Nursing care
Why chronic kidney disease causes anaemia, and what that means for nursing
Written and reviewed by Dana Whitfield, RN, MSN · 4 min read · Updated October 2026
Short answer
The kidneys make erythropoietin, the hormone that tells bone marrow to produce red blood cells. As kidney tissue is lost, erythropoietin falls and fewer red cells are made, causing a normocytic anaemia with fatigue and breathlessness. Iron deficiency and blood loss often add to it, so treatment combines iron with erythropoiesis-stimulating agents under careful monitoring.
The kidney's role in making red blood cells
Specialised cells in the kidney sense how much oxygen is reaching the tissues. When oxygen delivery falls, they release erythropoietin, often shortened to EPO. EPO travels to the bone marrow and signals it to produce more red blood cells. This feedback loop normally keeps haemoglobin steady and responds to blood loss or altitude.
In chronic kidney disease, functional kidney tissue is lost, so EPO production falls short of what the body needs. The marrow is not damaged, but it receives a weaker signal and produces fewer red cells. The resulting anaemia is typically normocytic and normochromic, meaning cells are normal in size and colour, just fewer in number.
Other factors that deepen the anaemia
Low EPO is the main cause, but rarely the only one. Red cells survive for a shorter time in kidney disease, and iron deficiency is common because of reduced absorption, poor intake and blood loss. Clients on haemodialysis lose some blood with each treatment and through frequent blood tests. Deficiencies of vitamin B12 and folate, infection and inflammation can also contribute.
These extra factors matter because they change treatment. Bone marrow cannot build haemoglobin without iron, so an erythropoiesis-stimulating agent works poorly if iron stores are low. Iron studies are therefore checked alongside haemoglobin, and iron is often given by IV in dialysis clients. When a client responds less than expected, the team looks for iron deficiency, bleeding or infection.
What the anaemia looks like at the bedside
Because the anaemia develops slowly, clients may adapt and underreport symptoms. Common findings include fatigue, weakness, pallor, shortness of breath on exertion, dizziness, poor concentration and reduced exercise tolerance. In clients with heart disease, anaemia can provoke chest pain because the heart must work harder to deliver oxygen.
An expected trend on treatment is a gradual rise in haemoglobin with improving energy. Concerning findings include a sudden fall in haemoglobin, which suggests bleeding rather than kidney disease alone, new chest pain, or signs of a clot. Ask about black stools and other bleeding, and report abrupt changes rather than attributing every low value to the kidneys.
ESA therapy: why it helps and why limits matter
Erythropoiesis-stimulating agents such as epoetin alfa replace the missing EPO signal and can reduce the need for transfusion. Their labelling carries a boxed warning that ESAs increase the risk of death, heart attack, stroke, venous thromboembolism and thrombosis of dialysis access, particularly when haemoglobin is pushed too high, so the team uses the lowest effective dose to reach a modest target.
Before each dose, check blood pressure, because uncontrolled hypertension is a contraindication and ESAs can raise pressure. Review the latest haemoglobin and report a rapid rise or a value above the prescribed range. Monitor dialysis access for loss of thrill or bruit, and teach clients to report headache, chest pain, leg swelling or neurological symptoms promptly.
Apply the mechanism to a hypothetical scenario
A hypothetical client with stage 4 CKD is due for a scheduled epoetin alfa injection. Haemoglobin has risen faster than expected over two weeks and is now above the prescribed target, and blood pressure is higher than usual. Options include giving the dose as scheduled, giving a double dose next week instead, giving oral iron only, or holding the dose and contacting the prescriber.
Holding and contacting the prescriber is correct, following local protocol. A rapid rise above target and raised blood pressure increase the cardiovascular and clotting risks that the boxed warning describes. Giving the dose ignores those risks, and doubling a later dose makes no sense. Iron alone does not address the decision about whether the ESA should continue.
Sources and further reading
NIDDK: Anemia in chronic kidney disease. Reduced EPO, shorter red cell survival, iron, B12 and folate deficiency, dialysis blood loss, symptoms, iron and ESA treatment, and transfusion risks including transplant antibodies.
MSD Manual Professional: Chronic kidney disease. Deficient EPO from loss of renal mass, normochromic normocytic anaemia, ESA use at the lowest effective dose, higher haemoglobin targets increasing stroke and thrombosis, and iron replacement.
DailyMed: Epogen (epoetin alfa) prescribing information. Boxed warning on death, myocardial infarction, stroke, venous thromboembolism and vascular access thrombosis, and uncontrolled hypertension as a contraindication.
The next step on this is the same as on everything else here: answer questions and read the rationales. Our renal and genitourinary practice questions are the closest set to what this page covers.
Common questions
Why is anaemia of CKD usually normocytic?
The main problem is too little EPO signal, not faulty cell production, so the marrow makes fewer red cells of normal size. Coexisting iron deficiency can change this pattern.
Why do clients on ESAs also need iron?
Bone marrow needs iron to build haemoglobin. Without adequate iron stores, ESA therapy produces a poor response, so iron levels are checked and replaced as prescribed.
Why is a blood transfusion not the first choice for CKD anaemia?
Transfusion raises haemoglobin quickly but can cause iron overload and antibodies that may make a future kidney transplant harder. It is usually reserved for specific situations.