The initial diagnosis, based on the history and initial laboratory data, was anemia of chronic disease (ACD). This is a large group of conditions second only to iron deficiency as a cause of anemia. This class of anemias can be due to chronic infectious or inflammatory conditions, carcinoma, autoimmunity, or chronic renal disease.1 Patients with ACD typically have a mild, normocytic anemia and inappropriately low reticulocyte response. Cytokines, including interleukin-1 (IL-1), interferon gamma (IF-g), and tumor necrosis factor a (TNF-a), produced in response to chronic inflammatory states, such as gout, cause anemia through multiple mechanisms, including direct suppression of erythropoi-esis, blunted renal production of erythropoietin (EPO) in response to anemia, and increased uptake and sequestration of iron within macrophages. A key effecter of iron sequestration is hepcidin, a peptide synthesized by hepatocytes in response to IL-6 and liposaccharide. Hepcidin blocks release of iron from duodenal enterocytes and macrophages, causing hypoferremia and anemia.
Indirect measurements of iron stores can be confusing in ACD. Serum iron and transferrin saturation are typically low, but unlike simple iron deficiency, transferrin concentration is not elevated. Intracellular iron is bound to ferritin, and serum ferritin concentration accurately reflects iron stores in most individuals. However, serum ferritin concentrations can be elevated in ACD states, reflecting increased hepatic synthesis of apoferritin (non-iron-containing ferritin), reducing the sensitivity and negative predictive value of a normal or elevated ferritin concentration for excluding iron deficiency. An alternative to performing a bone marrow biopsy to assess iron stores in patients with ACD and possible coexisting iron deficiency is to measure serum soluble transferrin receptor (sTfR).2 In iron deficiency, both transferrin receptor expression on the surface of erythroid progenitors and soluble shed TfR are increased. Optimal detection of iron deficiency in patients with ACD is achieved by determining the ratio of sTfR to the logarithm of serum ferritin.3 A sTfR/log ferritin ratio >2 is consistent with ACD and iron deficiency, while a ratio <l is predictive of ACD alone. While evelated sTfR is a sensitive indicator of iron deficiency, it is nonspecific, and will be elevated in patients with chronic hemolytic anemias such as sickle cell disease, thalassemias, and hereditary spherocytosis. Currently, sTfR assays are not available on most automated chemistry instruments, and demand for the test is low. In this case presentation, a sTFs/log transferrin ratio of 0.9 is consistent with ACD with adequate iron stores despite the low serum iron and transferrin saturation. While chronic inflammation due to untreated gout may contribute to the patient's anemia, the markedly low serum erythropoietin concentration, blood chemistries, and loss of renal parenchyma point to renal disease as the primary cause of his anemia.
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