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Renal anaemia is a form of blood deficiency caused by chronic kidney disease. Damaged kidneys produce insufficient erythropoietin, reducing red blood cell production and impairing oxygen transport.
Renal anaemia is a form of blood deficiency caused by chronic kidney disease. Damaged kidneys produce insufficient erythropoietin, reducing red blood cell production and impairing oxygen transport.
Renal anaemia is a condition of reduced red blood cell mass that develops as a direct consequence of chronic kidney disease (CKD). Healthy kidneys produce the hormone erythropoietin (EPO), which stimulates the bone marrow to generate red blood cells (erythrocytes). As kidney function declines, EPO production falls, leading to a deficiency of haemoglobin -- the protein responsible for carrying oxygen in the blood. Renal anaemia commonly appears when the glomerular filtration rate (GFR) drops below 60 ml/min and is nearly universal in patients receiving dialysis.
The primary cause of renal anaemia is insufficient EPO synthesis by the damaged kidneys. Additional contributing factors include:
The symptoms of renal anaemia reflect insufficient oxygen delivery to tissues and may be aggravated by the underlying kidney disease:
Diagnosis is based on blood tests. Key parameters include:
ESAs are synthetic analogues of endogenous erythropoietin, including epoetin alfa, epoetin beta, darbepoetin alfa, and methoxy polyethylene glycol-epoetin beta. They are administered subcutaneously or intravenously to stimulate bone marrow red blood cell production. The treatment target is a haemoglobin level of 10 to 12 g/dl.
Iron is essential for red blood cell production and is frequently deficient in CKD patients. Iron supplementation is often given alongside ESA therapy. In dialysis patients, intravenous iron is preferred as oral absorption is frequently inadequate.
A newer class of oral agents -- including roxadustat, daprodustat, and vadadustat -- work by inhibiting the breakdown of the transcription factor HIF (hypoxia-inducible factor), which naturally triggers EPO production in response to low oxygen levels. This stimulates endogenous erythropoiesis without requiring injections.
Transfusions are reserved for severe, symptomatic anaemia due to associated risks such as iron overload, infection transmission, and sensitisation against donor antigens.
Untreated renal anaemia significantly increases the risk of cardiovascular disease, hospitalisation, and mortality in CKD patients. Early and adequate treatment improves quality of life, reduces cardiovascular complications, and may slow the progression of kidney disease.
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