Abstract:
Background: Anemiaisafrequentcomplicationin patients withchronic kidney disease (CKD),with theincidencerising in stages
3–5. Iron defciency and defective erythropoiesis are the major causes. Still, the role of iron status and the stimulating capability of
ESAs on the progression of CKD have hardly been evaluated.
Objective: To assess the efect of iron defciency and ESA therapy with respect to the correction of anemia and preservation of
kidney function in patients with CKD stages 3–5.
Methods: Afollow-upobservational study was carried out in 120 CKDpatients at nephrology department in a tertiary institution,
from January 2023 to December 2024. Te patients were classifed into three groups: Group 1 and Group 3 considered iron
defcient, with no ESA and ESA therapy, respectively, while Group 2 was non–iron-defcient with no ESA. Te parameters tested
were hemoglobin levels, serum ferritin, transferrin saturation (TSAT), and estimated glomerular fltration rate (eGFR) at baseline
andat 6monthsafter treatment. Te ESAtreatmentgiven consisted of epoetin alfa or darbepoetin alfa, with iron supplementation
given according to iron-defciency status.
Results: Baseline hemoglobin levels were signifcantly lower in Group 1 (9.5±1.2g/dL), and these subjects were associated with
a faster decline of eGFR by value per year (annual decline in eGFR: 3.5±2.3mL/min/1.73m2) compared to Groups 2 and 3 (p<0.01).
Te ESA-treated group (Group 3) exhibited relatively the greatest improvement in hemoglobin level (to 12.3±1.5g/dL) and the
slowest decline in kidney function (1.7±1.2mL/min/1.73m2). Iron supplementation produced greater changes in ferritin and TSAT.
Conclusion: Iron defciency is a paramount modifable driver of anemia and CKD progression. ESA treatment improves anemia
and retards renal deterioration, especially when coupled with iron supplementation. Early detection and correction of anemia
might merit interplay in pursuit of optimized CKD outcomes.
