Inflammation, serum C‐reactive protein, and erythropoietin resistance

The anaemia associated with chronic renal failure has many causes. The main reason is deficient erythropoietin synthesis with serum levels of erythropoietin which are too low for the degree of anaemia. Blood loss, either iatrogenic from the puncture sites of the vascular access and blood sampling, or from other sources such as the gastrointestinal tract are contributive. As a result, iron requirements are often increased more than fivefold in dialysis patients. Most patients with chronic renal failure achieve the desired target haemoglobin (Hb) level when supplemented with relatively low doses (50–150 IU/kg/week) of recombinant human erythropoietin (epoetin) and parenteral iron (usually 1500–3000 mg/year) [1]. About a quarter of the dialysis patients, however, have a poor response and need higher doses (>200 IU/kg/week) to reach the target Hb level. This relative resistance to epoetin and iron is often associated with co‐morbid conditions, particularly inflammatory conditions. The inflammatory process may be acute, leading to transient resistance to epoetin, or chronic, with a persistently poor response to epoetin.