ABSTRACT
Contexto: la deficiencia de hierro es un trastorno frecuentemente observado en pacientes con enfermedad renal crónica (ERC), sobre todo en estadios avanzados. Su presencia se asocia a una mayor morbilidad y mortalidad. La deficiencia de hierro puede ser absoluta o funcional. La deficiencia absoluta se refiere a una ausencia o una reducción de las reservas de hierro, mientras que la deficiencia funcional se define por la presencia de depósitos de hierro adecuados pero con una disponibilidad insuficiente de hierro para su incorporación en los precursores eritroides. Varios factores de riesgo contribuyen a la deficiencia absoluta y funcional de hierro en ERC, incluyendo pérdidas hemáticas, absorción alterada de hierro e inflamación crónica. Objetivo: con esta revisión narrativa se pretende presentar las definiciones, los aspectos fisiopatológicos, los criterios diagnósticos y las medidas terapéuticas en el paciente con diagnóstico de ERC con deficiencia de hierro. Metodología: se realizó una revisión no sistemática de la literatura en la base de datos PubMed, incluyendo además las guías internacionales más utilizadas que abordan el tema de deficiencia de hierro en ERC. Resultados: se incluyeron un total de 30 referencias bibliográficas. La deficiencia de hierro puede ser absoluta o relativa y el déficit absoluto de hierro se produce con valores de ferritina 100 mcg/l, pero con una TSAT < 20 %. El tratamiento del déficit absoluto consta de reposición de hierro oral o endovenoso y en pacientes que aún no reciben diálisis, se puede hacer una prueba terapéutica con hierro oral, de no haber respuesta se optará por hierro endovenoso, mientras que en pacientes que sí reciben diálisis, la medida ideal es el hierro endovenoso, preferiblemente en preparaciones que permitan esquemas de altas dosis y bajas frecuencias de administración. Las metas propuestas por las distintas guías presentan variaciones entre 500 y 700 mcg/l de ferritina. Conclusiones: el déficit de hierro debe buscarse activamente en pacientes con ERC, ya que su presencia y la falta de intervención conlleva a un incremento en los desenlaces adversos. La terapia con hierro es el pilar del tratamiento y la elección del agente a utilizar dependerá de las características individuales del paciente y de la disponibilidad de las preparaciones de hierro oral o endovenoso.
Background: Iron deficiency is a disorder frequently observed in patients with chronic kidney disease (CKD), especially in advanced stages. Its presence is associated with increased morbidity and mortality. Iron deficiency can be absolute or functional. Absolute deficiency refers to absent or reduced iron stores, while functional deficiency is defined by the presence of adequate iron stores but insufficient iron availability for incorporation into erythroid precursors. Several risk factors contribute to absolute and functional iron deficiency in CKD, including blood fi, impaired iron absorption, and chronic inflammation. Purpose: With this narrative review, it is intended to present the details, pathophysiological aspects, diagnostic criteria and therapeutic options in patients diagnosed with chronic kidney disease with iron deficiency. Methodology: A non-systematic review of the fi ron ra was carried out, in the PubMed database, also including the most used international guidelines that address the issue fi ron deficiency in chronic kidney disease. Results: A total of 30 bibliographical references were included. Iron deficiency can be absolute or relative. The absolute iron deficiency occurs with ferritin values 100 mcg/l but with a TSAT <20 % Treatment of absolute deficiency consists of oral or intravenous iron replacement. In a patient who is not yet receiving dialysis, a therapeutic trial with oral iron can be done, if there is no response, intravenous iron will be chosen. In patients receiving dialysis, the ideal measure is intravenous iron, preferably in preparations that allow high-dose schemes and low frequencies of administration. The goals proposed by the different guidelines present variations between 500 and 700 mcg/l d ferritin. Conclusions: iron deficiency should be actively sought in patients with CKD, since its presence and lack of intervention leads to an increase in adverse outcomes. Iron therapy is the mainstay of treatment; the choice of the agent to be used depends on the individual characteristics of the patient and the availability of oral or intravenous iron preparations.
ABSTRACT
Iron deficiency due to blood loss, absorption disorders and dietary deficiencies causes iron-deficiency anaemia, whose treatment seeks to eliminate the underlying cause and restore haemoglobin and iron deposits. Typically, the latter 2 of these objectives can be achieved through oral iron therapy. Intravenous iron administration (IIA) should be limited to those patients refractory or intolerant to oral preparations or who require rapid repletion. The indiscriminate use of IIA can increase morbidity and mortality due to iatrogenic overload. This fact, coupled with the growing popularity of IIA and the lack of reference guidelines in Spanish, led the Spanish Erythropathology Group of the Spanish Society of Haematology and Haemotherapy to develop this study, which presents the main recommendations on the optimal use of IIA in iron deficiency and attempts to constitute reference guidelines on good practices for the clinical management of these conditions.
ABSTRACT
Iron deficiency has become a new target to improve functional outcomes in patients with heart failure, and intravenous preparations seem to be the only effective treatment for that purpose. However, the relation among iron and oxygen in this population is far from understood as hepcidin is generally upregulated, potentially avoiding iron availability and harm in the context of excess oxidative stress. Laboratory markers used to detect tissue iron deficiency are highly dependent on needs for hemoglobin synthesis, so that reaching peak hemoglobin for each individual should rationally be the first goal of any attempt with therapeutic iron. A subset of patients receiving intravenous iron may have a worse outcome related to admissions and mortality compared to placebo, suggesting that the laboratory thresholds used to detect iron deficiency in heart failure are highly sensitive but less specific to identify patients that would not benefit of this therapy. A gradual delivery of iron over time with parallel measurement of its uptake for hemoglobin synthesis could therefore be recommended to fulfill tissue needs. Standard oral iron therapy should not be dismissed in heart failure patients with anemia and depleted iron stores (ferritin <30 ng/ml) as, contrary to intravenous iron trials, these patients were not included in a trial resulting in neglectable effect of oral iron on exercise capacity.
