Diagnosis of iron deficiency in chronic renal failure

Fernández-Rodríguez, Ana; Guindeo-Casasús, María C.; Molero-Labarta, Teresa; Domínguez-Cabrera, Casimira; Hortal-Cascón, Luis; Pérez-Borges, Patricia; Vega-Díaz, Nicanor; Santana, Pedro Saavedra; Palop-Cubillo, Leocadia

doi:10.1016/s0272-6386(99)70079-x

Cited by 109 publications

(54 citation statements)

References 29 publications

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“…If one is trying to determine whether an ESA is having its intended effect of stimulating bone marrow RBC production, before an increase in reticulocytes is noted and well before the Hb rises, then an increase in the sTfR may be the first detectable measure. It is not affected by inflammation (13), which one would think would make sTfR a more reliable test than serum ferritin, but Fernandez-Rodriguez et al (14) found sTfR to be less accurate than serum ferritin. Those authors demonstrated an sTfR sensitivity of 70% and a specificity of 59% at a cutoff of 2.6 mg/L.…”

Section: Soluble Transferrin Receptormentioning

confidence: 99%

Assessing Iron Status

Wish¹

2006

Clinical Journal of the American Society of Nephrology

504

427

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The increasing prevalence of multiple comorbidities among anemic patients with chronic kidney disease has made the use of serum ferritin and transferrin saturation more challenging in diagnosing iron deficiency. Because serum ferritin is an acute-phase reactant and because the inflammatory state may inhibit the mobilization of iron from reticuloendothelial stores, the scenario of patients with serum ferritin >800 ng/ml, suggesting iron overload, and transferrin saturation <20%, suggesting iron deficiency, has become more common. This article revisits the basis for the Kidney Disease Outcomes Quality Initiative recommendations regarding the use of serum ferritin and transferrin saturation in guiding iron therapy, then explores some of the newer alternative markers for iron status that may be useful when serum ferritin and transferrin saturation are insufficient. These newer tests include reticulocyte hemoglobin content, percentage of hypochromic red cells, and soluble transferrin receptor, all of which have shown some promise in limited studies. Finally, the role of hepcidin, a hepatic polypeptide, in the pathophysiology of iron mobilization is reviewed briefly.

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Section: Soluble Transferrin Receptormentioning

confidence: 99%

Assessing Iron Status

Wish¹

2006

Clinical Journal of the American Society of Nephrology

504

427

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“…Patients with chronic liver disease may have elevated sTfR levels when they experience either iron deficiency or stimulated erythropoiesis in response to hemolysis or hemorrhage [109]. Renal failure patients have low sTfR levels as a result of erythroid hypoplasia [12,42] and iron deficiency is then associated with a relative elevation of sTfR levels that nevertheless remain within the normal range [33,110]. Active malaria is associated with changes in erythropoietic activity brought about by hemolysis (which would tend to increase sTfR levels) as well as inflammation (which would rather decrease sTfR levels).…”

Section: Soluble Tfr: a Marker Of Iron Status And/or Erythropoiesis?mentioning

confidence: 99%

Soluble transferrin receptor for the evaluation of erythropoiesis and iron status

Béguin

2003

Clinica Chimica Acta

395

316

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Iron transport in the plasma is carried out by transferrin, which donates iron to cells through its interaction with a specific membrane receptor, the transferrin receptor (TfR). A soluble form of the TfR (sTfR) has been identified in animal and human serum. Soluble TfR is a truncated monomer of tissue receptor, lacking its first 100 amino acids, which circulates in the form of a complex of transferrin and its receptor. The erythroblasts rather than reticulocytes are the main source of serum sTfR. Serum sTfR levels average 5.0 F 1.0 mg/l in normal subjects but the various commercial assays give disparate values because of the lack of an international standard. The most important determinant of sTfR levels appears to be marrow erythropoietic activity which can cause variations up to 8 times below and up to 20 times above average normal values. Soluble TfR levels are decreased in situations characterized by diminished erythropoietic activity, and are increased when erythropoiesis is stimulated by hemolysis or ineffective erythropoiesis. Measurements of sTfR are very helpful to investigate the pathophysiology of anemia, quantitatively evaluating the absolute rate of erythropoiesis and the adequacy of marrow proliferative capacity for any given degree of anemia, and to monitor the erythropoietic response to various forms of therapy, in particular allowing to predict response early when changes in hemoglobin are not yet apparent. Iron status also influences sTfR levels, which are considerably elevated in iron deficiency anemia but remain normal in the anemia of inflammation, and thus may be of considerable help in the differential diagnosis of microcytic anemia. This is particularly useful to identify concomitant iron deficiency in a patient with inflammation because ferritin values are then generally normal. Elevated sTfR levels are also the characteristic feature of functional iron deficiency, a situation defined by tissue iron deficiency despite adequate iron stores. The sTfR/ferritin ratio can thus describe iron availability over a wide range of iron stores. With the exception of chronic lymphocytic leukemia (CLL) and high-grade non-Hodgkin's lymphoma and possibly hepatocellular carcinoma, sTfR levels are not increased in patients with malignancies. We conclude that soluble TfR represents a valuable quantitative assay of marrow erythropoietic activity as well as a marker of tissue iron deficiency. D

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“…Expert reviews have suggested the use primarily of serum ferritin (with or without transferrin saturation) (18)(19)(20), with some indicating that the addition of sTfR could enhance the ascertainment of iron deficiency in IBD, considering that serum ferritin is an acute phase reactant and thus can be difficult to interpret in the presence of inflammation (19,20). Soluble transferrin receptor (sTfR) is thought to be more sensitive than ferritin at detecting iron deficiency, although the incremental utility of this index continues to be debated (24,25). That is, the sTfR receptor is elevated in iron deficient states, but is significantly less affected by inflammation than typical iron indices (ferritin, serum iron and total iron binding capacity, and percent transferrin saturation) (24,26,27).…”

Section: Introductionmentioning

confidence: 99%