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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.
Chronic kidney disease (CKD) carries substantial residual risk of kidney function loss despite guideline-directed therapies. Astragalus (Huangqi)–based formulations have multi-target anti-inflammatory and antifibrotic actions and may complement standard care, but high-quality randomized evidence remains limited. To evaluate the efficacy and safety of an Astragalus-dominant formulation (Eefooton, EFT) as adjunctive therapy in CKD stages 3–5 over 24 weeks, and to explore fluid-status mechanisms using bioimpedance.
In a double-blind, placebo-controlled, parallel-group trial, adults with CKD stages 3–5 were randomized 2:1 to EFT (n=80) or placebo (n=40) in addition to usual care. The intention-to-treat primary analysis used analysis of covariance (ANCOVA) at each month (Months 1–6) for Δ estimated Glomerular Filtration Rate (ΔeGFR, post-baseline minus baseline), adjusting for baseline eGFR. Secondary outcomes included monthly Δcystatin C and log₁₀- Urine Albumin to Creatinine Ratio (UACR); Creatinine clearance rate and 24-h total protein were assessed at Months 3 and 6. Pre-specified subgroups (Stage 3 vs 4–5; UACR <300 vs ≥300 mg/g; baseline Angiotensin-Converting Enzyme Inhibitors / Angiotensin II Receptor Blockers or Sodium-Glucose Cotransporter-2 Inhibitors use) and bioimpedance were examined.
EFT produced early eGFR gains vs placebo that attenuated by Month 6: adjusted mean differences were +4.30, +6.48, +7.16, +6.35, and +5.57 mL/min/1.73 m² at Months 1–5 (all p<0.001), and +3.11 (95% CI −0.13 to +6.36; p=0.060) at Month 6. Stage-3 patients showed sustained benefit to Month 6 with significant Treatment×Stage interaction, corroborated by Mixed-Effects Model for Repeated Measures (MMRM) sensitivity analyses. Δcystatin C showed no between-group differences through Month 5, with a modest EFT increase at Month 6. UACR and 24-h protein showed no treatment effect. Bioimpedance did not support extracellular decongestion as the driver (no overhydration reduction with EFT). Safety was acceptable; calcium was unchanged, while phosphate and intact parathyroid hormone rose slightly with EFT; albumin increased modestly.
As an adjunct to usual care, EFT yielded clinically meaningful early improvements in eGFR—most durable in Stage-3 CKD—without antiproteinuric effects and with a manageable safety profile. Findings support targeted evaluation of EFT as a complementary renoprotective strategy, with attention to mineral metabolism monitoring and adherence over time.
