Synopsis
Distinguish renal anaemia from treatable alternatives, assess iron availability correctly, and use iron, erythropoietic therapy and transfusion safely.
- CKD anaemia is usually isolated, normocytic and hypoproliferative, becoming more plausible below eGFR 30 mL/min/1.73 m², but blood loss, iron or vitamin deficiency, inflammation, haemolysis and marrow disease must still be excluded.
- The 2024 UK Kidney Association guideline advises investigation when haemoglobin is below 110 g/L or symptoms are attributable to anaemia, regardless of CKD stage or dialysis status.
- Do not measure serum erythropoietin routinely: concentrations do not reliably separate renal anaemia or guide treatment.
- Assess iron with red-cell indices and, where available, reticulocyte haemoglobin or hypochromic cells; otherwise combine transferrin saturation and ferritin with CRP because ferritin rises during inflammation.
- Absolute iron deficiency requires a source assessment, especially gastrointestinal or menstrual blood loss; CKD causes impaired iron use but does not explain depleted stores by itself.
- Correct iron deficiency before starting an ESA or HIF-prolyl-hydroxylase inhibitor; most haemodialysis patients need intravenous rather than oral iron.
- For adults receiving an ESA, UKKA recommends a haemoglobin range of 100–120 g/L; normalising haemoglobin increases vascular and hypertensive harm without proven additional benefit.
- ESA resistance is a diagnosis prompt, not a command to escalate indefinitely: check iron, infection, inflammation, bleeding, dialysis adequacy, hyperparathyroidism, adherence, haemolysis and marrow disease.
- Roxadustat is a NICE option for eligible adults with symptomatic stage 3–5 CKD, no iron deficiency and no dialysis at initiation; use its current oral regimen and thrombotic safety framework through renal services.
- Avoid transfusion when possible in a transplant candidate because HLA sensitisation can reduce future donor compatibility, but do not withhold life-saving blood for severe symptomatic anaemia or haemorrhage.
Key red flags
Haemodynamic instability, active haemorrhage, syncope, ischaemic chest pain or severe hypoxia with anaemia needs urgent resuscitation, crossmatch and transfusion assessment rather than waiting for iron or ESA response.
A sudden haemoglobin fall with haemolysis, dialysis-circuit loss, retroperitoneal bleeding or gastrointestinal haemorrhage requires same-day cause control and cannot be labelled renal anaemia.
Severe uncontrolled hypertension or hypertensive neurological symptoms during ESA therapy require immediate blood-pressure management and specialist dose interruption.
A paradoxical haemoglobin fall with very low reticulocytes after prior ESA response raises rare antibody-mediated pure red-cell aplasia; stop the implicated strategy and seek specialist haematology-nephrology assessment.
Chest pain, unilateral swelling, acute dyspnoea or access dysfunction on ESA or HIF-PHI therapy may represent thrombosis and needs emergency evaluation.
Investigation priorities
Define severity, cell size and whether abnormalities extend beyond the erythroid line.
Management branches
Haemoglobin falls below 110 g/L or symptoms plausibly relate to anaemia.
- Assess urgency, bleeding, cardiovascular symptoms and trajectory, and compare renal stage with the severity and morphology of anaemia.
- Obtain FBC indices, reticulocytes, iron availability and CRP, adding B12, folate, haemolysis, paraprotein or marrow testing according to phenotype.
- Investigate absolute iron deficiency for a source rather than assigning it to CKD and review medicines, dialysis losses, inflammation and nutrition.
- Treat the identified cause, then reassess symptoms and haemoglobin before selecting renal-specific erythropoietic therapy.