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.
Chronic kidney disease (CKD) is a worldwide public health problem with steadily increasing incidence, prevalence and cost. By 2050, CKD is predicted to become the fifth leading age-standardized cause of death worldwide. Secondary hyperparathyroidism (SHPT) develops as CKD advances, and persistently elevated parathyroid hormone (PTH) may be nephrotoxic and associated with earlier dialysis onset. A post-hoc analysis of two Phase 3 studies conducted in the United States has shown that sustained reduction of elevated intact PTH (iPTH) of ≥30% from baseline (BL) with extended-release calcifediol (ERC) treatment was associated with slower rates of estimated glomerular filtration rate (eGFR) decline in patients with SHPT and stage 3-4 CKD. This post-hoc analysis of a phase 3 bridging study in China examined whether the reduction of iPTH in Chinese SHPT patients treated with ERC could also delay CKD progression.
Chinese patients (n=67) with eGFR ≥15 to <60 mL/min/1.73m², plasma iPTH ≥85 pg/mL and serum total 25-hydroxyvitamin D (25D) <30 ng/mL received oral ERC once daily at bedtime for 26 weeks. Dosing started at 30 µg/day and increased, as needed, to 60 µg/day after 3 months. Calcium, phosphorus, 25D, 1,25-dihydroxyvitamin D (1,25D), iPTH, eGFR and urine albumin-to-creatinine ratio (uACR) were measured at BL and regular intervals. Participants were categorized by response (or non-response) of attaining a sustained mean decrease of ≥30% from BL in iPTH by the efficacy assessment period (EAP), defined as the last 6 weeks of treatment, to evaluate differences in eGFR decline. A total of 60 ERC-treated subjects were analyzed in whom eGFR was measured at both weeks 13 and 26. The observed changes from BL (CFB) of mean eGFR in the two response groups were compared by t-test.
For the 60 participants, mean (SD) 25D increased from 17±5 ng/mL at BL to 96±25 ng/mL (p<0.001) by the EAP, iPTH decreased from 160.1±67.9 pg/mL to 120.3±69.8 (p<0.001), BL eGFR in the response group (n=34) was 23.1±6.4 mL/min/1.73m², which was similar to the non-response group (n=26; 23.0 ± 8.1). The rate of eGFR decline was >2-fold higher (p=0.036) in the non-response group (eGFR CFB -5.1±5.3 mL/min/1.73m²) compared with the response group (eGFR CFB -2.4±3.8 mL/min/1.73m²). There was no statistically significant difference in the changes of serum P (CFB 0.2±0.4 vs 0.4±0.6 mg/mL, p=0.13) between the two groups. Serum calcium sightly increased from BL in the response group (CFB 0.2±0.2 mg/dL) but not in the non-response group (CFB 0.0±0.2 mg/dL). Duration of iPTH reduction had no impact on safety parameters.
Sustained mean reductions of ≥30% in elevated iPTH with ERC treatment were associated with slower eGFR decline in Chinese patients with SHPT and stage 3-4 CKD without raising safety concerns, a finding which was consistent with the results of the similar United States studies.
