Overview
Clinical Meaning
Anemia of CKD results primarily from decreased erythropoietin (EPO) production by peritubular fibroblasts in the kidney as nephron mass declines.
Anemia of CKD results primarily from decreased erythropoietin (EPO) production by peritubular fibroblasts in the kidney as nephron mass declines. EPO stimulates erythroid progenitor cells in the bone marrow to differentiate and mature into red blood cells. Additional factors contributing to CKD anemia include functional iron deficiency (inadequate iron supply for erythropoiesis despite normal iron stores), chronic inflammation (hepcidin elevation sequesters iron in macrophages), shortened RBC lifespan (uremic toxins damage erythrocyte membranes), and blood loss from dialysis procedures and uremic platelet dysfunction. KDIGO guidelines recommend evaluating anemia when hemoglobin (Hgb) falls below 130 g/L in males or 120 g/L in females with CKD. Iron status must be assessed before initiating erythropoiesis-stimulating agents (ESAs): transferrin saturation (TSAT) and serum ferritin are the key markers. Iron replacement is first-line: IV iron (ferric carboxymaltose, iron sucrose, ferumoxytol) is preferred in dialysis patients and CKD 3-5 with oral iron intolerance. ESAs (epoetin alfa, darbepoetin alfa) are second-line when Hgb remains <100 g/L despite adequate iron stores (TSAT >30%, ferritin >500 µg/L). The target Hgb with ESA therapy is 100–115 g/L — normalizing hemoglobin to...