26rhk048 10.3205/26rhk048 urn:nbn:de:0183-26rhk0480 Meeting Abstract Claßen Claßen Paul P

I. Medizinische Klinik und Poliklinik, Universitätsmedizin der Johannes Gutenberg-Universität Mainz, Mainz, Deutschland

author Meineck Meineck Myriam M

I. Medizinische Klinik und Poliklinik, Universitätsmedizin der Johannes Gutenberg-Universität Mainz, Mainz, Deutschland

author Filippi Filippi Edoardo E

I. Medizinische Klinik und Poliklinik, Universitätsmedizin der Johannes Gutenberg-Universität Mainz, Mainz, Deutschland

author Marini Marini Federico F

IMBEI, Universitätsmedizin der Johannes Gutenberg-Universität Mainz, Mainz, Deutschland

author Weinmann-Menke Weinmann-Menke Julia J

Innere Medizin X: Klinik für Nephrologie, Universitätsklinikum Heidelberg, Heidelberg, Deutschland

author German Medical Science GMS Publishing House

Düsseldorf

610 20260909 engl This is an Open Access article distributed under the terms of the Creative Commons Attribution 4.0 License. Dieser Artikel ist ein Open-Access-Artikel und steht unter den Lizenzbedingungen der Creative Commons Attribution 4.0 License (Namensnennung). M0656 048 Deutsche Gesellschaft für Rheumatologie Deutsche Gesellschaft für Orthopädische Rheumatologie Gesellschaft für Kinder- und Jugendrheumatologie 54. Kongress der Deutschen Gesellschaft für Rheumatologie und Klinische Immunologie (DGRh), 36. Jahrestagung der Gesellschaft für Kinder- und Jugendrheumatologie (GKJR), 40. Jahrestagung der Deutschen Gesellschaft für Orthopädische Rheumatologie (DGORh) Deutscher Rheumatologiekongress 2026 Experimentelle & Translationale Rheumatologie Leipzig 20260909 20260912 ET.24 TextIntroduction: Lupus nephritis is characterized by inflammatory and tissue remodeling processes in the kidney, but the metabolic pathways associated with renal disease remain incompletely understood. Among these, nucleotide and purine metabolism may contribute to inflammatory stress and tissue injury. We therefore used an integrated multi-omics approach to investigate whether purine-related metabolic pathways are altered in kidneys from lupus-prone mice.Methods: Kidneys from lupus-prone MRL Faslpr mice and congenic MRL Fas+/+ control mice were analyzed using untargeted metabolomics, proteomics and bulk RNA sequencing. Differential abundance and expression analyses were performed in each omics layer, followed by pathway and gene set enrichment analyses. Cross-platform integration was used to identify metabolic pathways consistently altered in lupus-prone kidneys.Results: Across metabolomic, proteomic and transcriptomic datasets, lupus-prone kidneys showed a clear separation from controls and a strong inflammatory transcriptional background. Within this context, integrated analyses highlighted purine and nucleotide metabolism as a prominently altered pathway. Metabolomic profiling indicated accumulation of metabolites consistent with enhanced purine turnover, while proteomic and transcriptomic analyses supported changes in enzymes and regulatory programs linked to nucleotide catabolism and related metabolic stress responses. These alterations were accompanied by signatures suggestive of disturbed redox balance and broader metabolic adaptation in diseased kidneys. Overall, the findings support the presence of coordinated purine-associated metabolic remodeling in the lupus-prone kidney.Conclusion: Integrated kidney multi-omics identifies altered purine metabolism as a prominent feature of lupus-prone mouse kidneys. These findings suggest that purine-related pathways may contribute to the metabolic phenotype of lupus nephritis and provide a basis for further mechanistic studies. 0 0 0 0