Identification of a Novel Urinary Biomarker for Interstitial Inflammation and Renal Prognosis in Kidney Diseases

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 *

Identification of a Novel Urinary Biomarker for Interstitial Inflammation and Renal Prognosis in Kidney Diseases

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

Kaho Yamasaki kahoyamasaki@chiba-u.jp Chiba University Nephrology Chiba Japan *

Co-author 2

Yusuke Kashiwagi ykashiwagi@chiba-u.jp Chiba University Nephrology Chiba Japan -

Co-author 3

Yuuki Yoshioka yuukiy@chiba-u.jp Chiba University Nephrology Chiba Japan -

Co-author 4

Yasuhiro Yoshimura yyoshimura@chiba-u.jp Chiba University Nephrology Chiba Japan -

Co-author 5

Hanae Wakabayashi hawakaba@chiba-u.jp Chiba University Nephrology Chiba Japan -

Co-author 6

Atsuhiro Taguchi ataguchi@chiba-u.jp Chiba University Nephrology Chiba Japan -

Co-author 7

Katsuhiko Asanuma kasanuma@chiba-u.jp Chiba University Nephrology Chiba Japan -

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

Histopathological evaluation plays a pivotal role in the diagnosis and therapeutic decision-making of kidney diseases. However, renal biopsy, which is indispensable for such evaluation, is invasive, limited to assessing only a small portion of the organ, and poses challenges for quantitative assessment. Therefore, the development of noninvasive and quantitative biomarkers that can reflect the global pathological status of the kidney is highly desirable. In particular, reliable markers that correlate with renal interstitial inflammation remain limited. In this study, we focused on substance X (SubX) and aimed to elucidate its clinical utility and biological significance in the management of kidney diseases.

Methods

We established a clinical cohort comprising 24 healthy individuals and 139 patients with various types of kidney diseases. Serum and urinary levels of SubX were quantified using ELISA. Statistical analyses were performed to assess correlations between SubX levels and renal pathological findings across defined histopathological categories, as well as to evaluate its diagnostic performance and prognostic value for renal outcomes. Finally, immunohistochemical analyses were conducted to identify SubX-expressing cells in healthy and diseased kidneys.

Results

Urinary SubX levels showed the strongest correlation with interstitial inflammation among all renal pathological parameters and demonstrated high diagnostic performance for its detection. Renal survival was significantly poorer in patients with high urinary SubX levels compared with those with low levels. Immunohistochemical analyses, together with reanalysis of a published single-cell RNA sequencing dataset, revealed markedly increased SubX expression in fibroblasts in cases with elevated urinary SubX, suggesting that these cells may represent a major source of SubX production.

Conclusion

These results suggest that urinary SubX is a promising noninvasive biomarker reflecting renal interstitial inflammation and disease progression. Its correlation with histopathological severity and apparent association with fibroblast expression highlight a potential role in kidney disease pathophysiology.

Kewords