122 - Hematologic abnormalities in kidney disease
Autor(s): M. Golato, B. Biasioli, D. D’Alonzo, M. Liani, A. Pedrotta, P. Staffolani
Issue: RIMeL - IJLaM, Vol. 6, N. 3-S1, 2010 (MAF Servizi srl ed.)
Page(s): 122-128
Anaemia, white blood cell anomalies and platelet dysfunctions are the haematological anomalies more common found in patients with chronic kidney diseases. Both the uraemic environment and the dialysis process, to which the patients are necessarily subjected, are involved in the multifactorial aetiology of the disorders. The onset of anaemia is mainly due to the reduced production of erythropoietin (EPO), the hormon responsible for the blood cell maturation from red blood cell precursors. Red cell hypoplasia is complicated by the increased concentration of several cytokines such as interleukin 1 (IL-1) and interleukin 6 (IL-6), which inhibit the immature precursors maturation and stimulate a larger hepcidin production responsible for the reduced iron absorption. Recombinant Human Erytropoietin (rHuEPO) introduction has allowed the correction of anaemia avoiding to the patients the continuous blood transfusion; increased thrombotic risk is one of the adverse effects and the development of auto-anti body against erythropoietin and red cell aplasia (PRCA) is another unusual adverse effect. The increased erythropoietic activity, produced by rHuEPO treatment, may lead to iron stores depletion whereas the chronic inflammation, cause and accompanying process of kidney disease, may cause a reduced iron mobilization from the deposits, hence it is necessary to give iron supplement to patients during the treatment and it is necessary to evaluate the iron status throughout direct hematologic markers (haemoglobin content of reticulocytes, percent hypochromic reticulocytes) and indirect biochemical markers (serum ferritin, transferrin saturation ratio). Haemorrhagic diathesis and the tendency of the thrombotic phenomenons to happens, reduced chemotaxis with a greater infections susceptibility has implicated functional anomalies in the platelets membrane glicoproteins GPIb and GPIIb/IIIa and MAC-1 and LAM-1of white blood cells. The uremic toxins, inflammation, the utilization of dialysis membranes involve monocytes functional alteration and activation followed by increased plasmic levels of IL-1 and Tumor Necrosis Factor (TNF). Afterwards the dialysis treatments may produce an altered blood cells functionality with a variability linked to the characteristic of the patient with chronic kidney disease and to interaction with the dialysis membrane.