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Changes in Iron Availability with Roxadustat in Nondialysis- and Dialysis-Dependent Patients with Anemia of CKD. | LitMetric

AI Article Synopsis

  • Roxadustat is a treatment for anemia in chronic kidney disease (CKD) that works by enhancing hemoglobin levels through promoting erythropoietin production and improving iron availability.
  • In a study involving nearly 8,000 patients, those treated with roxadustat experienced significant increases in hemoglobin, serum iron, and total iron-binding capacity, while also observing reduced levels of hepcidin and serum ferritin over 52 weeks.
  • Compared to standard treatments like epoetin alfa and placebo, roxadustat led to better iron management and required less intravenous iron supplementation for achieving target hemoglobin levels.

Article Abstract

Background: Roxadustat, a hypoxia-inducible factor prolyl hydroxylase inhibitor, increases hemoglobin by stimulating erythropoietin synthesis and improving iron availability through facilitation of iron uptake and/or release from stores. In this exploratory analysis, we assessed the effect of roxadustat treatment on laboratory parameters related to iron metabolism in patients with anemia of chronic kidney disease (CKD).

Methods: Data were pooled from pivotal, randomized, phase 3 roxadustat trials: three placebo-controlled, double-blind trials in nondialysis-dependent (NDD) CKD and three open-label, active-comparator (epoetin alfa) trials in dialysis-dependent (DD) CKD. In this exploratory analysis, mean changes from baseline in hemoglobin, iron parameters, and hepcidin, and intravenous (iv) iron use were evaluated. Pooled results in NDD CKD and DD CKD patients are reported.

Results: Overall, 4277 patients with NDD CKD and 3890 patients with DD CKD were evaluated. Hemoglobin increases with roxadustat treatment were accompanied by increases in serum iron and total iron-binding capacity (TIBC) and decreases in serum ferritin and hepcidin from baseline through week 52. With epoetin alfa, the hemoglobin increase was accompanied by decreases in serum ferritin and hepcidin, but serum iron decreased, and there was no change in TIBC. With placebo, there were no changes in hemoglobin, iron parameters, or hepcidin. During treatment, iv iron use was reduced with roxadustat versus placebo and epoetin alfa.

Conclusions: In patients with NDD CKD and DD CKD, roxadustat treatment is associated with increases in serum iron and TIBC, accompanied by reduced hepcidin and indicative of improved iron kinetics. Patients treated with roxadustat achieved target hemoglobin levels with less iv iron use versus comparators. Practitioners treating patients with anemia of CKD with roxadustat should consider its unique effects when interpreting iron parameters.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9528373PMC
http://dx.doi.org/10.34067/KID.0001442022DOI Listing

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