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Abstract
Thromboembolic disease is an important complication in childhood nephrotic syndrome affecting about 5 % of patients (Ozkay et al., 2006).
Thrombosis in nephrotic syndrome may arise from the loss of proteins involved in the inhibition of systemic hemostasis (low antithrombin III and protein S levels ), the increased synthesis of factors promoting thrombosis ( factors I, V, VIII and von Willebrand factor ), or by the local activation of the glomerular hemostasis systems (intra-glomerular fibrin deposition ) ( Singhal and Brimble, 2005 ).
Protein Z (PZ) is a glycoprotein with structural similarities to protein C and coagulation factors VII, IX, and X. A key role for this liver-synthesized protein seems to be the down regulation of coagulation by inhibition of activated coagulation factor X (Broze, 2001).
Increased blood concentrations of protein Z therefore might be expected to result in greater inhibition of blood coagulation, predisposing to bleeding, whereas reduced blood concentrations of protein Z might be expected to cause reduced inhibition of blood coagulation, predisposing to thrombosis (Staton et al., 2005 ).