The persistence of the anemia, might be explained by iron disturbances (Fig 3) and/or by a reduced (altered) EPO activity, and both changes may result from the glomerular kidney lesions (Fig 5) and from the developed local inflammatory milieu, as showed by the increased gene expression of different protein mediators of inflammation, hypoxia and fibrosis in the remnant kidney (Figs 6 and 7). The gene discussed is EPO; the disease is anemia (phenotype).