Intravenous Versus Oral Iron for Treatment of Iron Deficiency in Non-hemodialysis-dependent Patients With Chronic Kidney Disease

Anne Marie Liles

Disclosures

Am J Health Syst Pharm. 2012;69(14):1206-1211. 

In This Article

Abstract and Introduction

Abstract

Purpose The evidence evaluating the efficacy of i.v. versus oral iron for the treatment of iron deficiency in non-hemodialysis-dependent patients with chronic kidney disease (CKD) is reviewed.
Summary Although erythropoiesis-stimulating agents (ESAs) are the mainstay of anemia treatment, concomitant iron supplementation is often required. Patients with CKD are at risk for developing iron deficiency due to frequent blood testing, decreased dietary intake, inflammation, decreased gastrointestinal absorption, the use of phosphate binders, hemodialysis, and treatment with ESAs. Seven randomized, controlled trials compared i.v. and oral iron in this population, six in patients treated with ESAs and one in patients not receiving ESAs. Two studies found no difference between i.v. and oral iron. An additional study found the two formulations to be equivalent when evaluating ESA dosage requirements. All studies found i.v. iron to be superior in increasing ferritin and transferrin saturation (TSAT) levels. Five of the studies compared baseline laboratory values for patients treated with i.v. and oral iron; all of these found oral iron to significantly increase hemoglobin, ferritin, or TSAT levels. Only one trial found a significant decrease from baseline in ferritin and TSAT for oral iron. Interpretation of the results of these studies is limited by several factors, the most significant of which is a short study duration, ranging from 21 days to six months.
Conclusion Published evidence does not support the use of i.v. iron over oral iron to treat deficiencies in non-hemodialysis-dependent patients with CKD. While studies found that i.v. iron significantly increased serum levels of ferritin and TSAT, hemoglobin levels were not consistently raised.

Introduction

Anemia develops in the early stages of chronic kidney disease (CKD), primarily due to the progressive decrease in erythropoietin production by the kidneys.[1] Even at stage 1 or 2 CKD, 25% of patients have hemoglobin levels of ≤12 g/dL.[2] Although erythropoiesis-stimulating agents (ESAs) are the mainstay of anemia treatment, concomitant iron supplementation is often required. Patients with CKD are at risk for developing iron deficiency due to frequent blood testing, decreased dietary intake, inflammation, decreased gastrointestinal absorption, the use of phosphate binders, hemodialysis, and treatment with ESAs.[3] While patients receiving hemodialysis are at greater risk, iron deficiency has been demonstrated in patients not receiving hemodialysis. The National Health and Nutritional Examination Survey found that approximately 60% of men and 70% of women with glomerular filtration rates of <60 mL/min had a transferrin saturation (TSAT) level of <20%, a ferritin concentration of <100 ng/mL, or both.[4] Gotloib et al.[5] performed bone marrow biopsies in patients with non-hemodialysis-dependent CKD (ND-CKD) with hemoglobin concentrations of <12 g/dL and found an absence of blood iron in the sternal bone marrow in 46 of 47 patients. Therefore, iron supplementation is an essential component in the treatment of anemia in ND-CKD patients. This article evaluates the current evidence of the efficacy of i.v. versus oral iron in ND-CKD patients.

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