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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.
Please follow the instructions below to input your abstract title.
Abstract titles should be brief and reflect the content of the abstract.
Glomerulonephritis (GN) comprises a heterogeneous group of kidney disorders driven by immune-mediated inflammation and structural injury within the glomeruli. Thrombin, a serine protease central to both coagulation and inflammation, has emerged as a potential mediator of glomerular damage. Beyond its role in clot formation, thrombin activates protease-activated receptors (PARs), promoting pro-inflammatory, pro-coagulant, and profibrotic cascades within renal tissue. Despite its biological plausibility, the utility of thrombin as a clinical biomarker in GN remains underexplored. This study aimed to quantify urinary and serum thrombin levels in patients with GN and to determine their relationship with established clinical, biochemical, and histopathological indicators of disease activity and chronicity.
In this cross-sectional observational study, 72 adult patients with biopsy-confirmed GN and 40 healthy age- and sex-matched volunteers were enrolled. Urinary and serum thrombin concentrations were measured using standardized enzyme-linked immunosorbent assay (ELISA) kits. Additional measurements included urinary and serum levels of interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), and transforming growth factor-beta1 (TGF-β1). Renal biopsies were evaluated for both activity and chronicity indices by experienced nephropathologists blinded to biomarker levels. Spearman’s rank correlation was used to assess associations between biomarkers and clinical/histological parameters. Comparisons between groups were performed using non-parametric statistical methods with a significance threshold of p<0.05.
Urinary thrombin levels were significantly elevated in GN patients (median 9.4 ng/ml; IQR 2.1–15.3) compared to healthy controls (median 0.38 ng/ml; IQR 0.2–0.7), p=0.013. Serum thrombin concentrations did not differ significantly between groups (p=0.623). Thrombinuria was detected in 80.6% of GN patients and showed moderate to strong positive correlations with 24-hour proteinuria (r=0.514; p=0.013), urinary IL-6 (r=0.438; p=0.021), and TNF-α (r=0.372; p=0.037). Conversely, significant inverse correlations were observed between urinary thrombin and urinary TGF-β1 (r=–0.534; p=0.028), as well as the chronicity index derived from renal biopsies (r=–0.783; p=0.006). Notably, serum thrombin levels were not correlated with either systemic cytokines or histological parameters, underscoring the specificity of thrombinuria for intrarenal processes.
Thrombinuria is a common and quantifiable feature in patients with GN, with robust associations to proteinuria, urinary pro-inflammatory cytokines, and histopathological indicators of active disease. These findings support the hypothesis that urinary thrombin may serve as a sensitive, non-invasive biomarker of glomerular inflammation and coagulopathy. Its inverse relationship with chronicity parameters suggests its potential role in distinguishing active from fibrotic lesions. Incorporating thrombinuria into clinical assessment tools may enhance disease monitoring and guide therapeutic decision-making. Longitudinal studies are warranted to evaluate its prognostic significance and responsiveness to treatment.
