Kidney Fibrosis
Kidney Fibrosis - 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.
08:19
The Mouse Isolated Perfused Kidney Technique
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Cited by 24 •
2016
The mouse isolated perfused kidney (MIPK) is a technique for keeping a mouse kidney under ex vivo conditions perfused and functional for 1 hr. The buffers and surgical technique are described in detail.
04:37
Unilateral Ureteral Obstruction Model for Investigating Kidney Interstitial Fibrosis
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Cited by 1 •
2025
This protocol describes a method for inducing unilateral ureteral obstruction (UUO) in mice to study the progression of tissue fibrosis in obstructive nephropathy. It includes surgical procedures, post-operative care, and methods for fibrosis assessment.
01:45
Kidney Structure
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2019
The kidneys are two large bean-shaped organs located in the upper abdomen. They filter the blood several times a day to remove toxins and rebalance water and electrolytes of the circulatory system via the renal veins. The kidneys receive blood directly from the heart via the renal arteries. These arteries enter the kidney at the hilum, the concave surface of the bean, where they branch and divide into smaller vessels and capillaries. The renal cortex is the thick outer layer of the kidney. It...
10:42
Normothermic Machine Perfusion of Rat Kidneys for Transplantation
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2026
This protocol describes the ex vivo normothermic machine perfusion of a rat kidney for subsequent transplantation into a recipient rat.
FAQs
Persistent injury and repeated inflammation activate renal fibroblasts and related cell populations. These cells can become myofibroblasts, a more matrix-producing state, and increase production of extracellular matrix proteins such as collagen. This cellular shift connects ongoing tissue damage with progressive structural remodeling in the kidney.
Excess extracellular matrix accumulates in the renal interstitial space and changes the organization of kidney tissue. The resulting remodeling can disrupt tubular and vascular function, reducing nephron performance. As these structural effects continue, filtration may become impaired, linking tissue-level scarring with declining renal function.
Fibrotic remodeling provides a pathway through which persistent kidney injury can progress toward organ failure. Its importance in chronic kidney disease lies in the cumulative loss of effective nephron performance and filtration. For medicine, this makes fibrosis a relevant target for research intended to slow disease progression and preserve renal function.
Biomarkers can help researchers identify and characterize fibrotic disease processes associated with persistent renal injury. In this context, they support investigation of disease mechanisms and may help evaluate whether an antifibrotic strategy is influencing the course of tissue remodeling. Their value is therefore tied to both biological understanding and treatment research.
A supported investigation can connect several observations: persistent injury and inflammation, activation of renal fibroblasts, transformation toward matrix-producing myofibroblasts, and collagen accumulation in the interstitial space. Researchers can then relate these changes to tubular, vascular, nephron, and filtration outcomes while assessing possible biomarkers or antifibrotic approaches.
Antifibrotic strategies are studied according to whether they could slow the remodeling associated with chronic kidney disease and help preserve renal function. Evaluation focuses on the fibrosis-related cellular and matrix changes, as well as their consequences for nephron performance and filtration. This approach connects molecular mechanisms with clinically relevant kidney outcomes.