Discussion
iron deficiency anemia, CKD, TIBC
IRON DEFICIENCY ANEMIA, IRON DEFICIENCY, SECONDARY
In our study, the changes in %TSAT, serum iron and TIBC did not differ significantly between OD and BD dosing groups over 12 weeks. However, serum ferritin increased significantly in the BD group as compared to the OD group. Either repletion of intracellular stores or sequestration of iron within the cellular stores will lead to rise in serum ferritin concentrations. Overall, in the study population, serum hepcidin concentrations increased significantly over 12 weeks though there was no difference between the groups. This is in line with expected biological response in hepcidin concentrations to oral iron supplementation and repletionAt 12 weeks, MCHC increased in the OD group as compared to decrease in the BD group. It is not surprising that the change in MCHC was not statistically significant when overall study population was considered as the directions of change between the groups were opposite. MCHC is a calculated value and expressed in g/dL as a ratio of hemoglobin to hematocrit. It represents the average concentration of hemoglobin per unit of volume of red blood cell (RBC). MCHC has been traditionally regarded as a reliable marker of availability of iron within the preceding 3–4 months and its incorporation in intracellular hemoglobinWith iron repletion, changes in MCV and hemoglobin lag changes in hemoglobin content within RBCs as reflected by MCH and MCHCOur study has several strengths. The study was a randomized, controlled trial. We did serial measurements at baseline, 2, 5 and 12 weeks on the same platform. We selected participants according to the prevalent KDIGO clinical practice guideline, which is more aligned with practice. We have excluded patients who would have required erythropoietin therapy or would have been at risk of poor iron absorption or iron loss from gut. However, lack of a placebo arm, open-label design, restriction to single center and short duration of follow up are few limitations of our study. We have also not measured other biomarkers of iron deficiency like serum soluble transferrin receptor. Also, wide entry criteria with respect to iron status and already higher hemoglobin levels at baseline might have led to limited hemoglobin response in the study population.In our study, we did not find any significant difference in %TSAT between the groups. Differences in secondary outcomes like ferritin or MCHC between groups are just hypothesis generating. These observations need to explored in patients with more objectively defined true or functional iron deficiency so that effects of less frequent oral iron dosing on long term clinical end points in patients with iron deficiency anemia and CKD can be uncovered.