Synopsis
Confirm renal anaemia without diagnostic anchoring, correct iron restriction, select erythropoiesis-stimulating therapy safely, and balance transfusion, cardiovascular and transplant-sensitisation risks.
- CKD anaemia is usually normocytic and hypoproliferative, driven by inadequate erythropoietin response, inflammation, iron restriction and shortened red-cell survival.
- Do not attribute anaemia to kidney disease solely from a reduced eGFR; blood loss, iron deficiency, B12 or folate deficiency, haemolysis and marrow disease still require assessment.
- Check full blood count, reticulocytes, ferritin and transferrin saturation, with CRP and clinical context because ferritin rises during inflammation and may mask unavailable iron.
- Absolute iron deficiency means depleted stores, while functional deficiency means iron is present but hepcidin-mediated sequestration limits delivery to erythroblasts.
- Oral iron may suit non-dialysis CKD when tolerated and likely to work; intravenous iron is often required in haemodialysis or after inadequate oral response.
- Erythropoiesis-stimulating agents are considered after correctable causes and iron status are addressed, particularly in dialysis or symptomatic anaemia where transfusion avoidance matters.
- ESA treatment aims for an individual stable haemoglobin range rather than normalising population values; high targets and rapid rises increase vascular risk.
- Blood pressure must be controlled before and during ESA therapy, and dose changes use the rate of haemoglobin response rather than reflexively chasing a single result.
- Hypoxia-inducible-factor prolyl-hydroxylase inhibitors are oral alternatives for selected adults under current NICE recommendations, with class-specific thrombotic and tumour cautions.
- A poor ESA response should prompt review of iron availability, inflammation, infection, blood loss, dialysis adequacy, hyperparathyroidism, medicines and marrow disorders before escalating dose.
Key red flags
Rapid decline, bleeding, fragments, leucopenia, thrombocytopenia or marked macrocytosis requires urgent investigation beyond CKD.
Investigation priorities
Confirm phenotype and detect competing marrow or haemolytic disease.
Management branches
Haemoglobin falls below the reference range in a person with CKD.
- Review tempo, symptoms, bleeding, medicines and dialysis losses and obtain count, reticulocytes, film, iron indices, B12 and folate.
- Investigate gastrointestinal or gynaecological loss, inflammation, haemolysis and marrow disease when indices, trajectory or other cell lines are not typical.
- Attribute a renal component only after integrating kidney stage and competing causes, then agree symptom, transfusion-avoidance and transplant goals with nephrology.
Key medicines
Intravenous ironThe renal service calculates product-specific elemental iron and gives divided or total-dose infusions within licensed limits, haemodialysis timing and current ferritin and transferrin-saturation thresholds.Observe for hypersensitivity and extravasation, avoid indiscriminate dosing during active systemic infection and monitor cumulative iron rather than treating ferritin in isolation.
Epoetin alfaUse a renal-protocol subcutaneous or intravenous starting dose and interval, then titrate no more often than recommended according to haemoglobin trajectory, dialysis and individual response.Control hypertension and monitor rapid haemoglobin rise, stroke, vascular-access thrombosis and pure red-cell aplasia; avoid targeting a normal population haemoglobin.