Abstract
Abstract
Chronic kidney disease (CKD) is a global health problem that disrupts iron homeostasis and leads to anemia. The complex interactions among hepcidin, erythropoietin, and anemia play important roles in CKD management. Increased hepcidin levels in CKD patients disrupt iron bioavailability for erythropoiesis, whereas altered erythropoietin production affects red blood cell synthesis. This study explored the interaction between these factors in a cohort of 100 nondiabetic CKD patients. A cross-sectional study was conducted on 100 nondiabetic CKD patients at the Urology and Nephrology Center, Mansoura University, Egypt. Crucially, all included patients were completely naive to prior iron supplementation and erythropoiesis-stimulating agents (ESAs), eliminating these major therapeutic confounders. Hemoglobin levels were determined to create two groups: anemia (Hb p
= 0.753). Hepcidin levels were slightly higher in anemic patients (median 226.75 [202–268.38] ng/ml) than in nonanemic patients (196 [170.25–247.25] ng/ml), but the difference was not statistically significant (
p
= 0.077). Transferrin saturation (TSAT) was lower in the anemia group (median 23.4% [19.35–31.76]) compared to the control group (26.37% [21.45–31.52]), yet this difference also did not reach statistical significance (
p
= 0.282). Hepcidin levels remained statistically comparable across the varying stages of CKD and showed a significant negative correlation with hemoglobin (ρ = -0.277,
p
= 0.012), whereas TSAT demonstrated a modest positive correlation (ρ = 0.188,
p
= 0.071). In the adjusted regression model, TSAT was independently associated with hemoglobin (β = 0.047, 95% CI 0.012–0.082,
P
= 0.009), while hepcidin and erythropoietin were not. Transferrin saturation is independently associated with hemoglobin levels in non-diabetic chronic kidney disease, whereas serum hepcidin and erythropoietin are not. These findings indicate that functional iron bioavailability, rather than circulating hepcidin or erythropoietin, is the primary correlate of hemoglobin variance in this cohort.