Related Experiment Video
Updated: Jun 28, 2025

09:02
A Large Animal Model for Acute Kidney Injury by Temporary Bilateral Renal Artery Occlusion
Published on: February 2, 2021
4.5K
Complement activation in wasp venom-induced acute kidney injury
Rui Cheng1,2, Liang Xu2, Jianhua Gong2
1School of Medicine, Wuhan University of Science and Technology, Wuhan, China.
Renal Failure
|April 21, 2024
Summary
Complement activation significantly contributes to acute kidney injury (AKI) from wasp stings. Depleting complement pathways with cobra venom factor (CVF) reduced kidney damage, confirming complement
Area of Science:
- Nephrology
- Immunology
- Toxicology
Background:
- Complement activation is implicated in various kidney injuries.
- The specific role of complement in wasp venom-induced acute kidney injury (AKI) is not well understood.
Purpose of the Study:
- To identify the complement pathways involved in wasp venom-induced AKI.
- To investigate the effect of complement depletion on wasp venom nephrotoxicity.
Main Methods:
- Utilized a complement-depleted mouse model using cobra venom factor (CVF).
- Compared kidney pathology and blood urea nitrogen (BUN) levels between AKI and CVF+AKI groups.
- Assessed renal expression of key complement components (C3, C5, C1q, FB, MBL, C5b-9).
Main Results:
- Complement depletion via CVF improved kidney pathology and reduced BUN levels in wasp venom-induced AKI.
- Wasp venom induced upregulation of multiple complement components (C3, C5, C1q, FB, MBL, C5b-9) in renal tissue.
- Complement depletion significantly decreased these upregulated complement markers.
Conclusions:
- Complement activation occurs via all three major pathways in wasp venom-induced AKI.
- Complement plays a critical role in the pathogenesis of wasp venom-induced nephrotoxicity.
- Complement depletion offers a potential therapeutic strategy for wasp venom-induced kidney injury.
Related Concept Videos
Inflammation
53.4K
Overview
53.4K
Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors
627
Angiotensin-converting enzyme (ACE), a vital component of the renin-angiotensin-aldosterone system, is abundant in lung endothelial cells. ACE converts the inactive decapeptide, angiotensin I, into the active octapeptide, angiotensin II. This potent vasoconstrictor narrows blood vessels, increasing resistance to blood flow and elevating blood pressure. Angiotensin II also stimulates aldosterone production, encouraging kidney cells to reabsorb more sodium and water from urine, thereby increasing...
627

