Overview
Anaemia is a common complication of chronic kidney disease and contributes to fatigue, reduced exercise tolerance and left ventricular hypertrophy. It is typically normochromic and normocytic.
Causes
- Reduced erythropoietin production by the diseased kidney — the dominant mechanism
- Iron deficiency (poor absorption, blood loss, dialysis losses)
- Reduced red-cell survival and marrow suppression from uraemia
- Deficiencies of folate/B12 in some patients
Assessment
- Confirm the anaemia is proportionate to the degree of CKD (typically emerges as eGFR falls, often at G3b–G4)
- Check and optimise iron status (ferritin, transferrin saturation) before considering an ESA
- Exclude other contributing causes (bleeding, haematinic deficiency)
Management
- Optimise iron — oral iron in early CKD; intravenous iron is often needed, especially in dialysis
- Erythropoiesis-stimulating agents (ESAs) — e.g. epoetin, darbepoetin — for symptomatic anaemia once iron replete
- Target haemoglobin ~100–120 g/L — deliberately not fully normalised
- Monitor blood pressure
ESA cautions
- Hypertension, thrombosis and (at high haemoglobin targets) increased stroke risk
- ESA hyporesponsiveness — reconsider iron deficiency, infection/inflammation, hyperparathyroidism or occult blood loss
MRCP-specific traps
- Check iron before blaming erythropoietin — a classic exam step; ESAs fail in iron deficiency.
- Aiming for a normal haemoglobin is harmful — the target is deliberately modest.
- A previously stable patient who becomes ESA-resistant should prompt a search for infection, bleeding or hyperparathyroidism.
Summary
CKD anaemia is mainly due to erythropoietin deficiency (normochromic normocytic). Optimise iron first, then use ESAs to a modest haemoglobin of ~100–120 g/L — not normalisation — while watching for hypertension and thrombosis.
nephrologyhaematologychronic kidney diseasemrcp part 2