9 Iron is absorbed in the gastrointestinal tract and bound to serum transferrin. Hence, iron deficiency will limit responsiveness to EPO.
Although the development of erythroid lineage from a multipotential myeloid stem cell is regulated by EPO, the differentiation from erythroblasts into reticulocytes is an iron-dependent process. Iron metabolism is tightly regulated at multiple stages of the red blood cell (RBC) life cycle ( Figure 2). We furthermore provide an in-depth discussion of the current literature as it pertains to target levels of Hgb and iron indices. In this text, we review the mechanisms of IDA, the potential aids and pitfalls in the diagnosis of IDA, and the available treatment formulations for IDA in patients with CKD. To best manage IDA in CKD, a thorough understanding of its pathophysiology and treatments is necessary.
The traditional biomarkers used to detect iron deficiency in CKD are often unreliable, rendering the diagnostic and monitoring processes difficult. 8 Repletion of iron stores is often necessary in patients with CKD for the treatment of IDA and to maximize the efficacy of ESAs. 1, 7 This is due to both true paucity of iron stores (absolute IDA) and relative (functional) iron deficiency the latter being due to underlying inflammation which impairs the body’s ability to appropriately utilize the iron sequestered in the tissues. Many patients with anemia and CKD suffer from iron-deficiency anemia (IDA). 3– 6 Thus, the current guidelines advise a target Hgb below the definition of normal in patients with CKD.
Several well conducted studies in patients with CKD indicate that use of ESAs to normalize Hgb in patients with CKD may worsen cardiovascular (CV) outcomes. As such, erythropoiesis-stimulating agents (ESAs) have been considered a staple for the management of anemia in patients with CKD ( Figure 1). 2 Multiple mechanisms contribute to the development of anemia in CKD, the most important being relative deficiency of erythropoietin (EPO). Two important issues are addressed, including the potential risks of a more liberal approach to iron supplementation as well as the potential risks and benefits of IV versus oral iron supplementation in patients with CKD.Īnemia, defined as a hemoglobin (Hgb) concentration of 50% in the more advanced stages of the disease. Here, we review the pathophysiology and available diagnostic tests for IDA in CKD, we discuss the literature that has informed the current practice guidelines for the treatment of IDA in CKD, and we summarize the available oral and intravenous (IV) iron formulations for the treatment of IDA in CKD. The traditional biomarkers used for the diagnosis of iron-deficiency anemia (IDA) in patients with CKD have limitations, leading to persistent challenges in the detection and monitoring of IDA in these patients. Several risk factors contribute to absolute and functional iron deficiency in CKD, including blood losses, impaired iron absorption, and chronic inflammation. This may be due to a true paucity of iron stores (absolute iron deficiency) or a relative (functional) deficiency which prevents the use of available iron stores. Iron deficiency plays a significant role in anemia in CKD.
#HEARTS OF IRON IV NOT RESPONDING DRIVER#
Although relative deficiency of erythropoietin production is the major driver of anemia in CKD, iron deficiency stands out among the mechanisms contributing to the impaired erythropoiesis in the setting of reduced kidney function. Anemia is a complication that affects a majority of individuals with advanced CKD.
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