Diagnosing and treating anemia and iron deficiency in hemodialysis patients. (Educational Supplement).
Given the high prevalence of iron deficiency in hemodialysis patients, the iron status of patients diagnosed with anemia should be evaluated. Unfortunately, the common laboratory measurements for determining iron status are not reliable because they are influenced by other factors, such as inflammation. Health care providers are, therefore, encouraged to use newer methods, particularly reticulocyte hemoglobin content (CHr), which provides a real-time estimate of iron availability (Fishbane, Galgano, Langley, Canfield, & Maesaka, 1997). Once iron deficiency has been diagnosed and treated with iron supplementation, patients must continue therapy with maintenance doses of iron to sustain adequate iron stores for red blood cell production. This phase of iron therapy is crucial for good patient outcome but is often neglected. The goal of this report is to highlight guidelines for diagnosing and treating anemia and iron deficiency in hemodialysis patients.
Anemia and Iron Deficiency
Causes. Understanding the etiology of anemia and iron deficiency can help health care providers diagnose and treat these conditions. The underlying cause of anemia in most hemodialysis patients with chronic renal failure is the inadequate production of erythropoietin (EPO) (Adamson & Eschbach, 1998). Erythropoietin is a growth factor that is mainly produced in the kidney and is essential for erythropoiesis in the bone marrow. The cause of insufficient EPO production is not fully understood, but it is likely that chronic renal failure is accompanied by damage to the fibroblasts in the renal cortex where EPO is produced (Donnelly, 2001).
While reduced synthesis of EPO is usually the primary cause of anemia, several additional factors can lead to anemia and/or increase the severity of anemia caused by EPO deficiency. These factors include hyperparathyroidism, decreased red cell lifespan, blood loss, infection/inflammation, and iron deficiency.
During hyperparathyroidism, excessive amounts of parathyroid hormone (PTH) are produced, which causes bones to become depleted of calcium. The result is a reduced ability of the bone marrow to produce erythrocytes, which can be reversed with a parathyroidectomy (Kotzmann et al., 1997; Rault & Magnone, 1996). Decreased red cell lifespan in patients with chronic renal failure may be due to osmotic fragility of red cells caused by the presence of uremic toxins in the blood (Wu et al., 1998). Correcting uremia through hemodialysis has been shown to reduce osmotic fragility and, therefore, may increase red cell lifespan (Wu et al., 1998). Blood loss, which occurs as a result of the hemodialysis procedure, diagnostic sampling, and gastrointestinal bleeding, contributes to iron deficiency and increases the severity of anemia (Marcuard & Weinstock, 1988; Nissenson & Strobos, 1999).
Inflammation is a frequent characteristic of chronic renal failure and is now recognized as contributing to morbidity and mortality. Several factors can cause inflammation in hemodialysis patients, including the dialysis procedure, infection, and chronic intestinal bleeding (Stenvinkel, 2001). A recent study by Qureshi and colleagues (2002) detected markers of inflammation in 48% of hemodialysis patients and found that inflammation was a significant independent risk factor for mortality; inflammation was more prevalent in the nonsurvivors (44%) than in the survivors (13%). Inflammation also appeared to be interrelated with the occurrence of malnutrition and with cardiovascular disease, which is the leading cause of death in hemodialysis patients (USRDS, 2000). Also, correlative evidence indicates that inflammation may increase the severity of anemia by reducing the patient's ability to respond to therapy. For example, the presence of serum C-reactive protein (CRP), a marker of inflammation, is a strong predictor of resistance to epoetin alfa therapy in hemodialysis patients (Barany, Divino Filho, & Bergstrom, 1997). Inflammation caused by infection may also cause anemia by reducing iron transfer into the bone marrow and/or by inhibiting the synthesis of transferrin, an iron-binding transport protein in the plasma and extracellular fluid (Rosenthal, 1995). This results in iron deficiency and, therefore, a decrease in the production of red blood cells.
In addition to blood loss and infection, iron deficiency may also result from inadequate intestinal absorption and/or when the need for iron exceeds dietary intake. Since iron is necessary for Hgb production, iron deficiency can cause anemia and reduce the ability of a patient to respond to epoetin alfa therapy. Iron deficiency has been shown to occur in as many as 40% of hemodialysis patients with chronic renal failure (Tessitore et al., 2001). Therefore, it is important that hemodialysis patients be evaluated for anemia and iron deficiency concurrently.
Anemia is defined in terms of Hgb and hematocrit (Hct) levels. The mean values of Hgb and Hct for healthy adult men are 15.5 [+ or -] 2.0 g/dl and 47 [+ or -] 60/0, respectively, and the values for healthy menstruating women are 14.0 [+ or -] 2.0 g/dl and 41 [+ or -] 5%, respectively (see Table 1) (National Kidney Foundation, 2000). According to the National Kidney Foundation Clinical Practice Guidelines for Anemia of Chronic Kidney Disease (NKF-KDOQI), an anemia work-up should be initiated in patients with chronic renal failure when Hgb levels are less than 12 g/dl and the Hct is less than 37% for adult males and postmenopausal women (National Kidney Foundation, 2000). Compared with Hct, Hgb is a more accurate measure of anemia for several reasons. First, Hgb is stable when blood is stored at room temperature, but Hct is not. The mean corpuscular volume (MCV) from which Hct is calculated is stable for only 8 hours at room temperature and 24 hours when a blood sample is refrigerated (National Kidney Foundation, 2000). Also, the analyzers that measure Hgb produce consistent results that can be compared between laboratories, while the instruments that measure Hct have a higher margin of error (Fraser et al., 1989; Paterakis et al., 1994). Therefore, Hgb should be the primary means of quantifying the level of anemia in patients with chronic renal failure.
Evaluation of anemia should consist of at least the following measurements: Hgb, Hct, red blood cell count, reticulocyte count, iron parameters (i.e., serum iron, total iron binding capacity [TIBC], percent transferrin saturation [TSAT; serum iron x 100 divided by TIBC], serum ferritin), and a test for occult blood in the stool. Red blood cell counts range from 4.5 to 6.2 million/[micro]L in healthy men and 4.2 to 5.4 million/[micro]l in healthy women, and the normal range for reticulocyte count, which is the measure of slightly immature red blood cells, is 0.5% to 2.0%. The reticulocyte count is an important measure of the body's ability to make new red blood cells to replace those lost during dialysis, laboratory sampling, bleeding, or normal cell turnover. A greater-than-normal percentage of reticulocytes may indicate bleeding, while lower-than-normal numbers may indicate several problems, including bone marrow failure and iron deficiency. Since gastrointestinal bleeding is not uncommon in hemodialysis patients with chronic renal failure, a stool guaiac test for occult blood is recommended to test for this condition (Marcuard & Weinstock, 1988). Hemodialysis patients who are diagnosed with anemia should be tested for elevated levels of serum PTH in order to determine whether secondary hyperparathyroidism is causing their anemia. Levels of PTH in healthy individuals range from 10 to 55 pg/ml.
Since iron is necessary for Hgb production, iron deficiency can increase the severity of anemia. Consequently, the iron status of hemodialysis patients who are diagnosed with anemia should be evaluated. Available iron is usually determined by measuring parameters that assess circulating iron and storage iron. Circulating iron parameters include serum iron, TIBC, and TSAT, which indicate the amount of iron immediately available for Hgb synthesis. Serum iron reflects the amount of iron in the blood and varies widely in healthy individuals, ranging from 60 to 170 [micro]g/dl. The TIBC is a test that measures the total binding capacity of transferrin; TIBC is usually elevated when iron is low. In contrast, the TSAT measures the iron occupancy of transferrin, which is reduced when iron levels are low. Normal TIBC values range from 240 to 450 [micro]g/dl, and TSAT values of healthy individuals range from 30% to 40%. Serum ferritin is the most frequently used parameter to assess the amount of iron stored in the body. In healthy individuals, serum ferritin ranges from 30 to 200 ng/ml.
Iron deficiency can be either absolute or functional. Absolute iron deficiency in patients with chronic renal failure occurs when circulating iron and iron stores are depleted, indicated by a TSAT of less than 20% and a serum ferritin value of less than 100 ng/ml (National Kidney Foundation, 2000). In contrast, functional iron deficiency results when not enough iron from iron stores is released to support Hgb synthesis. This can occur in the presence of adequate iron stores when erythropoiesis is increased during therapy with epoetin alfa. As a result, TSAT decreases to levels consistent with absolute iron deficiency, but serum ferritin remains normal or slightly elevated. Although patients appear to have adequate levels of storage iron, they may still demonstrate an erythroid response when administered iron therapy. This raises the question as to whether clinicians should rely exclusively on TSAT and serum ferritin parameters for determining iron deficiency.
Although serum ferritin and TSAT are the common parameters used to determine iron deficiency, they do not accurately reflect the iron status of the patient. Saturated transferrin measurements have limited sensitivity and specificity. For example, a TSAT cutoff level of 21% has a sensitivity of 81% but a specificity of only 63% (Fishbane, Kowalski, Imbriano, & Maesaka, 1996). Decreasing the cutoff value improves the specificity but also reduces the sensitivity, while increasing the cutoff value has the opposite effects. Serum ferritin is also not reliable because it is an acute-phase reactant, which means that its levels increase during inflammation (Harrison & Arosio, 1996). Since inflammation is common in hemodialysis patients, serum ferritin levels may appear normal or even elevated in iron-deficient patients.
Recently, several studies have found that CHr is a more accurate measure of iron status compared with TSAT or serum ferritin (Brugnara, Zurakowski, DiCanzio, Boyd, & Platt, 1999; Fishbane, Shapiro, Dutka, Valenzuela, & Faubert, 200I). Reticulocytes are closely related to the cells in the bone marrow that are actively using iron for the synthesis of Hgb. The Hgb content of the reticulocytes, therefore, reflects the amount of iron available during red blood cell development (Besarab, 2001). In a study by Fishbane and colleagues, a CHr below 26 pg was shown to predict iron deficiency with 100% accuracy (Fishbane et al., 1997). This analysis provides a real-time estimate of iron availability and can detect an increase in CHr within 48 hours after the intravenous (IV) infusion of iron (Fishbane et al., 1997). Health care providers should, therefore, consider adding CHr to their panel of biochemical indicators of iron status in hemodialysis patients who have been diagnosed with anemia. A CHr value less than 29 pg indicates iron deficiency (Besarab, 2001).
An effective treatment strategy for anemia in hemodialysis patients addresses the underlying cause of the condition and the additional factors that influence its severity. Since EPO deficiency is usually the cause of anemia in hemodialysis patients, most patients are treated with epoetin alfa, a recombinant version of human EPO (rEPO). The goal of rEPO therapy is to achieve a target range of 11 to 12 g/dl for Hgb and 33% to 36% for Hct (National Kidney Foundation, 2000). Hemoglobin/Hct should be monitored every 1 to 2 weeks following initiation of rEPO therapy until stable target Hgb/Hct levels and rEPO dose have been achieved. Thereafter, Hgb/Hct should be monitored every 2 to 4 weeks (National Kidney Foundation, 2000). The objective when choosing the correct initial rEPO dose is to achieve the target Hgb/Hct within a 2- to 4-month period. The NKF-K/DOQI recommends that the initial dose of rEPO should be 80 to 120 units/kg/wk (typically 6,000 units/wk) for a 70-kg individual, given in 2 or 3 doses per week if administered subcutaneously (SC), while the IV dose should be 120 to 180 units/kg/wk (typically 9,000 units/wk) given in 3 divided doses (National Kidney Foundation, 2000). Pharmacokinetic studies have shown that the half-life of rEPO is prolonged in the circulation when administered SC (Winearls, 1998). The weekly dose of rEPO needed to. maintain target levels of Hct is lower when rEPO is administered SC (Kaufman et al., 1998). Therefore, the SC administration of rEPO may have advantages over the IV route, but both methods yield good results.
In addition to rEPO therapy, an attempt should be made to minimize the secondary factors that increase the severity of anemia. The most common condition that increases the severity of anemia and causes an incomplete response to rEPO treatment is iron deficiency (National Kidney Foundation, 2000; Winearls, 1998). Hemodialysis patients who are not responding to rEPO treatment and who have been diagnosed with absolute or functional iron deficiency should receive iron supplementation.
Currently, three IV iron supplements are available in the United States: iron dextran, sodium ferric gluconate, and iron sucrose. Therapy with oral iron is another option, but this treatment usually cannot maintain adequate iron stores (Macdougall et al., 1996). Each of the IV forms of iron has been shown to improve the response to rEPO in hemodialysis patients (Besarab et al., 2000; Richardson, Bartlett, & Will, 2001; Taylor, Peat, Porter, & Morgan, 1996). The goal with iron supplementation is to maintain the target Hgb/Hct levels described for rEPO therapy. To achieve this, sufficient iron should be administered to maintain a TSAT of greater than or equal to 20%, a serum ferritin level of greater than or equal to 100 ng/ml, and a CHr of greater than 29 pg (Besarab, 2001; National Kidney Foundation, 2000). To determine the correct dosing regimen, health care providers should refer to the prescribing information of the specific iron supplement they are administering.
In general, target levels of iron indices can be achieved with the administration of 1 g of IV iron given over an 8- or 10-week period. For sodium ferric gluconate, the recommended dosage is 125 mg diluted in 100 ml of 0.9% sodium chloride administered by IV infusion over 1 hour (Ferrlecit[R] package insert, 2001). Alternatively, sodium ferric gluconate can also be administered undiluted as a slow IV push at a rate of up to 12.5 mg/min (Ferrlecit[R] package insert, 2001). Usually, 1 g administered over 8 sessions will increase iron stores and Hgb to target levels. For iron sucrose, it is recommended that a dosage of 100 mg in 5 ml be administered as a slow IV injection at a rate of 1 ml per minute or as an infusion diluted in 100 ml of 0.90/0 sodium chloride (Venofer[R] package insert, 2000). Most patients will require a minimum of 1 g administered over 10 sequential dialysis sessions (Venofer[R] package insert, 2000). It should be noted that the use of iron dextran is associated with a risk of anaphylaxis and that a test dose of 25 mg is required before initiating therapy with this iron supplement (Infed[R] package insert, 2001). In contrast, anaphylactic reactions are not associated with sodium ferric gluconate and iron sucrose, and test doses of these supplements are not required (Ferrlecit[R] package insert, 2001; Venofer[R] package insert, 2000).
Health care providers who are administering iron supplementation to anemic hemodialysis patients should be aware that maintenance doses of iron are critical for maintaining Hgb/Hct and laboratory parameters of iron storage at target levels once these targets are reached. Chronic conditions, such as chronic bleeding, may continue to cause iron depletion after iron supplementation has been stopped. Maintenance doses usually range between 25 to 125 mg of IV iron per week. For sodium ferric gluconate, 62.5 mg given once per week is an effective maintenance dose (Fishbane & Wagner, 2001). Maintenance iron status should be monitored at least once every 3 months to ensure that an adequate dose of iron is being administered.
As mentioned above, iron status should not be determined using only serum ferritin levels, since infection/inflammation can increase ferritin to normal or elevated levels, thereby giving the appearance of proper iron stores. Distinguishing between functional iron deficiency and inflammation is a common clinical problem, since the TSAT may be less than 20% and serum ferritin may be greater than 100 ng/ml during both situations. When this TSAT/serum ferritin profile occurs, measuring CHr in conjunction with serum CRP can help distinguish between functional iron deficiency and inflammation (Besarab, 2001). C-reactive protein is an ideal indicator of inflammatory events because it is almost undetectable in healthy individuals, whereas during inflammation its levels will rise hundreds or thousands of times above normal. Baseline values of CRP should be determined when a hemodialysis patient is first diagnosed with anemia, since some patients may have chronically elevated levels. As discussed by Besarab, the increase in serum ferritin levels caused by inflammation can be dramatically higher (>500 ng/ml) than levels found during functional iron deficiency (Besarab, 2001). Reticulocyte hemoglobin content and CRP are particularly helpful in determining the presence of inflammation when serum ferritin is greater than 500 ng/ml and TSAT is less than 20%. Iron deficiency in the presence of inflammation is indicated when CHr levels are below 29 pg and CRP levels are higher than 15 mg/ml, while low levels of CHr (<29 pg) and 0 to low levels of CRP (<1.5 mg/ml) suggest iron deficiency in the absence of inflammation (see Table 2). When high levels of CRP are observed, reversible causes of inflammation should be investigated and, if found, treated accordingly.
The accurate diagnosis of anemia and iron deficiency is essential in hemodialysis patients, since these conditions are prevalent during chronic renal failure. When anemia is diagnosed, efficient patient care includes the monitoring of confounding factors, such as inflammation and bleeding, that may worsen the effects of anemia. Iron deficiency is especially problematic because it increases the severity of anemia and impairs the patient's response to rEPO therapy. Therefore, clinicians should use accurate laboratory parameters when determining the iron status of their patients. Once anemia and iron deficiency are diagnosed, therapy should be initiated with the understanding that these are the result of a chronic condition and, thus, may require long-term therapy. Given this, health care providers are encouraged to administer maintenance doses of iron when target Hgb and iron stores are achieved.
Table 1 Normal Hematologic Values for Healthy Individuals Parameter Value Hemoglobin, g/dl * 15.5 [+ or -] 2.0 Hematocrit, % * 47 [+ or -] 6 Red blood cell count, million/[micro]l 4.5-6.2 in men, 4.2-5.4 in women Reticulocyte count, % 0.5-2.0 Iron parameters Serum iron, [micro]g/dl 60-170 TIBC, [micro]g/dl 240-450 TSAT, % 30-40 Serum ferritin, ng/ml >100 CHr, pg >29 * Value for adult men/postmenopausal women. TIBC indicates total iron binding capacity; TSAT, transferrin saturation (serum iron x 100 divided by TIBC)' and CHr, reticulocyte hemoglobin content. Table 2 Changes in Iron Status During Anemia Parameter Absolute Iron Functional Iron Inflammation- Deficiency Deficiency induced * Serum ferritin, ng/ml <100 >100 >100 TSAT, % <20 <20 <20 CHr, pg <29 <29 <29 CRP, mg/ml ([dagger]) 0-15 0-15 >15 * During inflammation serum ferritin levels are normal or elevated, while TSAT and CHr are below normal, indicating inadequate iron levels. ([dagger]) CRP levels are usually 0 in healthy individuals and increase during inflammation, but hemodialysis patients may have slightly elevated levels at baseline. TSAT indicates transferrin saturation; CRP, C-reactive protein; and CHr, reticulocyte hemoglobin content.
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., & Eschbach, J.W. (1998). Erythropoietin for endstage renal disease. New England Journal of Medicine, 339, 625-627.
Barany, P., Divino Filho, J., & Bergstrom, J. (1997). High C-reactive protein is a strong predictor of resistance to erythropoietin in hemodialysis patients. American Journal of Kidney Diseases, 29, 565-568.
Besarab, A. (2001). Evaluating iron sufficiency: A clearer view. Kidney International, 60, 2412-2414.
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.
Brugnara, C., Zurakowski, D., DiCanzio, J., Boyd, T., & Platt, O. (1999). Reticulocyte hemoglobin content to diagnose iron deficiency in children. Journal of the American Medical Association, 281, 2225-2230.
Donnelly, S. (2001). Why is erythropoietin made in the kidney? The kidney functions as a critmeter. American Journal of Kidney Diseases, 38, 415-425.
End Stage Renal Disease Clinical Performance Measures Project Annual Report. (2001). Department of Health and Human Services, Centers for Medicare and Medicaid Services, Center for Beneficiary Choices, Baltimore, Maryland.
Ferrlecit[R] [package insert] (2001). Morristown, NJ: Watson Pharma, Inc.
Fishbane, S., Galgano, C., Langley, R.C. Jr., Canfield, W., & Maesaka, J.K. (1997). Reticulocyte hemoglobin content in the evaluation of iron status of hemodialysis patients. Kidney International, 52, 217-222.
Fishbane, S., Kowalski, E.A., Imbriano, L.J., & Maesaka, J.K. (1996). The evaluation of iron status in hemodialysis patients. Journal of the American Society of Nephrology, 7, 2654-2657.
Fishbane, S., Shapiro, W., Dutka, P., Valenzuela, O.F., & Faubert, J. (2001). A randomized trial of iron deficiency testing strategies in hemodialysis patients. Kidney International, 60, 2406-2411.
Fishbane, S., &Wagner, J. (2001). Sodium ferric gluconate complex in the treatment of iron deficiency for patients on dialysis. American Journal of Kidney Diseases, 37, 879-883.
Fraser, C.G., Wilkinson, S.P., Neville, R.G., Knox, J.D., King, J.F., & MacWalter, R.S. (1989). Biologic variation of common hematologic laboratory quantities in the elderly. American Journal of Clinical Pathology, 92, 465-470.
Harrison, P.M., & Arosio, P. (1996).The ferritins: Molecular properties, iron storage function and cellular regulation. Biochimica et Biophysica Acta, 1275, 161-203.
Ifudu, O., Feldman, J., & Friedman, E.A. (1996). The intensity of hemodialysis and the response to erythropoietin in patients with end-stage renal disease. New England Journal of Medicine, 334, 420-425.
INFeD[R] [package insert]. (1996). Morristown, NJ: Watson Pharma, Inc.
Kaufman, J.S., Reda, D.J., Fye, C.L., Goldfarb, D.S., Henderson, W.G., Kleinman, J.G., & Vaamonde, C.A. (1998). Subcutaneous compared with intravenous epoetin in patients receiving hemodialysis. New England Journal of Medicine, 339, 578-583.
Kotzmann, H., Abela, C., Heindl, J., Clodi, M., Riedl, M., Barnas, U., Heinzl, H., Niederle, B., Geissler, K., Waldhausl, W., & Luger, A. (1997). Effect of successful parathyroidectomy on hematopoietic progenitor cells and parameters of red blood cells in patients with primary hyperparathyroidism. Hormone and Metabolic Research, 29, 387-392.
Macdougall, I.C., Tucker, B., Thompson, J., Tomson, C.R. V., Baker, L.R.I., & Raine, A.E.G. (1996). A randomized controlled study of iron supplementation in patients treated with erythropoietin. Kidney International, 50, 1694-1699.
Marcuard, S.P., & Weinstock, J.V. (1988). Gastrointestinal angiodysplasia in renal failure. Journal of Clinical Gastroenterology, 10, 482484.
National Kidney Foundation. (2000). National Kidney Foundation-K/DOQI Clinical Practice Guidelines for Anemia of Chronic Kidney Disease. (2000). American Journal of Kidney Diseases, 37, S182-S238.
Nissenson, A.R., & Strobos, J. (1999). Iron deficiency in patients with renal failure. Kidney International, 55 (suppl 69), S18-S21.
Paterakis, G.S., Laoutaris, N.P., Alexia, S.V., Siourounis, P.V., Stamulakatou, A.K., Premetis, E.E., Sakellariou, C., Terzoglou, G.N., Papassotiriou, I.G., & Loukopoulos, D. (1994). The effect of red cell shape on the measurement of red cell volume. A proposed method for the comparative assessment of this effect among various haematology analysers. Clinical and Laboratory Haematology, 16, 235-245.
Qureshi, A.R., Alvestrand, A., Divino-Filho, J.C., Gutierrez, A., Heimburger, O., Lindholm, B., & Bergstrom, J. (2002). Inflammation, malnutrition, and cardiac disease as predictors of mortality in hemodialysis patients. Journal of the American Society of Nephrology, 13 (suppl 1), S28-S36.
Rault, R., & Magnone, M. (1996). The effect of parathyroidectomy on hematocrit and erythropoietin dose in patients on hemodialysis. American Society for Artificial Internal Organs Journal, 42, M901-M903.
Richardson, D., Bartlett, C., & Will, E.J. (2001). Optimizing erythropoietin therapy in hemodialysis patients. American Journal of Kidney Diseases, 38, 109-117.
Rosenthal, D.S. (1995). Hematologic manifestations of infectious disease. In R. Hoffman, E.J. Benz, S.J. Shattil, B. Furie, H.J. Cohen, & L.E. Silberstein (Eds.), Hematology: Basic principles and practice (pp. 2161-2166). New York: Churchill Livingstone.
Stenvinkel, P. (2001). The rote of inflammation in the anaemia of end-stage renal disease. Nephrology, Dialysis, Transplantation, 16 (suppl 7), 36-40.
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, Transplantation, 11, 1079-1083.
Tessitore, N., Solero, G.P., Lippi, G., Bassi, A., Faccini, G.B., Bedogna, V., Gammaro, L., Brocco, G., Restivo, G., Bernich, P. Lupo, A., & Maschio, G. (2001). The role of iron status markers in predicting response to intravenous iron in haemodialysis patients on maintenance erythropoietin. Nephrology, Dialysis, Transplantation, 16, 1416-1423.
United States Renal Data System Annual Report. (2000). National Institutes of Health, National Institute of Diabetes and Digestive and Kidney Diseases, Section H:583-662, Bethseda, MD.
Venofer[R] [package insert]. (2000). Shirley, NY: American Regent Laboratories, Inc.
Winearls, C.G. (1998). Recombinant human erythropoietin: 10 years of clinical experience. Nephrology, Dialysis, Transplantation, 13 (suppl 2), 3-8.
Wu, S.-G., Jeng, F.-R., Wei, S.-Y., Su, C.-Z., Chung, T.-C., Chang, W.J., & Chang, H.-W. (1998). Red blood cell osmotic fragility in chronically hemodialyzed patients. Nephron, 78, 28-32.
Jamie P. Foret, BSN, RN, is a registered nurse with a bachelor's degree in nursing. As a medical liaison for Watson Pharmaceuticals, his primary responsibility is to educate nephrology nurses on the latest advances in anemia management.
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|Author:||Foret, Jamie P.|
|Publication:||Nephrology Nursing Journal|
|Article Type:||Statistical Data Included|
|Date:||Jun 1, 2002|
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