Highlights of the Annual Dialysis Conference: Chronic Kidney Disease Related-Anemia

February 18-20, 2007; Denver, Colorado

Anne G. Le, PharmD, RPh


April 02, 2007

In This Article

Introduction to Anemia of Chronic Kidney Disease

Anemia is a common complication in patients with chronic kidney disease (CKD), but early recognition and correction of hemoglobin levels may improve clinical outcomes. The majority of patients with CKD who are undergoing dialysis need long-term treatment with erythropoiesis-stimulating agents (ESAs) to achieve and maintain a target hemoglobin level of 11 to 13 g/dL. Epoetin alfa and darbepoetin, 2 current ESAs, are effective treatments for anemia in patients undergoing dialysis. Moreover, iron deficiency is a common cause of anemia in CKD and can often be corrected with iron supplementation. In addition to the currently available iron preparations, 2 investigational unique, iron preparations, ferumoxytol and VIT-45, may be potentially given as total dose infusions, and might be a much needed addition to the clinicians' armamentarium.

Management of Iron Deficient Anemia: An Update

One of the major issues surrounding management of iron deficiency is how clinicians should manage anemic patients who have high ferritin and low transferrin saturation (TSAT) and are undergoing dialysis. Daniel Coyne, MD, from Washington University in St. Louis, Missouri, presented data from the recent Dialysis Patients' Response to IV Iron With Elevated Ferritin (DRIVE) Study,[1] which helps answer this question. The DRIVE study was a prospective, randomized, controlled, parallel-group, multicenter, clinical trial evaluating the use of intravenous (IV) iron vs no iron in dialysis patients with a hemoglobin ≤ 11 g/dL, a TSAT of ≤ 25% and serum ferritin values between 500 and 1200 ng/mL. Patients also had to be taking high epoetin doses (≥ 225 IU/kg/week or ≥ 22,500 IU/week). Patients were then randomized to receive 1 g of ferric gluconate (125 mg for 8 hemodialysis sessions) or no IV iron. Both groups received a 25% increase in epoetin dose. At the end of 6 weeks, the difference in hemoglobin change was the primary end point. DRIVE II was a follow-up study observational study to see how physicians manage these patients after exiting DRIVE and to determine whether or not there was a persistent difference in hemoglobin and the effect of epoetin usage. In the DRIVE study, at 6 weeks, the hemoglobin levels in the control group had increased with epoetin alone from 10.2 to 11.3 mg/dL and with IV iron, it increased from 10.4 to 11.9 mg/dL, which was significantly in favor of administration of iron with the epoetin increase. Similarly, the number of patients who responded (had ≥ 2 g/dL increase in hemoglobin) during the 6 weeks was 47% in the IV iron group and 29% in the control group, which significantly favored IV iron. The DRIVE II study results showed that when physicians and nurses took control of their patients, there was a dramatic decrease in the epoetin requirements and prescriptions in the IV iron group. In conclusion, in patients with elevated ferritin and TSAT ≤ 25%, the most effective strategy may be to increase the epoetin dose by 25% and to administer 1 g iron. Furthermore, using iron with an epoetin increase results in higher hemoglobin and lower epoetin requirements over a 12-week period.


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