Anemia in CKD Flashcards
Most patients with CRF (chronic renal failure) and ESRD enhibit
normochromic, normocytic anemia that is proportionate to renal failure
Cause of anemia in CKD
EPO deficiency
**Where does the majority of EPO come from?
Kidneys (90%) and the rest is from hepatocytes in the liver
Where are EPO producing cells fround?
Proximal tubular segment
Do cells store EPO?
No they make it de nova by increasing gene expression and translation
What transcription factor has to do with increased production of EPO?
Hypoxia-indeducible factor (HIF-1)
***What is a stimulus for erythropoiesis?
Tissue hypoxia
Carbohydrate moiety =
Rich in sialic acid (required for it to be active)
Critical to in vivo reactivity
EPO promotes
RBC differentiation
RBC that is most sensitive to EPO is
A cell between the CFU-E and the proerythroblast
Other causes of anemia with CRF
Blood loss through GI ulcers or retention in dialysis
Iron, folic acid or vit B12 deficiency
Osteitis fibrosis (bone can’t respond to EPO)
Systemic or infection or inflammatory illness)
Aluminum toxicity (blocks iron)
Hypersplenism (filters RBC too early)
Goals of Therapy
- prevent or reverse the signs and symptoms of tissue oxygen deprivation and left ventricular hypertrophy
- improve exercise capacity
- optimize survival
- improve quality of life of patients
Begin epoetin therapy in all CKD patients that have Hb levels
between 9 and 10g/dL.
Prior to initiation of epoetin,
iron balance should be assessed, since iron deficiency is the most common cause of suboptimal response to epoetin.
To prevent an absolute or functional iron deficiency in renal patients receiving epoetin,
it is suggested that ferritin should be at least 100ng/mL and TSAT values should be at least 20%
