Coagulation factors IX and X in patients with nephrotic syndrome and correlation of their activity to the underlying renal pathology

Nephrotic syndrome [NS] is characterized by significant protein loss in urine. Coagulation factors are expected to be lost in urine among the other proteins. Several studies on coagulation factors in patients with NS revealed changes in the various factors concerned with coagulation. This study included 30 patients with NS and 10 healthy subjects as control. All patients were subjected to renal biopsy to know the underlying pathological lesion. Beside the baseline investigations, the activities of coagulation factors IX and X were assayed. The results of this study showed that most of patients [except those with minimal lesion glomerulopathy] had significant increase in the activity of both factors IX and X [p < 0.05] with a significant decrease in clotting time. The cause of this increase in the activity may be due to increased synthesis by the liver which exceeds the rate of urinary loss. These changes in coagulation may have their effect on the course of the underlying renal disease

Protein C and protein S deficiency in thalassemic patients.

To investigate the status of the protein C-protein S anticoagulant pathway in thalassemic patients, we measured protein C and protein S levels of plasma of 30 adults and 18 children with beta-thalassemia/HbE disease, beta-thalassemia major and HbE disease. Mean +/- 1 SD values of protein C, protein S and other coagulant proteins produced by the liver were as follows: protein C 50.4 +/- 17.2%; protein S 58.8 +/- 25.5%; antithrombin III 78.1 +/- 12.8%; PLG 86.4 +/- 18.4%; prothrombin 71.0 +/- 13.1%; factor VII 72.7 +/- 21.5%; and factor X 79.2 +/- 15.6%. Protein C and protein S levels of thalassemic patients were significantly lower than those of other coagulant proteins produced by the liver. Decrease in protein C level was stronger than that of proteins S. gamma-Carboxylated protein C levels of splenectomized patients were significantly lower than those of nonsplenectomized patients. Severe decrease of protein C and protein S may be responsible for occurrence of thrombosis in thalassemic patients.