Related Experiment Video
Updated: Jul 27, 2026

Renal Ischaemia Reperfusion Injury: A Mouse Model of Injury and Regeneration
Published on: June 7, 2014
The pathology of chronic renal ischemia
1Department of Pathology, State University of New York, Syracuse, USA.
Abstract:
Chronic ischemia may cause end stage renal disease, especially in older patients with atherosclerotic renal artery stenosis. Examining the pathology of the ischemic kidney is a fundamental first step toward understanding the mechanisms of this injury. In experimental renal hypoperfusion, there is evidence of a mixture of adaptive responses, tubular and endothelial cell damage and repair events. These processes are reflected in a wide spectrum of morphological changes that include atrophy, focal necrosis, epithelial regeneration, apoptosis, inflammation, interstitial fibrosis, and thrombosis. The most severe damage is seen in the outer medulla, a region with marginal oxygenation even in normal circumstances. In the usual clinical case, the effects of aging, pre-existent hypertension, and the process of atherosclerosis further complicate the pathological picture. Lesions related to these factors include arteriosclerosis, athero-emboli, various types of glomerulosclerosis, and severe tubulointerstitial damage leading to "atubular glomeruli" and regional cortical scarring (nephrosclerosis). In this article, some mechanisms determining the varied and complex pathological findings that may be observed in individual cases are outlined.
Insights
Chronic kidney ischemia, often seen in older adults with renal artery stenosis, can lead to end-stage renal disease. Understanding ischemic kidney pathology reveals complex cellular damage and repair mechanisms contributing to kidney disease progression.
Area of Science:
- Nephrology
- Pathology
- Cardiovascular Science
Background:
- Chronic ischemia is a significant factor in end-stage renal disease (ESRD), particularly in elderly patients with atherosclerotic renal artery stenosis.
- Understanding the pathological mechanisms of ischemic kidneys is crucial for comprehending kidney injury.
Purpose of the Study:
- To outline the mechanisms behind the varied and complex pathological findings in ischemic kidneys.
- To detail the cellular and morphological changes associated with renal hypoperfusion.
Main Methods:
- Review of experimental renal hypoperfusion models.
- Analysis of morphological changes in kidney tissue.
- Consideration of complicating factors like aging, hypertension, and atherosclerosis.
Main Results:
- Ischemic kidneys exhibit a spectrum of adaptive responses, cell damage (tubular, endothelial), and repair events.
- Morphological changes include atrophy, necrosis, regeneration, apoptosis, inflammation, fibrosis, and thrombosis.
- Severe damage is concentrated in the outer medulla; clinical cases show arteriosclerosis, athero-emboli, glomerulosclerosis, and tubulointerstitial damage.
Conclusions:
- The pathology of ischemic kidneys is complex, involving a mix of injury and repair processes.
- Factors like aging, hypertension, and atherosclerosis significantly alter the pathological landscape.
- Further understanding of these mechanisms is essential for managing ischemic kidney disease.
Related Concept Videos
Acute Kidney Injury I: Introduction
Acute Kidney Injury II: Pathophysiology
Acute Kidney Injury III: Clinical Manifestations
Chronic Kidney Disease I: Introduction
Chronic Kidney Disease III: Interprofessional Care
Ischemic Stroke ll: Pathophysiology

