The physiopathological mechanisms proposed to explain the harmful role of anaemia in the progression of the renal lesions during the IRC rest on the tissue hypoxia induced by the reduction in haemoglobin. The tissue hypoxia supports the development of the interstitial fibrosis by stimulating the production of type I collagen and some inhibitors of metalloproteases, implied in the extracellular matrix degradation. The hypoxia also stimulates the synthesis of TGF-beta, pro-fibrosing factors implied in the progression of many renal diseases, in particular the nephropathy diabetic. By reducing the hypoxia thanks to the correction of anaemia by the EPO, one can hope to slow down the progression of the interstitial fibrosis, and thus the progression of the renal insufficiency. Lastly, the correction of anaemia reduces resistance to insulin and the secondary hyperinsulinism to uraemia, improves the dyslipidemia and the oxidizing stress, factors also implied in the progression of many nephropathies, diabetic or not.