FABROA, MARIA JESSICA ERLINDA P.

BSN III

Anemia of Renal Disease Narrative Pathophysiology

Anemia of renal disease is a hypo proliferative anemia resulting primarily from low
erythropoietin (EPO) or a diminished response to it; it tends to be normocytic and
normochromic. Treatment includes measures to correct the underlying disorder and
supplementation with EPO and sometimes iron. Anemia in chronic renal disease is
multifactorial. The most common mechanism is hypo proliferation due to decreased
erythropoietin (EPO) production; lack of EPO leads to loss of hepcidin suppression and
increased iron sequestration. Other factors include uremia, in which mild hemolysis is
expected due to increased red blood cell deformity, blood loss due to dysfunctional platelets,
dialysis and angiodysplasia, and secondary hyperparathyroidism.

When your kidneys are damaged, they produce less erythropoietin (EPO), a
hormone that signals your bone marrow—the spongy tissue inside most of your bones—to
make red blood cells. With less EPO, your body produces fewer red blood cells, and less
oxygen is delivered to your organs and tissues. In addition to your body makes fewer red
blood cells, the red blood cells of people with anemia tend to live in the bloodstream for a
shorter time than usual, causing the blood cells to die faster than they can be replaced.
People with anemia may have low levels of nutrients, such as iron, vitamin B12 NIH external
link, and folate NIH external link that are needed to make healthy red blood cells.

Many patients with renal failure will not respond to erythropoietin, which is essential
as it is a significant predictor of adverse cardiac events. Two factors that lead to
unresponsiveness include iron deficiency and inflammation. High levels of CRP predict
resistance to erythropoietin in dialysis patients. Iron supplements are recommended to
enhance responsiveness to erythropoietin.

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