The Relationship Between Anemia and Iron Metabolism Indicators in Chronic Kidney Disease

Abstract

Anemia developing secondary to chronic kidney disease (CKD) is a severe pathophysiological condition that compromises patients' quality of life and exponentially amplifies the risks of cardiovascular complications and end-stage renal disease. Although conventional nephrology recognizes erythropoietin (EPO) deficiency as the primary etiology of renal anemia, contemporary investigations illuminate that the disruption of iron homeostasis and hepcidin-mediated reticuloendothelial blockade play equally decisive roles. This study aims to quantitatively evaluate the pathogenetic correlation between iron metabolism indicators (ferritin, transferrin saturation – TSAT, serum hepcidin, soluble transferrin receptors – sTfR) and hemoglobin levels across various stages of CKD (Stages 3-5). Utilizing a prospective observational design, the clinico-laboratory parameters of 186 patients suffering from CKD were analyzed over an 18-month longitudinal period. Dispersion and multivariate regression models revealed that a decline in the estimated glomerular filtration rate (eGFR) below 30 mL/min/1.73 m² induces a pathological, almost fourfold elevation in serum hepcidin levels (reaching 68.5 ± 15.2 ng/mL). Consequently, despite elevated serum ferritin indices (385.4 ± 112.5 ng/mL), TSAT declines precipitously to 14.2 ± 3.8%, while sTfR elevates above 4.2 mg/L, unequivocally confirming the syndrome of "functional iron deficiency." This profound laboratory monitoring of iron metabolism (sensitivity 88%, specificity 85%) provides nephrologists with a highly accurate objective substrate for appropriately differentiating absolute from functional iron deficiency, pre-emptively assessing the risk of covert hemosiderosis, and personalizing strategies for the administration of erythropoiesis-stimulating agents alongside intravenous iron therapies.