Anaemia and Kidney Disease

The kidneys are not just filters — they are endocrine organs. specialised cells in the kidney called peritubular interstitial cells produce erythropoietin (EPO) in response to low oxygen levels. EPO travels to the bone marrow and signals it to produce red blood cells. When kidneys are scarred and damaged, these EPO-producing cells die off. Even if the bone marrow has plenty of iron and building materials, it lacks the 'instruction' to build red blood cells.

Anaemia typically first appears when eGFR falls below 45 ml/min/1.73m² (stage 3b). By stage 4 (eGFR 15–29), most people have some degree of anaemia. By stage 5 or dialysis, nearly all patients are anaemic without treatment. The degree of anaemia does not always match the eGFR — some people are more affected than others. Regular full blood count (FBC) tests are part of standard CKD monitoring.

In CKD, iron deficiency is often 'functional' — the body has iron stores but cannot mobilise them effectively due to inflammation and low EPO. This is diagnosed by blood tests showing low transferrin saturation (TSAT) or ferritin that is not as high as it appears. 'Absolute' iron deficiency means depleted stores, usually from blood loss (e.g. gut bleeding, heavy periods, frequent blood tests). Both types need treatment but the approach differs slightly.

Erythropoiesis-stimulating agents (ESAs) are injectable medicines that replace the missing EPO hormone. Epoetin alfa is usually given twice weekly or three times weekly; darbepoetin alfa and methoxy polyethylene glycol-epoetin beta have longer half-lives and can be given weekly or fortnightly. ESAs are usually started when haemoglobin falls below 100 g/L and the patient has symptoms. They are highly effective but require monitoring for blood pressure rises, and should not push haemoglobin above 120 g/L.

Many CKD patients cannot absorb enough oral iron due to inflammation, phosphate binders, or proton pump inhibitors. Intravenous iron (iron sucrose, ferric carboxymaltose, iron isomaltoside) is given as a hospital infusion. It rapidly replenishes iron stores and improves the response to ESA therapy. TSAT and ferritin are checked before and after treatment. Modern IV iron preparations are safe, with rare allergic reactions.

Hypoxia-inducible factor prolyl hydroxylase (HIF-PH) inhibitors — daprodustat, roxadustat — are oral tablets that stimulate the body's natural EPO response by mimicking low oxygen. They are an alternative to injectable ESAs and may also improve iron mobilisation. They are becoming available in the UK for non-dialysis and dialysis CKD patients. Your nephrologist can advise if they are suitable for you.

Take prescribed iron and ESA injections as directed. Eat iron-rich foods compatible with your renal diet — lean red meat (small portions), lentils (if potassium allowed), eggs, and iron-fortified cereals (check phosphate additives). Take vitamin C with iron-rich meals to boost absorption. Avoid tea and coffee around mealtimes. Report worsening fatigue, chest pain or breathlessness promptly — these may signal falling haemoglobin or heart strain.