Introduction:
Anemia in chronic kidney disease (CKD) often results from reduced erythropoietin production. Traditionally, treatment involves erythropoietin and intravenous (IV) iron. Desidustat, a novel hypoxia-inducible factor prolyl hydroxylase inhibitor (HIF-PHI), has been introduced to stimulate endogenous erythropoietin production. This retrospective study assesses the real-world outcomes of Desidustat in CKD-related anemia.
Methods:
This is a retrospective observational study in which we analyzed a cohort of 29 Patients diagnosed with CKD-associated anemia. Patients with mean Hb level of 8-10 gm/dl and whether receiving erythropoietin therapy or not, were administered Desidustat and included in this study. The dosage was set at 100 mg thrice weekly, with monthly follow-ups to monitor hemoglobin (Hb) levels. Dosage adjustments were made according to individual Hb responses.
Results:
In current study of 29 patients, Diabetic kidney disease (DKD) was the most common cause of CKD (n=22 patients) followed by hypertension(n=18). In 24 weeks, treatment follow up period, The baseline mean hemoglobin was 9.18 ± 0.87 gm/dL. An increase in hemoglobin was observed from baseline to end of study at 24 weeks, reaching at 10.78 ± 0.76 gm/dL, demonstrating a significant rise in hemoglobin level (P value <0.001). There was also an improvement shown in the serum creatinine level and there was no change in e-GFR of the patients during study period. There was also non-comparable change in the serum potassium level at the end of 24 weeks of study period. The rise in Hb was sustained during whole study period. There were no any reported adverse events during the treatment follow-up period.
Conclusions:
Desidustat effectively increases hemoglobin levels in CKD anemia patients. The effect of Desidustat on serum creatinine and e-GFR needs to be established.
I have no potential conflict of interest to disclose.
I did not use generative AI and AI-assisted technologies in the writing process.