Vol 2, No 4 (2011)
Review paper
Published online: 2011-12-28
Coagulation disturbances in kidney diseases
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
Hematologia 2011; 2, 4: 332–338
Keywords: coagulation disturbancesend-stage renal diseasechronic kidney diseaseendothelial dysfunction