Disturbances in iron metabolism play a key role in the pathophysiology of chronic kidney disease (CKD), contributing to clinical complications, particularly the development of anemia. Evaluating the diagnostic utility of iron metabolism proteins in CKD patients, depending on disease progression, is of great significance both diagnostically and therapeutically.

Aim: to evaluate the role of iron metabolism proteins in the pathogenesis of anemia and their clinical diagnostic value in patients with chronic kidney disease at both the conservative and terminal stages.

Materials and methods. The study included patients with stage II–III CKD (conservative group) and terminal-stage CKD undergoing hemodialysis (terminal group), as well as healthy controls. Serum levels of hemoglobin, iron, erythropoietin, ferritin, transferrin, lactoferrin, ferroportin, hepcidin, and haptoglobin were analyzed.

Results. In terminal-stage CKD, the concentrations of hemoglobin (22.1 %, p < 0.001 and 28.6 %, p = 0.001), erythropoietin (26.8 % and 32.5 %, p < 0.001), iron (18.3 %, p = 0.004 and 33.0 %, p < 0.001), TIBC (14.5 %, p < 0.001 and 17.3 %, p = 0.003), LIBC (14.4 %, p = 0.006 and 14.8 %, p = 0.039), and transferrin (11.3 %, p = 0.042 and 30.8 %, p = 0.008) were significantly lower in both men and women compared to the conservative group. In contrast, ferritin (2.3-fold and 2.1-fold, p < 0.001), hepcidin (82.2 % and 65.1 %, p < 0.001), ferroportin (50.0 % and 46.2 %, p < 0.001), and lactoferrin (2.2-fold and 87.5 %, p < 0.001) levels were significantly increased in the terminal stage group compared to the conservative group. Ferritin and hepcidin demonstrated the highest diagnostic performance in CKD, showing excellent sensitivity, specificity, and diagnostic efficiency. Lactoferrin and erythropoietin also showed strong diagnostic value, while ferroportin exhibited moderate diagnostic performance. Transferrin demonstrated the lowest diagnostic efficiency, indicating limited standalone clinical usefulness.

Conclusions. This study demonstrates that functional iron deficiency in end-stage renal disease is mediated by systemic inflammation. These findings underscore the pivotal role of iron metabolism proteins in the pathogenesis of renal anemia and validate their clinical utility as diagnostic biomarkers and therapeutic targets.