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Anemia In Chronic Kidney Disease PowerPoint Presentation

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Description : Check out this medical PowerPoint presentation titled "Anemia in Chronic Kidney Disease” by Andrew Narva, MD, FASN and Amy Barton Pai, PharmD, MHI, FASN, FCCP, FNKF.

This medical PowerPoint presentation is about anemia, a common complication of chronic kidney disease (CKD), which occurs when the kidneys are not functioning properly and are unable to produce enough erythropoietin (EPO), a hormone that stimulates the production of red blood cells in the bone marrow.

In CKD, anemia can develop as early as stage 3 of the disease and can worsen as kidney function declines. It is more common in patients with more severe CKD, especially those on dialysis.

The symptoms of anemia in CKD can include fatigue, weakness, shortness of breath, dizziness, and difficulty concentrating. Anemia can also exacerbate other complications of CKD, such as cardiovascular disease.

Treatment of anemia in CKD typically involves administering erythropoiesis-stimulating agents (ESAs), which are medications that stimulate the production of red blood cells. Iron supplementation may also be necessary to help support the production of red blood cells.

In addition to medical treatment, patients with anemia in CKD may also benefit from lifestyle changes such as increasing physical activity, eating a healthy diet, and quitting smoking. Close monitoring of anemia levels is important to ensure that treatment is effective and adjusted as necessary.

Tags : Anemia, Chronic Kidney Disease, erythropoietin, red blood cells, bone marrow, Nephrology, Nephrology PowerPoint presentation

Published on : Jun 07, 2023 | Views : 1887 | Downloads : 12

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Slide 1-

Module 3: Anemia in Chronic Kidney Disease Andrew Narva, MD, FASN & Amy Barton Pai, PharmD, MHI, FASN, FCCP, FNKF
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Andrew Narva, MD, FASN No financial disclosures/conflicts of interest Amy Barton Pai, PharmD, MHI, FASN, FCCP, FNKF Disclosure: Consultant for Keryx Slide 2 of 68 Faculty Disclosure Information
Slide 3-

About NKDEP This professional development opportunity was created by the National Kidney Disease Education Program (NKDEP), an initiative of the National Institute of Diabetes and Digestive and Kidney Diseases of the National Institutes of Health. With the goal of reducing the burden of chronic kidney disease (CKD), especially among communities most impacted by the disease, NKDEP works in collaboration with a range of government, nonprofit, and health care organizations to: raise awareness among people at risk for CKD about the need for testing; educate people with CKD about how to manage their disease; provide information, training, and tools to help health care providers better detect and treat CKD; and support health system change to facilitate effective CKD detection and management. To learn more about NKDEP, please visit: http://www.nkdep.nih.gov. For additional materials from NIDDK, please visit: http://www.niddk.nih.gov. Slide 3 of 68
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Meet our Presenters Amy Barton Pai, PharmD, MHI, FASN, FCCP, FNKF Dr. Barton Pai is Chair of the National Kidney Disease Education Program’s Pharmacy Working Group Dr. Amy Barton Pai, Pharm.D., MHI, FASN, FCCP, FNKF is Associate Professor of Clinical Pharmacy at the University of Michigan College of Pharmacy. She obtained her Bachelor of Science in Pharmacy from Albany College of Pharmacy in 1996 and then completed a Pharmacy Practice Residency at St. Peter’s Hospital in Albany, New York. She received her Doctor of Pharmacy from Albany College of Pharmacy in 1999. From 1999-2001 she was a Nephrology Research Fellow at the University of Illinois at Chicago. Dr. Pai was on faculty at the University of New Mexico College of Pharmacy and School of Medicine from 2001 to 2008 and at Albany College of Pharmacy and Health Sciences from 2008 to 2016. She earned a Master's degree in Healthcare Innovation in 2018. Slide 4 of 68
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Andrew S. Narva, M.D., F.A.C.P. Dr. Narva is the Director of the National Kidney Disease Education Program (NKDEP) at the National Institutes of Health. Prior to joining the NKDEP in 2006, he served as Director of the Kidney Disease Program for the Indian Health Service (IHS). Dr. Narva continues to serve as the Chief Clinical Consultant for Nephrology for IHS and to provide care for patients at Zuni Pueblo through a telemedicine clinic. Dr. Narva is a member of the American Board of Internal Medicine Nephrology Subspecialty Board. He has served as a member of the Eighth Joint National Committee (JNC 8) Expert Panel, the National Quality Forum Renal Steering Committee, the Kidney Disease Outcomes Quality Initiative Work Group on Diabetes in Chronic Kidney Disease, and the Medical Review Board of End Stage Renal Disease Network 15. Slide 5 of 68 Meet our Presenters
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After completing this module, you will be able to: Describe applications of erythropoiesis and iron metabolism in treating anemia of CKD and the role of the pharmacist in addressing current controversies in care. Discuss how laboratory, clinical, and medication data are used to assess and monitor anemia in chronic kidney disease (CKD) and identify optimal management strategies. Review the key differences in formulation, pharmacokinetics, pharmacodynamics and immunogenicity between the available intravenous iron products. Integrate the evidence-base for erythropoiesis stimulating agents (ESA) into care paradigms for different CKD settings (e.g. pre-dialysis vs. dialysis vs. transplant) Slide 6 of 68
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Slide 7 of 68 Anemia is a complication of CKD Anemia may: Result from inadequate erythropoietin synthesis. Develop early and worsen as CKD progresses. Occur earlier in people with diabetes. Involve inadequate iron intake, impaired iron absorption and chronic inflammation.
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Anemia may develop as eGFR declines Reference: Adapted from Stauffer PLoS ONE 2014 Slide 8 of 68 NHANES 2007-2010
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Kidneys act as oxygen sensors in the body Slide 9 of 68 Renal tissue hypoxia triggers erythropoietin production. Erythropoietin stimulates erythrocyte (red blood cell) synthesis in bone marrow. Hemoglobin is the primary iron-containing protein in erythrocytes that transports and delivers oxygen to tissues. Both erythropoietin and iron are required to produce hemoglobin (Hgb) and correct hypoxia.
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Red Blood Cell Cycle Slide 10 of 68
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Anemia in CKD Slide 11 of 68 Anemia of CKD
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Question Slide 12 of 68 A 66 year old patient with an eGFR of 20 mL/min/1.73m2 presents with symptoms of anemia. The patient has been taking ferrous sulfate orally and currently has a diabetic foot infection being treated with antibiotics. Which of the following is likely contributing to the patient’s anemia? Decrease in EPO production Decrease in iron absorption in GI tract Infection All of the above
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Answer Slide 13 of 68 A 66 year old patient with an eGFR of 20 mL/min/1.73m2 presents with symptoms of anemia. The patient has been taking ferrous sulfate orally and currently has a diabetic foot infection being treated with antibiotics. Which of the following is likely contributing to the patient’s anemia? Decrease in EPO production Decrease in iron absorption in GI tract Infection All of the above Answer: D Anemia in CKD is often multi-factorial. The principal cause of anemia in CKD is decreased EPO production but, in this patient decreased iron absorption in GI tract and current infection are also contributors.
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Iron transport & storage are dysregulated in CKD Slide 14 of 68 Reference: http://www.cdc.gov/ncbddd/hemochromatosis/training/pathophysiology/iron_cycle_popup.htm
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Additional factors for inadequate iron in CKD Slide 15 of 68 References: Kopple et al. Kidney Int 2000; 57(4):1688–1703; Young et al. Clin J Am Soc Nephrol 2009;4(8):1384–1387. Both a spontaneous decrease in intake and aversion to foods with protein may occur as eGFR declines. Hepcidin may accumulate in CKD. Hepcidin is the hormone that controls iron homeostasis. This hormone regulates iron absorption in the gut and mobilization of stored iron. Inflammation may reduce absorption of iron.
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Hepcidin-Master iron regulator Slide 16 of 68 Iron regulates hepcidin; increased iron levels stimulates hepcidin production Increased erythropoietin activity reduces hepcidin levels Inflammation and infection increases hepcidin synthesis Hepcidin inhibits iron release from macrophages as well as intestinal iron absorption.
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Anemia in CKD is associated with morbidity and mortality Toto. Kidney Int 2003; 64(suppl 87):S20–S23. Slide 17 of 68 Observational data show association with: Coronary artery disease Left ventricular hypertrophy Hospitalization for cardiac disease Death from congestive heart failure All-cause mortality
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Question Slide 18 of 68 Which of the following is a possible cause of anemia in chronic kidney disease patients? Increased GI iron absorption Decreased erythropoietin synthesis Increased red blood cell life span Decreased inflammation
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Answer Slide 19 of 68 Which of the following is a possible cause of anemia in chronic kidney disease patients? Increased GI iron absorption Decreased erythropoietin synthesis Increased red blood cell life span Decreased inflammation Answer: B As kidney function declines, the kidney becomes unable to produce adequate erythropoietin and poor erythropoiesis is compounded by reduced iron absorption. Answer C and D are incorrect because red blood cell life span decreases and systemic inflammation typically increases in patients with CKD.
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Slide 20 of 68 USING LABORATORY DATA TO GUIDE CKD MANAGEMENT
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How do we know if the patient has anemia? Slide 21 of 68 Diagnosis of anemia Hemoglobin Males: Hb <13 g/dL Females: Hb <12 g/dL Additional workup CBC RBC indices Ferritin Transferrin saturation (TSAT) Stool screen for occult blood Serum folate Vitamin B12
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Symptoms and Signs Slide 22 of 68 Symptoms Signs Palpitations Vertigo Pica (with iron deficiency) Irritability Fatigue Dizziness ↓ exercise tolerance Shortness of breath Weakness Tachycardia Pale appearance ↓ mental acuity Neurological symptoms (with vitamin B12 deficiency)
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Assessing iron status Slide 23 of 68 Serum iron Measures ferric iron (Fe3+), subject diurnal variation Total iron-binding capacity (TIBC) TIBC measures the amount of iron binding sites available on serum transferrin. Transferrin saturation (TSAT) Generally reflects iron available for transport to the bone marrow Calculated as serum iron/TIBC x 100 = TSAT Serum ferritin Ferritin in the liver reflects stored iron, however, serum ferritin may not be as robust in reflecting stored iron Acute phase reactant and will be elevated in acute & chronic inflammation http://www.cdc.gov/nutritionreport/report.html
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Laboratory for healthy adults Slide 24 of 68 Suggested laboratory targets to initiate iron supplementation in CKD patients
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Hemoglobin target is controversial: Boxed Warning for ESAs Slide 25 of 68 Chronic Kidney Disease: In controlled trials, patients experienced greater risks for death, serious adverse cardiovascular reactions, and stroke when administered erythropoiesis-stimulating agents (ESAs) to target a hemoglobin level of greater than 11 g/dL (5.1). No trial has identified a hemoglobin target level, ESA dose, or dosing strategy that does not increase these risks (2.2). Use the lowest ESA dose sufficient to reduce the need for red blood cell (RBC) transfusions (5.1).
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Case Slide 26 of 68 The patient is a 68 year-old male (95 kg, BMI 31kg/m2) with CKD and a history of diabetes for several years. He is a chronic smoker referred for management of anemia. He is currently on furosemide 40mg BID, metoprolol tartrate 50mg BID, aspirin 81mg once daily, and insulin glargine 15 units in the morning. His pertinent labs include:
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Question Slide 27 of 68 His anemia is likely due to: Iron deficiency Folate/vitamin B12 deficiency Reduced erythropoietin production A and C
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Answer Slide 28 of 68 His anemia is likely due to: Iron deficiency Folate/vitamin B12 deficiency Reduced erythropoietin production A and C Answer: D Answer A is correct because the patient is iron deficient (TSAT <30%, Ferritin <500 ng/mL). Answer B is incorrect does not have laboratory data to support B12or folate deficiency. Answer C is correct because patient has advanced kidney disease (eGFR 25).
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Slide 29 of 68 IRON THERAPY
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Treatment Goal Slide 30 of 68 Goals Reduce blood transfusion requirements Minimize hospitalizations Decrease signs and symptoms of anemia Improve quality of life Treatment Approaches Typically utilizes the combination of iron therapy and erythropoiesis stimulating agents (ESA)
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Iron Therapy (KDIGO recommendations) Goal: TSAT<30% and ferritin <500 ng/mL CKD patients with anemia not on iron Increase in hemoglobin without starting ESA desired CKD non-dialysis patients (ND) 1-3 months of oral iron Choice of route should be chosen based on severity of iron deficiency, ongoing blood losses, iron status tests, Hgb concentration, ESA responsiveness, ESA dose and clinical statu Hemodialysis patients (HD) Trial of IV iron Slide 31 of 68
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Amount of elemental iron differs between oral iron supplements Slide 32 of 68 Absorption: Ferrous+2 iron > ferric+3 iron A 325 mg dose of: Ferrous fumarate has 108 mg elemental iron (33%). Ferrous sulfate has 65 mg elemental iron (20%). Ferrous gluconate has 35 mg elemental iron (12%). Reference: http://www.anemia.org A Physician’s Guide to Oral Iron Supplementation. Nov 2008.
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What needs to be considered before starting oral iron? Slide 33 of 68
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Tips on oral iron supplements Slide 34 of 68 Impaired absorption with: Caffeinated beverages (especially tea) Calcium (foods and beverages, supplements) Antacids H-2 receptor blockers Proton pump inhibitors Consider: Start with half of the recommended dose, gradually increase. Take with food. Try different preparation. Take in divided doses. Stool softener may help. Reference: http://www.anemia.org A Physician’s Guide to Oral Iron Supplementation. Nov 2008.
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Take iron supplement separate from calcium-based phosphate binders Slide 35 of 68 Calcium supplements may be prescribed with meals to bind dietary phosphorus. Calcium may interfere with iron absorption. Indications of when to take iron supplements: Iron absorption is increased when supplement is taken between meals and separate from phosphate binders.
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IV Iron may be used in CKD patients Slide 36 of 68 Five formulations available in the US IV iron formulations are nanoparticle suspensions comprised of iron oxide cores with carbohydrate shells Limits free iron plasma, thus reducing toxicity Metabolized via reticuloendothelial system (i.e. macrophage phagocytosis) There are unresolved potential bioavailability and safety challenges (related to labile iron) with IV iron formulations Zager, Clin J Am Soc Nephrol 2006; 1(suppl 1):S24–S31. Charytan et al CJASN 2015
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What do I need to consider before starting IV Iron? Slide 37 of 68 Zager et al. Kidney Int 2004; 66(1):144–156; Zager, Clin J Am Soc Nephrol 2006; 1 (suppl 1):S24–S31; Hörl, J Am Soc Nephrol 2007; 18(2):382–393; Charytan DM, et al. J Am Soc Nephrol. 2015 Jun;26(6):1238-47; Macdougall IC et al. Kidney Int. 2016 Jan;89(1):28-39
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IV Iron Formulations Slide 38 of 68
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Question Slide 39 of 68 A patient with CKD was recently diagnosed with iron deficiency anemia. The provider wants to start her on a intravenous iron product. Which of the intravenous iron products requires a test dose? a. Ferumoxytol b. Iron Dextran c. Iron Sucrose d. Sodium Ferric Gluconate e. Ferric Carboxymaltose
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Answer Slide 40 of 68 Answer: B Iron dextran requires a test dose because of documented anaphylactoid reactions. Ferumoxytol also has a boxed warning about hypersensitivity, however no test dose is required, infusion over at least 15 minutes is recommended with a minimum of 30 minutes of observation post infusion A patient with CKD was recently diagnosed with iron deficiency anemia. The provider wants to start her on a intravenous iron product. Which of the intravenous iron products requires a test dose? a. Ferumoxytol b. Iron Dextran c. Iron Sucrose d. Sodium Ferric Gluconate e. Ferric Carboxymaltose
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Slide 41 of 68 Considerations for IV iron administration when inflammation is present Administered dose of elemental iron is not able to be fully utilized (incorporated into RBCs) Clearance of IV iron compounds is ZERO-ORDER (capacity-limited, saturable) Clearance decreases as molecular weight increases
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Question Slide 42 of 68 Which of the following is true regarding IV iron formulations? Their pharmacokinetic profiles are well-characterized They are all colloidal suspensions of nanoparticles The proportion of the elemental iron dose incorporated into RBCs is required by the FDA in the new drug application All of the above
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Answer Slide 43 of 68 Which of the following is true regarding IV iron formulations? Their pharmacokinetic profiles are well-characterized They are all colloidal suspensions of nanoparticles The proportion of the elemental iron dose incorporated into RBCs is required by the FDA in the new drug application All of the above Answer: B All FDA approved IV iron formulations are iron oxide-carbohydrate nanoparticles in colloidal suspension.
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Zero order pharmacokinetic profile of ferumoxytol Slide 44 of 68 Plasma ferumoxytol log concentration vs. time curve Pai AB et al. Clin Pharmacol Ther 2010 Aug;88(2):237-42
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The more IV iron, the better? Slide 45 of 68 Coyne DW et al. J Am Soc Nephrol 2007;18:975; Kapoian T et al. J Am Soc Nephrol 2008;`9;372; Spiegel G, Chertow G. Clin J Am Soc Nephrol 2009;41009
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Slide 46 of 68 Comparison of catalytically active iron among available products
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Generic IV Iron Formulations http://www.ema.europa.eu/ema/, www.fda.gov/GDUFARegScience Slide 47 of 68 Sodium ferric gluconate is the only US generic Iron Sucrose: Widely available in Europe, South America and Asia Referred to as “similars” Less expensive and considered equivalent to Venofer® Switches are often mandated in Europe European Medicines Agency suggests the terminology “Non-biological Complex Drugs”
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Laboratory Parameters Before and After Switching to an Iron Sucrose Similar Slide 48 of 68 Rottembourg J et al Nephrol Dial Transplant. 2011 Oct;26(10):3262-7
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Summary Slide 49 of 68 CKD patients can be treated with oral or IV iron therapy. Dialysis patients are usually treated with IV iron therapy. There are gaps in knowledge regarding pharmacokinetics, pharmacodynamics and outcomes related to IV iron administration in CKD. Clinical iron indices may be insufficient for the clinician to adequately evaluate iron storage and availability and should be used in the context of the individual patients response. Judicious use of IV iron formulations is warranted until more prospective data clarify long-term safety and efficacy.
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Slide 50 of 68 TREATING ANEMIA WITH ERYTHROPOIESIS STIMULATING AGENTS
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Erythropoietin Stimulating Agents (ESA) http://www.fda.gov/drugs/drugsafety/postmarketdrugsafetyinformationforpatientsandproviders/ucm200297.htm Slide 51 of 68 Genetically engineered forms of erythropoietin Biological so only dosed parenterally Must advise patient of risks and benefits Recombinant EPO first available in 1989 to treat anemia in end-stage renal disease (ESRD) Prior to availability, patients often symptomatic with Hemoglobin (Hb) in 6-7 g/dL range
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ESA Slide 52 of 68
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Slide 53 of 68 Dosing Conversion for ESAs Package Insert. Mircera.
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Case Question Slide 54 of 68 A 58 year old male (185 lb) currently receiving thrice weekly dialysis and 75units/kg of epoetin alfa three times per week is being switched to darbepoetin alfa in the hospital. What is the appropriate dose of darbepoetin alfa? 25mcg/week 40mcg/week 60mcg/week 100mcg/week
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Case Answer Slide 55 of 68 A 58 year old male (185 lb) currently receiving thrice weekly dialysis and 75units/kg of epoetin alfa three times per week is being switched to darbepoetin alfa in the hospital. What is the appropriate dose of darbepoetin alfa? 25mcg/week 40mcg/week 60mcg/week 100mcg/week Answer: C Patient weighs 83.9 kg, so his weekly dose of epoetin alfa equals 12,585 units (50 units/kg x 83.9 kg x 3times/week). This converts to 60 mcg/weekly of darbepoetin alfa by using the conversion table.
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ESA Slide 56 of 68 Common adverse events (≥20%) Hypertension (most common) Infection Hypotension Myalgia Nausea Diarrhea Monitoring Parameters Hemoglobin once weekly upon initiation of an ESA and until stable; then once monthly Evaluate transferrin saturation and serum ferritin
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Blood transfusions are associated with many risks Slide 57 of 68 Patients required frequent blood transfusions before ESA were available. Risks associated with blood transfusions include: Volume overload Iron overload Allosensitization (i.e. sensitization to donor blood) Transfusion reactions Bloodborne infection
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CHOIR Study Slide 58 of 68 Correction of Anemia with Epoetin Alfa in Chronic Kidney Disease (CHOIR study) Randomized Controlled Trial N=1432 patients with CKD stage 3 and 4 patients Dosing of epoetin alfa targeted to achieve a Hb of 13.5 vs 11.3 g/dL for an intended 36 month follow up period Primary end point time to composite of death, MI, hospitalization for CHF or stroke Secondary endpoints include time to RRT, hospitalization for any cause and quality of life Singh A, et al. N Engl J Med 2006;355:2085-98.
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CHOIR outcome Slide 59 of 68 Early termination with median follow up of 16 months More CV events (MI, stroke, CHF hospitalization) in higher Hgb group Similar QOL scores between the groups Hazard Ratio (95% CI) 1.34 (1.03-1.74) p=0.03
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CREATE Study Slide 60 of 68 Drueke TB, et al. N Engl J Med 2006;355:2071-84. Cardiovascular Risk Reduction by Early Anemia Treatment with Epoetin Beta N = 603 CKD patients (primarily stage 4) Hb 10.5-11.5 g/dL vs. 13-15 g/dL Primary endpoint: Composite cardiovascular events Secondary endpoint: left ventricular mass index, the progression of chronic kidney disease, and the quality of life
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CREATE Outcome Slide 61 of 68 No significant difference in the risk of a first cardiovascular (CV) event between the complete correction and partial correction groups (hazard ratio 0.78; 95% CI 0.53-1.14; P = 0.20) More frequent dialysis initiation and hypertensive episodes and headaches were more frequently reported in the higher Hb group Time to primary first CV event after censoring data of patients at the time of dialysis initiation Group 1= higher Hb Group 2= lower Hb
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TREAT Study Slide 62 of 68 A Trial of Darbepoetin Alfa in Type 2 Diabetes and Chronic Kidney Disease (TREAT study) N =4038 CKD stage 3 and 4 patients with diabetes Hgb 13 vs < 9.0 g/dL (placebo group with rescue darbepoetin when Hgb) Primary endpoints: Time to the composite outcome of death or a cardiovascular event and the time to the composite outcome of death or ESRD Pfeffer M, et al. N Engl J Med 2009;361:2019-32.
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Slide 63 of 68 TREAT outcome No difference in primary CV composite endpoint Higher risks of fatal/non-fatal strokes in normal Hgb group ( 5% vs 2.6% HR 1.92, P < 0.001) More patients in the rescue group required transfusions in the placebo group (496 vs 297 p<0.001) Patients with a history of cancer in the higherHb group also had a higher risk of death
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Hemoglobin in CKD: Guidelines Suggestions Slide 64 of 68 Note: Most institutions utilize their own ESA dosing protocol with more detailed dosing changes recommended based on Hb response. Some protocols have lower and upper limits of Hb that differ from guideline suggestions.
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Question Slide 65 of 68 A 71 year old female presents to the CKD clinic with the following laboratory data complaining of increasing fatigue and shortness of breath. She recently received 2 doses of 100 mg of iron sucrose IV. Hb 9.2 g/dL; TSAT 40%; Ferritin 550 ng/mL Which of the following is the most appropriate therapeutic intervention? Ferrous sulfate 325mg PO TID Iron sucrose 100mg IV X 5 doses Start an ESA No intervention necessary
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Answer Slide 66 of 68 A 71 year old female presents to the CKD clinic with the following laboratory data complaining of increasing fatigue and shortness of breath. She recently received 2 doses of 100 mg of iron sucrose IV. Hb 9.2 g/dL; TSAT 40%; Ferritin 550 ng/mL Which of the following is the most appropriate therapeutic intervention? Ferrous sulfate 325mg PO TID Iron sucrose 100mg IV X 5 doses Start an ESA No intervention necessary Answer: C The patient’s iron indices indicate repletion and still anemic and symptomatic therefore an ESA can be initiated
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Hyporesponse to anemia treatment in CKD Slide 67 of 68 Decreased responsiveness to erythropoietin Uremia Chronic inflammation Severe hyperparathyroidism Folate deficiency
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Summary Slide 68 of 68 ESAs should be used judiciously in CKD Consider potential reasons for hyporesponse that may facilitate dose reductions Doses should be individualized and the patient's clinical status desired outcomes from treatment should be integrated in goal setting
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