Back
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".
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.
EPO resistance and iron deficiency in CKD-related anemia are associated with an increase in inflammatory cytokines associated with the innate immune response, such as IL-6, IL-1, and TNF-α. Recently (Bandach et al, Sci Reports 2021) we reported that kidney fibrosis and anemia of CKD can be worsened or relieved when IL1 effects are enhanced or inhibited, respectively. The water lily Nuphar lutea plant has been widely used as a traditional remedy for the treatment of rheumatism, scars, pain, and more. Gopas et al (Cancer Biology Therapy 2009) extracted an active ingredient from the family of nupharidines, 6,6′-Dihydroxythiobinupharidine (DTBN), which showed anti-inflammatory properties, mainly through the inhibition of NF-κB. The purpose of this study was to test the effects of DTBN in a mouse model of CKD-associated anemia.
8 weeks old male C57BL/6 mice were divided into 3 groups: Control, CKD (induced by adenine diet) and CKD-DTBN. Animals were IP injected with saline-DMSO or 30 μg DTBN, every two days and sacrificed after 3 weeks from dietary intervention.
Serum urea (Fig. 1A) and kidney TGFβ mRNA (Fig. 1B) were significantly decreased in CKD-DTBN Vs CKD. Macrophage infiltration (Fig. 2A,C) and renal fibrosis (Fig. 2A,B) were ameliorated in CKD-DTBN Vs CKD. A significant improvement in systemic inflammation indices (blood lymphocytes (Fig. 3a), liver IL-6 (Fig. 3b) and CRP(Fig. 3C)), as well as kidney pSTAT3/STAT3 protein ratio (Fig. 3D), immunostainable NF-κB (Fig. 2A,D) and F4\80 (Fig. 3E), which were increased in CKD, were all decreased in CKD-DTBN. CKD anemia indices (hemoglobin (Fig.4A), hematocrit (Fig. 4B) and RBC (Fig. 4C) count) improved in CKD-DTBN Vs CKD. Kidney HIF-2α (Fig. 5A, B) and EPO mRNA (Fig. 5C) were significantly decreased in both uremic groups, but was unchanged in CKD- DTBN Vs CKD. However, serum iron (Fig. 5D) and transferrin saturation (Fig 5E) were increased in CKD-DTBN Vs CKD. Liver hepcidin (Fig. 5F) was elevated in DTBN treated group.
Treatment of uremic mice with DTBN ameliorated renal fibrosis, inflammation, and anemia, with improvements linked to enhanced iron utilization despite persistent hepcidin elevation. These findings identify DTBN as a candidate therapeutic agent for CKD and its complications.