# Roxadustat for Erythropoiesis-Stimulating Agent Hyporesponsive Anemia in Hemodialysis: Multicenter Retrospective Analysis

## TL;DR

This study examines the effectiveness of Roxadustat in treating anemia in hemodialysis patients who don't respond well to traditional treatments.

## Contribution

The study provides real-world evidence on Roxadustat's impact on anemia in ESA-hyporesponsive hemodialysis patients.

## Key findings

- Roxadustat significantly increased hemoglobin levels in ESA-hyporesponsive patients over six months.
- Baseline hemoglobin levels predicted final hemoglobin levels, regardless of treatment group.
- Transfusion requirements decreased in both treatment groups over the study period.

## Abstract

Background and Objectives: Anemia management in maintenance hemodialysis patients with erythropoiesis-stimulating agent (ESA) hyporesponsiveness remains challenging. Roxadustat, a hypoxia-inducible factor prolyl hydroxylase inhibitor, offers a mechanistically distinct alternative. Materials and Methods: This multicenter retrospective study analyzed 110 hemodialysis patients with persistent anemia (Hemoglobin (Hb) < 10 g/dL) despite ≥ 3 months of maximum-reimbursable-dose ESA therapy in Türkiye. Outcomes were evaluated between patients who switched to Roxadustat (n = 80) and those who continued ESA therapy (n = 30) over 6 months in a non-randomized, observational comparison. Results: At baseline, median Hb levels were significantly lower in the Roxadustat-group than in the ESA-group (8.70 vs. 9.50 g/dL; p < 0.001), while weight-adjusted ESA doses were comparable (p = 0.332). By Month 6, the Roxadustat group achieved a significant Hb increase (from 8.70 to 9.95 g/dL), whereas the ESA-group showed no significant change (9.50 to 9.65 g/dL), and end-of-treatment Hb did not differ significantly between groups. The unadjusted mean Hb rise was greater in the Roxadustat cohort than in the ESA cohort (+1.40 ± 1.55 vs. +0.65 ± 1.93 g/dL; p = 0.037). However, after adjustment for baseline Hb (ANCOVA), baseline Hb predicted final Hb, while treatment group was not independently associated with final Hb. Transfusion requirements declined over follow-up in both groups. No new short-term safety signal was identified based on available clinical documentation. Conclusions: Roxadustat improved Hb in ESA-hyporesponsive patients with lower baseline Hb, but adjusted analyses indicated that baseline severity influenced response. Targets were not consistently achieved; these findings are hypothesis-generating regarding dose optimization, treatment duration, and earlier initiation.