Management of Anemia in CKD Albert Ignatius V.

Amo, RN Anemia A condition where the body has an abnormally low supply of RBC Develops in the early stage of CKD when your kidneys have 20-50% of your normal kidney function = Chronic Renal Insufficiency Anemia worsens as kidney disease progresses Nearly everyone with ESRD has anemia Keeps people from feeling their best

Observations Mainly due to: o Decreased Oxygen delivery to the tissues Paleness, Fatigue, Dyspnea, Difficulty Concentrating, Sleep disorders, Dizziness, Cold intolerance, Headaches, o Hearts compensatory Changes Increased cardiac output, left ventricular hypertrophy, palpitations Can lead to: o Angina o Claudication o Transient Ischemic Attacks

Factors Decreased EPO production Decreased RBC lifespan because of wastes Loss of blood during hemodialysis treatment Too little iron (Fe)

EPO Action EPO Produced in kidney -> Acts on EPO Receptors -> Development of reticulocytes -> Increased RBC Pathophysiology Progression of CKD -> Increased tissue scarring -> Destruction of Kidneys interstitial fibroblasts -> ->Decreased EPO production -> Decreased RBC production = ANEMIA Too little iron Factors: Not enough iron in diet Body is not able to absorb iron Iron absorbed through diet is not enough to keep up with RBC demand for production ESA uses a lot of iron to make RBC Mantainance values for: HD patients 11-12 g/dl 35-40% 200-500 ng/ml 20% >29pg/cell CKD/non-PD Dialysis >11 g/dl > 33% 100-500 ng/ml >20%
None Recommended

Diagnostics for Anemia

Hemoglobin [Hgb] Hematocrit [Hct] Ferretin Transferrin Saturation [TSAT] Retuculocyte Hemoglobin Count [CHr]

Management of Anemia Erythropoietin Stimulating Agents [ESA] Iron Treatment RBC Transfusions Proper Nutrition Compliance to treatment regimen

Erythropoietin Stimulating Agents [ESA] Any agent that augments(enlarge or increase) erythropoiesis through direct or indirect action on the erythropoietin receptor. Acts on the EPO receptors present in the bone marrow Synthesized the Ovary cells of Chinese Hamsters (Cricetulus griseus) Indications: o Hgb < 11mg/dL Route: o Subcutaneous Reduces dosing requirement o Intravenous Painless, for Renogen Dosing: o Initial Dose of Epoetin: Should be treated in the CKD period prior to ESRD Starting for Hemodialysis patients 4000-6000 units, 3x/week Peritoneal Dialysis 8000 units once per week o Initial Dose of Darbepoetin alfa: Hemodialysis Patients 25 mcg once daily Peritoneal Dialysis Patients 60 mcg every 2 weeks o Selection of dose depends on starting Hgb level o Avoid excessive rise of dose to prevent worsening of hypertension Monitoring of Initial Dose effects: o Check Hgb every 2 weeks o Adjust ESA dose as needed o Watch out for Plateau Effect Hemoglobin stops rising Increase of ESA dose demand to reach therapeutic targets Cause: Induction of Iron therapy If target Hgb has been reached: o Monitor Hgb every 2-4 weeks o In maintenance phase: Adjust ESA dose based on subsequent changes in hemoglobin o Note patients with ESA resistance May signal iron deficiency or infection Side Effects: o Worsening of Hypertension o Seizures o Graft Clotting o Effect on Kt/V - Dialysis urea clearance may decrease slightly as Hgb Rises o Phosporus Balance More difficult to control in ESA therapy o Hyperkalemia No reported occurrence in clinical setting but can possibly occur

Causes of decreased response to ESA therapy Blood loss Functional Iron deficiency Reticuloendothelial blockade Poor absorption of dietary iron

Differences in ESA Types Epoetin alfa Renogen is administered TIVT Epoetin beta Contains more basic isoforms than alfa [Isoforms: A different protein with the same function as another protein] Darbepoietin alfa Has longer half life than Epoetin, Costs more than Epoetin Continuous Erythropoietin Receptor Activator [ CERA ] o Has longest half life because of polyethelyne glycol o Promotes increased stimulation of erythropoietin receptors o Banned for use in sports

Iron Treatment Helps increase Hgb and lowers ESA requirements Can be given Orally or Intravenous IV Iron is given: o Episodic basis when Fe deficiency develops o Repeated small doses to maintain Fe balance Oral Iron o Safe and Inexpensive o Side effects: Constipation, Diarrhea, Bloating, Dyspepsia o Not for hemodialysis patients because of troublesome side effects o Convenient for peritoneal dialysis patients because: PD patients have less chronic blood loss o Dosage: 200mg of elemental Iron/day, take on empty stomach to maximize efficiency Intravenous Iron o Superior effectivity and efficiency compared to Oral Iron o Used for Hemodialysis patients o Less safe that oral iron o Dosing Strategies: Repletive 1000 mcg dose over 8-10 consecutive HD Treatments or Weekly maintenance of 25-100mg For PD Patients: 250 infusions for 1-2 hours o Safety Concerns: Anaphylaxis Give slow IV push to avoid incidence of reaction [ > 2 mins ] Oxidation Give VitE to decrease oxidative stress Infection Discourage Fe treatment to prevent further growth of infection o Drugs: IV Iron Dextran Higher risk of anaphylaxis because of dextran Used for patients with long history of drug use Reactions can occur within 5 mins of injection or can be delayed by 45 mins or more Have Epinephrine or other anti anaphylactic meds on hand Sodium Ferric Gluconate Non-dextran preparation Less frequent reactions compared to Fe dextran Can be given in 1000mg divided in 8 consecutive treatments Iron sucrose Same rate of reactions as Sodium Ferric Gluconate May be used as Fe replacement therapy o 10mcg for 10 consecutive doses or o 25-100 mcg weekly dose

Pure Red Cell Aplasia

Clinical syndrome defined as the absence of mature erythroid precursors in a normocellular bone marrow. There are no requrements for RBC to mature in the normal bone marrow

Patients have: Severe Anemia Low reticulocyte cell count (baby RBC) Normal platelet granulocyte counts

Causes: Autoimmune disorders Thymoma Tumor from the epithelial cells of the thymus o The organ for the bodys immune defense Viral Infections o HIV, Herpes, parvovirus B19, Hepatitis Idiopathic Congenital o Hereditary Pure Red Cell Aplasia Erythropoietin Administration o Development of neutralizing anti-EPO antibodies after 6 months of drug exposure o Use of the stabilizer = Polysorbate Leaches organic compounds from uncoated rubber stoppers in pre filled syringes Substance could interact with erythropoietin and illicit immunogenicity Classified as a RARE DISEASE

Pathophysiology

Predisposing Factors Apply

T cells secrete factors to inhibit erythroid colonies in bone marrow

T-cells directly kills erythroblasts

Decreased RBC Production

Unresponsive to EPO Treatment Management: Immunosuppresive Drugs o Mycophenolate mofetil CellCept [Roche] Myfortic [Novartis]

Anemia

RESOURCES

Fundamentals of Nursing 7th Edition B. Kozier et al. Nursing Care Plans, 6th Edition M. Doenger et al. Handbook of Dialysis 4th Edition J. Daugirdas et al. The power of Iron Dialysis Patient Citizens, Fresenius Medical Care Parenteral Iron Therapy Options S. Silverstein, G. Rogers Anemia and Chronic Disease National Kidney Foundation