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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.
Erythropoietin-stimulating agent (ESA) resistance is a common challenge in patients with chronic kidney disease (CKD) and is associated with adverse outcomes. Vitamin D deficiency, particularly of its active form, 1,25-dihydroxyvitamin D (1,25(OH)₂D), has been implicated in the pathogenesis of anemia. However, the precise relationship between active vitamin D levels and ESA resistance remains unclear.
A total of 376 pre-dialysis CKD patients (estimated glomerular filtration rate [eGFR] < 60 mL/min/1.73 m²) treated with ESAs were analyzed. ESA resistance was defined based on the erythropoietin resistance index (ERI), calculated as the monthly continuous erythropoietin receptor activator (CERA) dose per kilogram of body weight divided by hemoglobin concentration. Patients in the highest tertile of ERI were categorized as the ESA-hyporesponsive group. Baseline characteristics—including 1,25(OH)₂D and 25(OH)D levels, renal function, iron metabolism, inflammatory markers, and parameters of mineral metabolism—were compared between ESA-resistant and non-resistant groups. Univariable and multivariable logistic and linear regression analyses were conducted to identify factors, including 1,25(OH)₂D and 25(OH)D levels, independently associated with ESA resistance and ERI values.
Among the participants, 33.5% were classified as ESA-resistant. The ESA-resistant group had significantly lower eGFR, hemoglobin, and 1,25(OH)₂D levels, but higher hsCRP, parathyroid hormone (PTH), and ESA dose requirements.
In multivariable logistic regression analysis, 1,25(OH)₂D levels (odds ratio [OR] 0.88, 95% CI 0.84–0.92, P < 0.001) were independently associated with ESA resistance. Other independent predictors included serum ferritin (OR 0.97, 95% CI 0.95–0.99, P = 0.001), transferrin saturation (TSAT) (OR 0.93, 95% CI 0.90–0.96, P < 0.001), hsCRP (OR 2.47, 95% CI 1.44–4.25, P = 0.001), and intact PTH (OR 1.07, 95% CI 1.02–1.13, P = 0.010).
In multivariable linear regression analysis, ERI was significantly correlated with 1,25(OH)₂D (β = −0.280, P < 0.001), TSAT (β = −0.168, P < 0.001), hsCRP (β = 0.166, P < 0.001), and intact PTH (β = 0.205, P < 0.001). Serum 25(OH)D levels were not significantly associated with ESA resistance or ERI.
Active vitamin D deficiency is independently associated with erythropoietin resistance in patients with CKD, even after adjusting for iron status and inflammation. Future prospective studies are warranted to determine whether correction of active vitamin D deficiency can improve ESA responsiveness in patients with pre-dialysis CKD.
