Achieving optimal patient outcomes with intravenous iron.
Iron deficiency must be aggressively addressed to achieve optimal patient outcomes. Most patients are iron deficient when they start hemodialysis, and despite increasing recognition of this condition, iron deficiency remains present in more than 50% of hemodialysis patients receiving rHuEPO (NKF, 2001).
Causes of Iron Deficiency
The cause of iron deficiency in dialysis patients is multifactorial. There are two kinds of iron deficiency: absolute iron deficiency denotes an insufficient total body store, whereas functional iron deficiency involves a relative inaccessibility of otherwise adequate total body iron stores. End stage renal disease (ESRD) patients are prone to both types of iron deficiency.
Causes of absolute iron deficiency may include malabsorption (Goch, Birgegard, Danielson, & Wikstrom, 1996; Kooistra et al., 1998), blood loss from frequent laboratory testing (weekly, bi-weekly, and monthly labs) (Fishbane & Maesaka, 1997), lowgrade gastrointestinal bleeding (Akmal, Sawelson, Karubian, & Gadallah, 1994), and hemolysis (Yee & Besarab, 2002). These contributing factors are common to all chronic kidney disease and ESRD patients. However, in hemodialysis patients, accidental blood loss from the vascular access, frequent surgical procedures, and blood loss from blood left in the extracorporeal circuit (i.e., blood lines and dialyzer) are primarily responsible for absolute iron deficiency (Fishbane & Maesaka, 1997). It is the magnitude of these blood losses, estimated to be up to 3 g per year, that make oral iron repletion particularly impractical in this patient population (Cook & Eschbach, 1975).
Even with adequate iron stores, which most dialysis patients lack, available iron may be insufficient to meet the demand caused by rHuEPO. This situation is termed fractional iron deficiency. Simple infection and inflammation, associated with ESRD, can increase synthesis of the iron storage protein, ferritin, resulting in the sequestration of iron in the reticuloendothelial system (RES) (Yee & Besarab, 2002). Anemia and inflammation-induced cytokine production can interfere with both the effect of erythropoietin on the bone marrow and release of stored iron from the RES (Goicoechea et al., 1998; Silverberg, Iaina, Wexler, & Blum, 2001; Yee & Besarab, 2002). Even without this "RES blockade," during rHuEPO therapy, a superphysiologic rate of erythropoiesis can cause iron demand to exceed supply. Functional iron deficiency may occur in 40% to 60% of rHuEPO-treated dialysis patients.
Consequences of Iron Deficiency
The result of iron deficiency is that the effect of rHuEPO is blunted (Adamson, 1994; Macdougall, Chandler, Elston, & Harchowal, 1999; Richardson, Bartlett, & Will, 2001; Taylor, Peat, Porter, & Morgan, 1996), with, at a minimum, an increased cost of rHuEPO estimated at $109 to $240 per patient per month (Besarab et al., 2000; Macdougall et al., 1999), and, at worst, persistent anemia. Anemia impairs activities of daily living (ADL), rehabilitation, quality of life, cognitive function, nutrition, and energy (Delano, 1989; Tong & Nissenson, 2001). Anemia reduces cardiac function and increases hospitalization and mortality (Levin, Singer, Thompson, Ross, & Lewis, 1996; Silverberg et al., 2001; Tong & Nissenson, 2001). Silverberg recently described the "Cardio renal anemia syndrome" in which anemia exacerbates chronic heart failure (CHF), accelerating renal deterioration, and in turn further worsening anemia (Silverberg et al., 2003). This necessitates a treatment plan that addresses the individual elements as a unit, all of which must be treated concurrently.
IV Iron Therapy
The considerations discussed above make iron supplementation a necessary corollary of rHuEPO treatment. Unfortunately, oral iron supplementation is generally inadequate in hemodialysis patients (Wingard, Parker, Ismail, & Hakim, 199,5; Yee & Besarab, 2002), failing to achieve a hemoglobin (Hgb) of 11 to 12 g/dL and hematocrit (Hct) of 33% to 36% according to guideline 6 of the K/DOQI clinical guidelines (NKF, 2001). Given the poor iron absorption in these patients, not enough iron can be absorbed to offset the heavy iron deficiency associated with the chronic blood loss. In addition, compliance with iron supplementation regimens is often poor due to GI adverse effects (NKF, 2001).
Prevention of anemia in hemodialysis patients requires both rHuEPO therapy and parenteral iron. However, this cannot be administered simply on an "as needed" basis, but can only be optimized by establishing an IV iron protocol, administering sate and effective IV iron supplements, closely monitoring iron indices and hematologic parameters, and understanding the nurse/patient relationship.
Establishing an IV Iron Protocol
Standardized patient care.
A therapeutic protocol creates a structured, consistent, standardized approach that facilitates stable iron and hematologic parameters consistent with the K/DOQI clinical guidelines recommendations. Each nurse follows an identical protocol, and each patient receives the same level of care.
Increased Patient Management Efficiency
A predefined protocol speeds the response time and accuracy of any therapeutic intervention and also predetermines a course of action for each scenario. Protocols also facilitate nurse independence. For example, a maintenance protocol, rather than periodic ("as needed") iron therapy, lends itself to a nurse managed program, requiring less physician involvement (Vail Wyck, Bailie, & Aronoff, 2002). However, maintenance therapy can instigate iron over load, highlighting the need for precise monitoring as a component of any good protocol.
Iron Administration Based on Hematologic Parameters That Reflect Iron Status
It is important to assess iron status before rHuEPO therapy using the K/DOQI clinical guidelines for target ranges: transferrin saturation (TSAT) 20% to 50%, serum ferritin 100 to 800 ng/mL, Hgb 11 to 12 g/dL, Hct 33% to 36% (NKF, 2001). Serum ferritin is used as a gauge of total body iron stores, TSAT as a measure of circulating iron available for erythropoiesis, and Hgb reflects the effect of iron status on the red blood cell (Fishbane & Maesaka, 1997).
Figure 1 outlines our protocol for IV iron supplementation in hemodialysis patients. However, it should be kept in mind that no single value for either serum ferritin or TSAT, nor any combination of values, equals an absolute diagnosis of iron sufficiency (Van Wyck et al., 2002). Ferritin can be elevated in inflammatory states, independent of iron stores. In addition, because of the "RES blockade," serum ferritin, reflecting iron sequestered in the total body iron storage pool, may underestimate actual iron needs.
If serum ferritin is above 800 ng/mL, IV iron is discontinued and the patient is checked for other causes of rHuEPO hyporesponsiveness, such as infection or inflammation (see Figure 1). Many hemodialysis patients may have elevated serum ferritin levels independent of their iron status, and the underlying problem causing the ferritin to rise should be uncovered. The distinction between functional anemia and inflammation is also crucial, because in both cases the ferritin is above 100 ng/mL and the TSAT is below 20%. An empiric approach to making the diagnosis of functional anemia is to give supplemental iron and observe whether there is a response in either increased Hgb or decreased rHuEPO requirement.
Choosing an IV Iron Supplement
There are four IV iron supplements available in the United States: two dextrans (INFeD[R], Watson Pharmaceuticals, Corona, Calif; Dexferrum[R], American Regent Laboratories, Inc, Shirley, NY) and two nondextrans (iron sucrose [Venofer[R], American Regent Laboratories, Inc, Shirley, NY] sodium ferric gluconate [Ferrlecit[R], R&D Laboratories, Marina Del Rey, Calif]). All have been shown in clinical studies to be effective in both replenishment and maintenance of iron stores (Charytan et al., 2001; Nissenson, Lindsay, Swan, Seligman, & Strobos, 1999; Park, Uhthoff, Tierney, & Nadler, 1998) and have been shown to be capable of optimizing the use of rHuEPO therapy needed to maintain target Hgb levels (Besarab et al., 2000; Macdougall et al, 1999; Taylor et al., 1996).
Iron dextrans (Dexfirrum[R], INFeD[R])
Until 1999, the iron dextrans were the only parenteral iron supplement available in the United States. A study by Park observed that rHuEPO doses were reduced by an average of 24 IU/kg/wk after 4 months of therapy with iron dextran (Park et al., 1998), or by about 40% compared to a control group (Besarab et al., 2000).
Sodium ferric gluconate (Ferrlecit[R])
Sodium ferric gluconate has long been used in Europe but was only approved in the United States in February 1999. It is considered safer than iron dextran, with no fatalities reported (Faich & Strobos, 1999; Michael et al., 2002). No test dose is required, and sodium ferric gluconate can be administered as an IV push. In two multicenter, randomized, prospective trials, the incidence of intolerance was low (0.3%-0.44%) (Coyne et al., 2003; Michael et al., 2002). Sodium ferric gluconate can be used in iron dextran-sensitive patients, although adverse events were approximately sevenfold higher than in dextran tolerant patients (Coyne et al., 2003; Robbins & Orfitelli, 2000). However, this increased reaction rate was similar to that of placebo, suggesting that it represented host idiosyncrasy and not immunologically mediated cross-reactivity. Like iron dextran, it has a low potential for causing oxidative stress, since it is processed exclusively by RES (Ferrlecit package insert, 2001).
Iron sucrose (Venofer[R])
Iron sucrose, also long used in Europe, is the most recent addition to the hematinic therapy armamentarium in the United States (November, 2000). As with sodium ferric gluconate, a test dose is not required and it can be used in iron dextran-sensitive patients (Van Wyck et al., 2000).
Iron sucrose is considered safer than iron dextran (Fishbane & Kowalski, 2000). It can also improve responsiveness to rHuEPO therapy; a recent study showed that iron sucrose decreased the median rHuEPO dose from 136 IU/kg/wk to 72 IU/kg/wk (Richardson et al., 2001). However, it may have greater potential of causing oxidative stress than the other iron supplements, since some iron is released directly to transferrin in the circulatory system (Danielson, Salmonson, Derendorf, & Geisser, 1996).
Determining Efficacy and Safety in Clinical Practice
Each dialysis unit should assess the safety and efficacy of IV iron supplements before permanently adding them to the unit's protocol. While published clinical studies can help guide the decision, differences between IV iron supplements may only surface when used in a real-world setting. Dialysis units treat a disparate population, unlike many clinical studies.
For example, although most clinical studies seem to indicate general efficacy equivalence between the available IV iron supplements, our experience revealed some variance. Our dialysis unit evaluated the efficacy and safety of sodium ferric gluconate before adding it to our IV iron management protocol. We initially treated 172 patients with iron sucrose for 5 months according to protocol (repletion dose, 100 mg; maintenance dose, 50 mg). We then switched to sodium ferric gluconate (new and maintenance patients) for 7 months (repletion dose, 125 mg; maintenance dose, 62.5 mg).
Overall, patients treated with sodium ferric gluconate had better iron and anemia outcomes. More patients achieved a TSAT of 20% or higher after treatment with sodium ferric gluconate than after treatment with iron sucrose (8.5.4% versus 51.2%, respectively; see Figure 2a). More patients were above target Hct level (>33%) after treatment with sodium ferric gluconate than after treatment with iron sucrose (84.4% versus 73.4%, respectively; see Figure 2b). As the TSAT increased, Hct increased owing to improved rHuEPO effectiveness.
Two patients (1.2%) showed mild hypersensitivity to sodium ferric gluconate (feeling flushed after slow 1V push). We are currently conducting a more structured comparative study of these two IV iron supplements.
Dynamics of the Nurse/Patient Relationship
Finally, because a patient's personal issues can negatively impact dialysis, the dialysis nurse should ideally be aware of the patient's personal situation (i.e., lifestyle, financial resources, home life)--not just the medical history and laboratory data. The patient's lifestyle (diet, smoking, stress, compliance with medications) and financial situation (does the patient have electricity and plumbing and access to adequate nutrition?) can greatly influence the overall outcome of anemia management. By knowing what resources are available to the patient--is (s)he able to cook for her- or himself?. Can the patient shop for food, or does someone else do this?--the dialysis nurse can recommend important support services. For some patients, it may be necessary for the nurse to involve a social worker to assist in providing services and ultimately helping them to achieve optimal IV iron management.
Parenteral iron supplementation is necessary for realizing the full benefits of anemia therapy in hemodialysis patients, and successful supplementation can result in considerable cost savings. Frequent monitoring of iron and hematologic indices can help to diagnose iron deficiency early, reduce the severity of iron deficiency, and help minimize anemia and its attendant complications.
When choosing an IV iron supplement, the prescriber should consult safety and efficacy information. However, evaluating IV iron efficacy in one's own hemodialysis unit may also be instructive. By assessing a real-world, diverse group of patients, differences between IV iron supplements may become apparent.
Optimizing IV iron management is essential to the overall health of hemodialysis patients. Establishing an IV iron protocol, administering a safe and effective IV iron supplement, and developing a strong nurse/patient relationship are all indispensable to an effective and efficient hemodialysis program.
Figure 1 IV Iron Protocol Hemodialysis Iron Protocol * Assess TSAT monthly and serum ferritin quarterly in all patients *Patients with TSAT <20% receive an IV iron repletion regimen Repletion [check] IV iron 1000 mg over 8-10 weeks in divided doses [check] Hematologic parameters (TSAT, serum ferritin) weekly or biweekly in resistant cases [check] After the initial 8-10 weeks, IV iron is continued until TSAT >20% and serum ferritin >500 ng/mL (If serum ferritin rises above 800 ng/mL, stop IV iron treatment) * Maintenance [check] If monthly TSAT falls below 20%, modify IV iron dose accordingly * If last serum ferritin <500 ng/mL, resume repletion weekly doses * If last serum ferritin >500 ng/mL, resume 50% repletion weekly [check] If monthly TSAT remains above 20% * Minimize weekly dose to lowest possible dose to maintain indices in target range * Hold iron if target range is exceeded Figure 2a & 2b Percentage successful iron repletion with iron sucrose versus sodium ferric gluconate. Percentage of patients with TSAT Levels [greater than or equal to] 20% Treatment Period Iron sucrose Sodium ferric gluconate Jan 51.2 Feb 53.1 Mar 50.3 Apr 57.5 May 57.9 Jun 59.7 Jul 60.0 Aug 71.3 Sep 71.8 Oct 72.2 Nov 75.8 Dec 85.4 Percentage of patients with Hct Levels >33% Treatment Period Iron sucrose Sodium ferric gluconate Jan 73.4 Feb 70.3 Mar 69.9 Apr 66.9 May 70.5 Jun 73.9 Jul 81.8 Aug 85.5 Sep 73.2 Oct 80.0 Nov 77.9 Dec 84.4 Note: Table made from bar graph.
Note: This article is supported by a financial grant from Watson Pharma, Inc. This article has undergone peer review. The information in this article does not necessarily reflect the opinions of ANNA or the sponsor
Adamson, J.W. (1994). The relationship of erythropoietin and iron metabolism to red blood cell production in humans. Seminars in Oncology, 21(suppl 3), 9-15.
Akmal, M., Sawelson, S., Karubian, F., & Gadallah, M. (1994). The prevalence and significance of occult blood loss in patients with predialysis advanced chronic renal failure (CRF), or receiving dialytic therapy. Clinical Nephrology, 42, 198-202.
Besarab, A., Amin, N., Ahsan, M., Vogel, S.E., Zazuwa, G., Frinak, S., Zazra, J.J., Anandan, J.V., & Gupta, A. (2000). Optimization of epoetin therapy with intravenous iron therapy in hemodialysis patients. Journal of the American Society of Nephrology, 11, 530-538.
Charytan, C., Levin, N., Al-Saloum, M., Hafeez, T., Gagnon, S., & Van Wyck, D.B. (2001). Efficacy and safety of iron sucrose for iron deficiency in patients with dialysis associated anemia: North American clinical trial. American Journal of Kidney Diseases, 37, 300-307
Cook, J.D., & Eschbach, J.W. (1975). Iron absorption and loss in chronic renal disease. In: Iron metabolism and its disorders. In H. Kief (Ed.). Amsterdam: Excerpta Medica.
Coyne, D.W., Adkinson, N.F., Nissenson, A.R., Fishbane, S., Agarwal, R., Eschbach, J.W., Michael, B., Folkert, V., Baffle, D., Trout, J.R., Dahl, N., Myirski, P., Strobos, J., & Warnock, D.G. (2003). Sodium ferric gluconate complex in hemodialysis patients. II. Adverse reactions in iron dextran sensitive and dextran-tolerant patients. Kidney International, 63, 217-224.
Danielson, B.G., Salmonson, T., Derendorf, H., & Geisser, P. (1996). Pharmacokinetics of iron(III)-hydroxide sucrose complex after a single intravenous dose in healthy volunteers. Arzneim-Forsch/Drug Res, 46, 615-621.
Delano, B.G. (1989). Improvements in quality of life following treatment with r-HuEPO in anemic hemodialysis patients. American Journal of Kidney Diseases, 14(2 suppl 1), 14-18.
Faich, G. & Strobos, J. (1999). Sodium ferric gluconate complex in sucrose: Safer intravenous into therapy than iron dextrans. American Journal of Kidney Diseases, 33, 464-470.
Ferrlecit[R]. (2001). Package insert. Corona, CA: Watson Pharma, Inc.
Fishbane, S. & Kowalski, E.A. (2000). The comparative safety of intravenous iron dextran, iron saccharate, and sodium ferric gluconate. Seminars in Dialysis, 13, 381-384.
Fishbane, S., & Maesaka, J.K. (1997). Iron management in end-stage renal disease. American Journal of Kidney Diseases, 29, 319-333.
Fletes, R., Lazarus, J.M., Gage, J., & Chertow, G.M. (2001). Suspected iron dextran-related adverse drug events in hemodialysis patients. American Journal of Kidney Diseases; 37, 743-749.
Goch, J., Birgegard, G., Danielson, B.G., & Wikstrom, B. (1996). Iron absorption in patients with chronic uremia on maintenance hemodialysis and in healthy volunteers measured with a simple oral iron load test. Nephron, 73, 403-406.
Goicoechea, M., Martin, J., de Sequera, R, Quiroga, J.A., Ortiz, A., Carreno, V., & Caramelo, C. (1998). Role of cytokines in the response to erythropoietin in hemodialysis patients. Kidney International, 54, 1337-1343.
INFeD[R]. (2001). Package insert. Corona, CA: Watson Pharmeceutical, Inc.
Kooistra, M.P., Niemantsverdriet, E.C., van Es, A., Mol Beermann, N.M., Struyvenberg, A., & Marx, J.J.M. (1998). Iron absorption in erythropoietin-treated haemodialysis patients: effects of iron availability, inflammation and aluminum. Nephrology, Dialysis, and Transplantation, 13, 82-88.
Levin, A., Singer, J., Thompson, C.R., Ross, H., & Lewis, M. (1996). Prevalent left ventricular hypertrophy in the predialysis population: Identifying opportunities for intervention. American Journal of Kidney Diseases; 27, 347-354.
Macdougall, I.C., Chandler, G., Elston, O., & Harchowal, J. (1999). Beneficial effects of adopting an aggressive intravenous iron policy in a hemodialysis unit. American Journal of Kidney Diseases, 34(suppl 2), S40-S46.
McCarthy, J.T., Regnier, C.E., Loebertmann, C.L., & Bergstralh, E.J. (2000). Adverse events in chronic hemodialysis patients receiving intravenous iron dextran--A comparison of two products. American Journal of Nephrology, 20, 455-462.
Michael, B., Coyne, D.W., Fishbane, S., Folkert, V., Lynn, R., Nissenson, A.R., Agarwal, R., Eschbach, J.W., Fadem, S.Z., Trout, J.R., Strobos, J., & Warnock, D.G. (2002). Sodium ferric glucomate complex in hemodialysis patients: Adverse reactions compared to placebo and iron dextran. Kidney International, 61, 1830-1839.
National Kidney Foundation (NKF). (2001). NKF-K/DOQI Clinical Practice Guidelines for Anemia of Chronic Kidney Disease, 2000. American Journal of Kidney Diseases, 37(suppl 1), S182-S238.
Nissenson, A.R., Lindsay, R.M., Swan, S., Seligman, R, & Strobos, J. (1999). Sodium ferric gluconate complex in sucrose is sale and effective in hemodialysis patients: North American clinical trial. American Journal of Kidney Diseases, 33, 471-482.
Park, L., Uhthoff, T., Tierney, M., & Nadler, S. (1998). Effect of an intravenous iron dextran regimen on iron stores, hemoglobin, and erythropoietin requirements in hemodialysis patients. American Journal of Kidney Diseases, 31, 835-840.
Richardson, D., Bartlett, C., & Will, E.J. (2001). Optimizing erythropoietin therapy in hemodialysis patients. American Journal of Kidney Diseases, 38, 109-117.
Robbins, K.C., & Orfitelli, C. (2000). Successful use of sodium ferric gluconate in sucrose in a patient with multiple drug allergies. Nephrology Nursing Journal, 27, 521-523.
Silverberg, D.S., Iaina, A., Wexler, D., & Blum, M. (2001). The pathological consequences of anaemia. Clinical Laboratory Haematology, 23, 1-6.
Silverberg, D.S., Wexler, D., Blum, M., Tchebiner, J.Z., Sheps, D., Keren, G., Schwartz, D., Baruch, R., Yachnin, T., Shaked, M., Sehwartz, I., Steinbruch, S., & Iaina, A. (2003). The effect of correction of anaemia in diabetics and non-diabetics with severe resistant congestive heart failure and chronic renal failure by subcutaneous erythropoietin and intravenous iron. Nephrology, Dialysis and Transplantation, 18, 141-146.
Silverberg, D.S., Wexler, D., Sheps, D., Blum, M., Keren, G., Baruch, R., Schwartz, D., Yachnin, T., Steinbruch, S., Shapira, I., Laniado, S., & Iaina, A. (2001). The effect of correction of mild anemia in severe, resistant congestive heart failure using subcutaneous erythropoietin and intravenous iron: A randomized controlled study. Journal of the American College of Cardiology, 37, 1775-1780.
Taylor, J.E., Peat, N., Porter, C., & Morgan, A.G. (1996). Regular low-dose intravenous iron therapy improves response to erythropoietin in haemodialysis patients. Nephrology, Dialysis, and Transplantation, H, 1079-1083.
Tong, E.M. & Nissenson, A.R. (2001). Erythropoietin and anemia. Seminars in Nephrology, 21, 190-203.
Van Wyck, D.B., Bailie, G., & Aronoff, G. (2002). Just the FAQs: Frequently asked questions about iron and anemia in patients with chronic kidney disease. American Journal of Kidney Diseases, 39, 426-432.
Van Wyck, D.B., Cavallo, G., Spinowitz, B.S., Adhikarla, R., Gagnon, S., Charytan, C., & Levin, N. (2000). Safety and efficacy of iron sucrose in patients sensitive to iron dextran: North American clinical trial. American Journal of Kidney Diseases, 36, 88-97.
Venofer[R]. (2003). Package insert. Shirley, NY: American Regent Laboratories, Inc.
Wingard, R.L., Parker, R.A., Ismail, N., & Hakim, R.M. (1995). Efficacy of oral iron therapy in patients receiving recombinant human erythropoietin. American Journal of Kidney Diseases, 25, 433-439.
Yee, J. & Besarab, A. (2002). Iron sucrose: the oldest iron therapy becomes new. American Journal of Kidney Diseases, 40, 1111-1121.
Achieving Optimal Patient Outcomes With Intravenous Iron
Posttest-1.2 Contact Hours Posttest Questions
(See posttest instruction on the answer form, on page 455.)
1. Absolute iron deficiency refers to
A. inaccessibility of adequate iron stores.
B. RES iron blockade.
C. Insufficient total iron stores.
D. Iron malabsorption.
2. Causes of absolute iron deficiency include all of the following EXCEPT
A. low-grade GI bleeding.
B. iron malabsorption.
C. accidental blood loss.
D. rHuEPO therapy.
3. Anemia can cause all the following EXCEPT
A. functional iron deficiency.
B. impairment of activities of daily living (ADL).
C. increased hospitalization.
D. exacerbation of CHF.
4. An IV iron protocol should be established because
A. it allows decreased nursing time.
B. rHuEPO treatment will cost less.
C. prevention of anemia is optimized.
D. laboratory testing of iron indices can be decreased.
5. According to the NKF-K/DOQI Guidelines, the target serum ferritin for an ESRD patient receiving rHuEPO therapy is
A. 100 to 500 ng/mL.
B. 100 to 800 ng/mL.
C. 200 to 500 ng/mL.
D. 200 to 800 ng/mL.
6. TSAT is useful to measure in ESRD patients because
A. a value >20% represents an absolute diagnosis of iron sufficiency.
B. it is elevated in inflammatory states.
C. it is a gauge of total body iron stores.
D. it is a measure of circulating iron available for erythropoiesis.
7. An anemic patient with a TSAT <20%, a serum ferritin of 300 ng/mL, and increased Hgb in response to iron probably has
A. functional iron deficiency.
B. absolute iron deficiency.
D. adequate iron stores
8. In developing an IV iron management protocol, each dialysis unit should
A. adhere strictly to published clinical studies.
B. adjust protocol to accommodate the local patient population.
C. prevent subjective patient issues from influencing treatment decisions.
D. attempt to minimize rHuEPO use.
9. Iron deficiency occurs in what percentage of rHuEPO-treated dialysis patients?
B. 10% to 30%
C. 30% to 50%
Martha Colfer, BSN, RN, CHN, is facility manager, Watson Wise Dialysis Center, Tyler, TX. She is a member of ANNA's Dallas Chapter.
|Printer friendly Cite/link Email Feedback|
|Title Annotation:||Sponsored Educational Supplement|
|Publication:||Nephrology Nursing Journal|
|Date:||Aug 1, 2003|
|Previous Article:||Renal hemodynamics: an overview.|
|Next Article:||Hemoglobin variability: impact on anemia management practices.|