COMPLEMENT OVERACTIVATION IN aHUS IS ATTENUATED BY RENIN INHIBITION VIA INTERACTION WITH COMPLEMENT FACTOR H

Certificate Output Instructions

For best output, select "Paper Size" as "A4" and "Margin" as "0" or "None".

To save or print to PDF, please select Print Destination > Save as PDF, enable Background Graphics under "More Settings", then click "Save".

Presented the abstract " "
(Abstract co-author(s): )

Back

E-Poster Presentation

During the congress, E-Posters will be accessible to all participants on the congress website 24/7, as well as in the E-poster stations in the congress center.

Preparing your E-Poster

Please review the E-Poster format requirements carefully when preparing your E-Poster. Should your E-Poster not meet the mentioned requirements, it may not be displayed as described above.

E-Poster Submission Deadline

Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.

E-Poster Format Requirements

PDF file
Layout: Portrait (vertical orientation)
One page only (Dim A4: 210 x 297mm or PPT)
E-Poster can be prepared in PowerPoint (one (1) PowerPoint slide) but must be saved and submitted as PDF file.
File Size: Maximum file size is 2 Megabytes (2 MB)
No hyperlinks, animated images, animations, and slide transitions
Language: English
Include your abstract number
E-posters can include QR codes, tables and photos

E-Poster

Abstract Title *

COMPLEMENT OVERACTIVATION IN aHUS IS ATTENUATED BY RENIN INHIBITION VIA INTERACTION WITH COMPLEMENT FACTOR H

Please follow the instructions below to input your abstract title.

Abstract titles should be brief and reflect the content of the abstract.

The title will not be accepted if it exceeds 25 words.
Type in CAPITAL LETTERS.
Lowercase may be used for abbreviations only, for example, mRNA.

Co-author 1

Chu-qiao Wang chuqiaowangjo@163.com Peking University First Hospital Renal Division, Department of Medicine Beijing China *

Co-author 2

Yi-fang Hu yifanghu9325@hotmail.com Department of Nephrology Zhongshan Hospital of Xiamen University; School of Medicine, Xiamen University Xiamen China -

Co-author 3

Fei-fei Chen chenfeif16@163.com Beijing Anzhen Hospital, Capital Medical University Renal Division, Department of Medicine Beijing China -

Co-author 4

Ying Tan tanying@bjmu.edu.cn Peking University First Hospital Renal Division, Department of Medicine Beijing China -

Co-author 5

Ming-hui Zhao mhzhao@bjmu.edu.cn Peking University First Hospital Renal Division, Department of Medicine Beijing China -

Co-author 6

Co-author 7

Co-author 8

Co-author 9

Co-author 10

Co-author 11

Co-author 12

Co-author 13

Co-author 14

Co-author 15

Introduction

Atypical hemolytic uremic syndrome (aHUS) is driven by dysregulation of the alternative complement pathway. While renin overexpression has been proposed as a potential activator of the complement system, the associations between renin and complement activation in aHUS remains unclear.

Methods

Renin expression and complement activation in renal biopsy specimens from patients with aHUS were assessed. We then utilized two distinct mouse models of aHUS mouse model to evaluate the effect of renin inhibition and complement activation. In addition, we performed proximity ligation assay, solid base binding assay and surface plasmon resonance to characterize the interaction between renin and complement factor H (CFH). A functional assay was used to assess the impact of renin on CFH regulatory activity.

Results

Renin expression was significantly elevated in aHUS, especially postpatrum aHUS, compared to controls. Renin inhibition in aHUS mice significantly alleviated proteinuria and complement activation. We validated the direct binding between renin and CFH. Renin binds to the regulatory site of CFH, impairing its complement-inhibitory function.

Conclusion

This study identifies a novel mechanism by which renin promotes complement activation in aHUS via direct interaction with CFH, which may serve as a potential therapeutic strategy for aHUS.

Kewords