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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.
Coagulation and complement systems interact, promoting inflammation and thrombosis, yet their involvement in chronic kidney disease (CKD) is not fully understood. This study aimed to clarify the relationship between the prothrombotic state and complement activity in the pathogenesis of CKD by studying a CKD cohort, public databases, and mouse models of kidney fibrosis. In addition, the therapeutic significance of nicotinamide (NAM), a precursor of NAD+ precursor with anti-inflammatory and antithrombotic properties, in modulating these pathways was demonstrated.
1) In a cohort of 71 CKD patients at our department, blood coagulation markers (i.e., fibrinogen and prothrombin time) and complement levels were analyzed to examine their correlations and associations with renal function parameters. 2) The Nephroseq database was used to explore the associations between coagulation- and complement-related genes in renal biopsy specimens. 3) In an adenine-induced nephropathy model (0.2% adenine diet), kidney samples were collected two weeks after NAM administration. The effects of NAM on the coagulation and complement pathways, as well as on innate immune responses, were evaluated.
In our CKD cohort, high plasma fibrinogen and low prothrombin time were independently correlated with high serum complement C3 and C4 after adjustment for age and renal function. Moreover, gene expression analysis of CKD renal tissues in the Nephroseq databases showed a positive correlation between fibrinogen β chain and C3 expression levels. Finally, tissue factor (factor III), fibrinogen, and C3 deposition and the genes related to coagulation and complement cascades were upregulated in fibrotic kidneys of mice. NAM improved renal function and histological injury scores in adenine-induced nephropathy. KEGG pathway analysis based on RNA sequencing identified a significant inhibition of the coagulation and complement cascades following NAM administration. Moreover, NAM suppressed innate immune responses linked to the prothrombotic state, including inflammasome activation and neutrophil extracellular trap formation.
The coagulation and complement cascades were elevated in the pathogenesis of CKD and may contribute to both kidney injury and cardiovascular risks. Our findings uncover a novel mechanism through which NAM may exert renoprotective effects, supporting its potential therapeutic application in CKD. This study was previously presented at the Annual Meeting of the Japanese Society of Nephrology, 2025.
