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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 Anginao Claudicationo 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

Diagnostics for Anemia Mantainance values for: HD patients CKD/non-PD Dialysis

Hemoglobin [Hgb] 11-12 g/dl >11 g/dl Hematocrit [Hct] 35-40% > 33% Ferretin 200-500 ng/ml 100-500 ng/ml Transferrin Saturation [TSAT] 20% >20% Retuculocyte Hemoglobin Count [CHr] >29pg/cell None Recommended

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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 onthe 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 requiremento 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 levelo Avoid excessive rise of dose to prevent worsening of hypertension

Monitoring of Initial Dose effects:o Check Hgb every 2 weekso Adjust ESA dose as neededo 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 weekso In maintenance phase:

Adjust ESA dose based on subsequent changes in hemoglobino Note patients with ESA resistance

May signal iron deficiency or infection Side Effects:

o Worsening of Hypertensiono Seizureso Graft Clottingo Effect on Kt/V - Dialysis urea clearance may decrease slightly as Hgb Riseso Phosporus Balance More difficult to control in ESA therapyo 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

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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 ofpolyethelyne glycolo Promotes increased stimulation of erythropoietin receptorso 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 developso Repeated small doses to maintain Fe balance

Oral Irono Safe and Inexpensiveo Side effects:

Constipation, Diarrhea, Bloating, Dyspepsiao Not for hemodialysis patients because of troublesome side effectso Convenient for peritoneal dialysis patients because:

PD patients have less chronic blood losso Dosage: 200mg of elemental Iron/day, take on empty stomach to maximize efficiency

Intravenous Irono Superior effectivity and efficiency compared to Oral Irono Used for Hemodialysis patientso Less safe that oral irono Dosing Strategies:

Repletive 1000 mcg dose over 8-10 consecutive HD Treatmentsor

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 therapyo 10mcg for 10 consecutive doses

or

o 25-100 mcg weekly dose

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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 marrowPatients 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 immunedefense

Viral Infectionso 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 exposureo Use of the stabilizer = Polysorbate

Leaches organic compounds from uncoated rubber stoppers in pre filledsyringes Substance could interact with erythropoietin and illicit immunogenicity

Classified as a RARE DISEASE

Pathophysiology

Management:

Immunosuppresive Drugso Mycophenolate mofetil

CellCept [Roche] Myfortic [Novartis]

Predisposing Factors Apply

T cells secrete factors to inhibiterythroid colonies in bone marrow

T-cells directly killserythroblasts

Decreased RBC Production

Unresponsive to EPO Treatment

Anemia

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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