This study aimed to confirm changes in biomarkers of erythropoiesis and iron metabolism and serum fibroblast growth factor 23 (FGF-23) during darbepoetin-α treatment and then switching to the hypoxia-inducible factor prolyl hydroxylase inhibitor roxadustat. A total of 28 patients on hemodialysis who received weekly doses of darbepoetin-α were switched to roxadustat. Biomarkers for erythropoiesis and iron metabolism and intact and C-terminal FGF-23 were measured in blood samples collected before the HD session on days − 7 (darbepoetin-α injection), − 4, and − 2, and days 0 (switch to roxadustat treatment, three times weekly), 3, 5, 7, 14, 21, and 28. Erythropoietin and erythroferrone levels were elevated on day − 4 by darbepoetin-α injection and decreased to baseline levels at day 0. Levels of erythropoietin were not significantly increased by roxadustat supplementation, but erythroferrone levels were continuously elevated, similar to darbepoetin-α treatment. Hepcidin-25 and total iron binding capacity were significantly decreased or increased in patients treated with roxadustat compared with darbepoetin-α. Changes of intact and C-terminal FGF-23 levels were parallel to changes of phosphate levels during roxadustat treatment. However, the actual and percentage changes of intact FGF-23 and C-terminal FGF-23 in patients with low ferritin levels were greater than those in patients with high ferritin levels. Roxadustat might stimulate erythropoiesis by increasing iron usage through hepcidin-25, which was suppressed by erythroferrone in the physiological erythropoietin condition. Changes of intact FGF-23 and C-terminal FGF-23 levels might be affected by roxadustat in patients on hemodialysis, especially those with a low-iron condition.
Daprodustat is a novel oral agent for renal anemia. This retrospective study examined 124 maintenance patients undergoing HD who had shifted from erythropoiesis-stimulating agents (ESA) or roxadustat to daprodustat (4mg daily). Anemia control, iron metabolism markers, and doses of daprodustat within 3 months after the shifting therapies were assessed. We used multivariate logistic regression analysis to determine the factors associated with the use of high doses of daprodustat 3 months after. The serum hemoglobin level significantly decreased after shifting therapies. Similarly, the proportion of patients who achieving a hemoglobin level within the appropriate range was also significantly lower, and median doses of daprodustat gradually increased. A significant increase in the serum iron, total iron-binding capacity, and transferrin saturation levels were found, but the serum ferritin level did not differ during the study period. Multivariate regression analysis showed that diabetes, a low Hb level, and use of high doses of ESA/roxadustat were independent predictors for the use of high doses of daprodustat 3 months after shifting therapies. We concluded that renal anemia control may worsen after shifting to daprodustat. Patients with diabetes, a low Hb level at baseline, and those receiving high doses of ESA/roxadustat may require high doses of daprodustat.
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