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A Modified Two Kidney One Clip Mouse Model of Renin Regulation in Renal Artery Stenosis
Published on: October 26, 2020
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Soluble urokinase receptor is a kidney-specific vasoconstrictor
Sebastian Buhl Rasmussen1, Rasmus Bo Lindhardt1, Georgina Gyarmati2
1Department of Anaesthesiology and Intensive Care, Odense University Hospital, Odense, 5000, Denmark; Department of Clinical Research, Faculty of Health Sciences, University of Southern Denmark, Odense, 5230, Denmark.
Ebiomedicine
|November 4, 2025
Summary
Soluble urokinase plasminogen activator receptor (suPAR) causes kidney blood vessel constriction, increasing acute kidney injury risk. This study reveals suPAR
Area of Science:
- Nephrology
- Immunology
- Vascular Biology
Background:
- Soluble urokinase plasminogen activator receptor (suPAR) is linked to kidney disease.
- Previous research focused on suPAR's effects on kidney epithelial cells.
- suPAR's impact on renal vasculature was previously unknown.
Purpose of the Study:
- To investigate the effects of suPAR on renal blood flow and glomerular dynamics.
- To determine if suPAR has a specific impact on kidney vasculature.
Main Methods:
- Utilized a translational approach combining clinical data, ex vivo kidney perfusion, and in vivo mouse imaging.
- Analyzed a propensity-score-matched cardiac surgery cohort.
- Employed intravital multiphoton microscopy in mice.
Main Results:
- High suPAR levels correlated with lower kidney function (eGFR) and increased acute kidney injury (AKI) occurrence.
- suPAR induced immediate renal blood flow reduction and calcium responses in renal contractile cells.
- These vasoconstrictive effects were kidney-specific and blocked by an anti-uPAR antibody.
Conclusions:
- suPAR acts as a kidney-specific vasoconstrictor, a novel class of innate immune mediators.
- suPAR-induced renal vasoconstriction contributes to AKI in high-risk patients.
- This finding has direct implications for understanding and managing AKI.
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