Vol 2, No 4 (2011)
Review paper
Published online: 2011-12-28

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Coagulation disturbances in kidney diseases

Elżbieta Mądro, Jolanta Małyszko
Hematologia 2011;2(4):332-338.

Abstract

Long-term hemodialysed patients reveal tendency to clot formation and haemorrhagic disorders. Haemostatic disturbances play essential role in their pathogenesis. They include plasmatic, vascular and platelet mechanisms. Abnormalities in blood platelets caused by chronic uraemia are partially corrected during hemodialysis. However, a direct contact between blood platelets and artificial surface of dialysis membrane during extracorporeal circulation, constitutes significant factor stimulating adhesion, retention of blood platelets inside the dialyser as well as formation of microaggregates and leukocyte-platelet aggregates. The increased concentrations of β-tromboglobulin and platelet factor 4 are the result of blood platelet activation as well. Expression of glycoproteins, in particular, glycoprotein IIb/IIIa (P-selectin and glycoprotein CD63) on the surface of blood platelets is the essential factor. Endothelial cell damage or injury is invariably associated witch such clinical condition as thrombosis, hypertension, renal failure and atherosclerosis and may be also responsible for accelerated atherosclerosis in patients with chronic renal failure. Endothelium secretes several vasoconstrictory substances including thromboxane A2 (TxA2), endothelins, angiotensin II, reactive oxygen species. Inflammatory modulators include adhesion molecules like intercellular adhesion molecule 1, vascular adhesion molecule 1, E-selectin, nitric oxide (NO). Hemostasis is modulated by endothelium by release of tissue plasminogen activator — plasminogen activator inhibitor type 1, von Willebrand factor, NO, prostacyclines, TxA2, tissue factor pathway inhibitor and fibrinogen.
Hematologia 2011; 2, 4: 332–338

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Hematology in Clinical Practice