Management of anemia

Anemia is a frequent complication of kidney disease. When severe, it causes symptoms that can be debilitating. The course of anemia tends to track the decline in kidney function, with prevalence increasing in more advanced disease. Although the most common cause is relative erythropoietin deficiency, other factors such as reduced iron availability contribute to the pathobiology. In this review, we use cases to explore the surprising complexity of decision-making in management of renal anemia. The prevalence and severity of anemia in CKD relate to the severity of CKD. We generally consider anemia as hemoglobin (Hb) <13 g/dL in men and <12 g/dL in women, with Hb <10 to 11 g/dL being more clinically relevant for intervention. Anemia in CKD is usually normocytic, normochromic, and hypoproliferative. 2 must have accompanying persistent proteinuria or hematuria, or other evidence of chronic kidney injury to be considered CKD. 2, anemia is relatively uncommon and unlikely to be related to the underlying CKD. Hepcidin plays a central role in iron metabolism and availability for erythropoiesis. When levels are elevated, intestinal iron absorption is diminished and release of stored reticuloendothelial system iron is blocked. The net effect is reduced iron availability for erythropoiesis. RBC, red blood cell. Republished with permission of the American Society of Nephrology from Babitt et al Hepcidin plays a central role in iron metabolism and availability for erythropoiesis. When l...

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Anemia of inflammation (AI), also known as anemia of chronic disease (ACD), is regarded as the most frequent anemia in hospitalized and chronically ill patients. It is prevalent in patients with diseases that cause prolonged immune activation, including infection, autoimmune diseases, and cancer. More recently, the list has grown to include chronic kidney disease, congestive heart failure, chronic pulmonary diseases, and obesity. Inflammation-inducible cytokines and the master regulator of iron homeostasis, hepcidin, block intestinal iron absorption and cause iron retention in reticuloendothelial cells, resulting in iron-restricted erythropoiesis. In addition, shortened erythrocyte half-life, suppressed erythropoietin response to anemia, and inhibition of erythroid cell differentiation by inflammatory mediators further contribute to AI in a disease-specific pattern. Although the diagnosis of AI is a diagnosis of exclusion and is supported by characteristic alterations in iron homeostasis, hypoferremia, and hyperferritinemia, the diagnosis of AI patients with coexisting iron deficiency is more difficult. In addition to treatment of the disease underlying AI, the combination of iron therapy and erythropoiesis-stimulating agents can improve anemia in many patients. In the future, emerging therapeutics that antagonize hepcidin function and redistribute endogenous iron for erythropoiesis may offer additional options. However, based on experience with anemia treatment in chronic...