Chronic Kidney Disease - Anemia Flashcards
Dr. Covert
How does CKD cause anemia?
-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
Symptoms of Anemia
-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)
Hg levels indicating anemia
Men: 13 g/dL
Women: 12 g/dL
Anemia screening for different CKD stages
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
Complete Blood count (CBC)
- Hemoglobin (if normal - no changes)
- 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
Iron studies
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)
Benefits of Iron in CKD patients
-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
Why would we want to delay the use of ESA agents?
-black-box warning: stroke, heart attacks, venous thromboembolic)
-tumor progression in certain cancer
-highest risk in patients with Hg over 11
Why is IV dextran (Dexferrum) dangerous?
-Blackbox warning for anaphylactic shock
-give an IV test dose
Which iron formulation is preferred in patients on dialysis
on dialysis: IV
not on dialysis: oral
Iron repletion dosing
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
How does the kidney interfere with low O2 levels?
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)
When is ESA initiated/stopped?
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
ESA agents
-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