Chronic Kidney Disease - Anemia Flashcards

Dr. Covert

1
Q

How does CKD cause anemia?

A

-the kidney produces EPO -> reduced EPO production -> reduced RBC

-CKD patients undergoing hemodialysis -> loss of iron, B12, folic acid, blood -> reduced RBC

-RAAS activation: fluid retention -> increases volume but RBC will be decreased
Q: Why is RAAS activated in RAAS patients

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2
Q

Symptoms of Anemia

A

-Fatigue, headache, weakness, vertigo, paleness

-higher risk for infection
-tachycardia (the body compensates for low RBC by pumping blood faster where it is needed), heart failure (a result of constantly pumping harder)

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3
Q

Hg levels indicating anemia

A

Men: 13 g/dL

Women: 12 g/dL

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4
Q

Anemia screening for different CKD stages

A

Stage 1: 90-60 when clinically indicated
Stage 2: 30-59 - annually
Stage 3: <30 2x a year
ESRD (end-stage renal disease): every 3 months

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5
Q

Complete Blood count (CBC)

A
  1. Hemoglobin (if normal - no changes)
  2. RBC indices:
    MCV (mean corpuscular volume, how large are the red blood cells)

if MCV is high (macrocytic): >100 fL: B12 or folate deficient
if MCV is low (microcytic): <80 fL: iron deficiency
-> check the iron

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6
Q

Iron studies

A

Ferritin: storage for iron (Ferritin is also made of iron -> so low iron -> low ferritin -> low iron storage)
<500 mcg/L = iron deficiency anemia

TIBC: total-iron-binding-capacity: if high it means there is a lot of space for iron to bind -> but there is no iron -> >450 = iron deficiency anemia

TSAT (transferrin saturation): transport capacity of iron, if less than 30% = iron deficiency anemia
(serum ion / TIBC) * 100

Others: B12 and Folic acid (folate) and Reticulate cell count - tells if the bone marrow responds well f.e. in case of an open wound (not on exam)

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7
Q

Benefits of Iron in CKD patients

A

-reduce the need for transfusion and the need for ESA (erythropoiesis-stimulating agent)!!
-increases ESA effectiveness when patients are using it
-iron therapy must be started before ESA bc if we stimulate EPO (more blood) there is not enough iron the blood can carry

-IV or PO
-not without risks

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8
Q

Why would we want to delay the use of ESA agents?

A

-black-box warning: stroke, heart attacks, venous thromboembolic)
-tumor progression in certain cancer
-highest risk in patients with Hg over 11

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9
Q

Why is IV dextran (Dexferrum) dangerous?

A

-Blackbox warning for anaphylactic shock
-give an IV test dose

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10
Q

Which iron formulation is preferred in patients on dialysis

A

on dialysis: IV

not on dialysis: oral

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11
Q

Iron repletion dosing

A

Dialysis patients: 1g IV given over 8-10 HD sessions which is 10 mg for each session
Maintenance dose: 50-125mg/week

Non-dialysis patients: 1 tablet q 24-48h for 1-3 months -> it is spaced out bc we can only absorb a limited amount of iron

Rule of 1s
1g = 1 repletion
only 10% of PO iron is absorbed
1 ml pack of blood (transfusion) = 1 mg elemental iron

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12
Q

How does the kidney interfere with low O2 levels?

A

the kidney senses low blood O2 -> the kidney secrets EPO -> signals to the bone marrow to produce more RBC -> Negative feedback: increased RBC shuts off the EPO secretion of the kidney

-in CDK patients, the kidney doesn’t secrete enough EPO -> drug ESA (erythropoietin-stimulating agents)

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13
Q

When is ESA initiated/stopped?

A

To minimize risks of ESA: heart attack, stroke, venous thromboembolic)
Non-dialysis patients:
Start: Hg <10 AND iron repleted
Stop: Hg >11.5
monitor: monthly, then Q3 months

Dialysis patients
Start: Hg 9-10 AND iron sufficiently depleted
Stop: > 11.5
monitor: monthly at therapy initiation

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14
Q

ESA agents

A

-Epoetin alpha (Epogen, Procrit, Reacrit) TIW - often used in dialysis patients bc they get their dialysis 3x a week

-Darbepoetin (Aranesp):
HD: q week
non-HD: q 4 weeks

-Mircera
SQ q 2weeks

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