relate experimental mechanisms to clinically relevant causes of acute renal damage and impaired recovery.