Effect of Albuminuria on the State of Plasma Hemostasis in Patients with Essential Hypertension

A.I. Pastushyna, O.M. Plenova


In recent decades, numerous scientific works are devoted to the study of the clinical and prognostic significance of albuminuria, methods of its detection, as well as treatment measures aimed at controlling this pathological condition. The objective of this work was to determine the features of changes of plasma hemostasis in patients with essential hypertension (EH), depending on the presence of albuminuria. Materials and methods. We have exa-mined 113 people: 14 apparently healthy ones (group 1, controls), 41 patients with EH stage II with concomitant albuminuria (group 2), 58 patients with EH stage II without concomitant albuminuria (group 3). We have conducted laboratory studies: measured activated partial thromboplastin time, prothrombin index, thrombin time, fibrinogen, soluble fibrin monomer complex (SFMC), time of XIIa-dependent fibrinolysis, antithrombin III, protein C. Results. There was found an increased content of SFMC, which in patients from group 3 was 135 % higher, and in patients of group 2 — 247 % higher than reference values. At that, in patients with albuminuria, this index was much higher even than in individuals with EH without albuminuria — exceeded by 48 %. Time of
XIIa-dependent fibrinolysis in both group 2 and 3 was much longer than normal one. Expressed changes occurred in the system of natural anticoagulants, which were statistically significant in relation to the control group only in patients with albuminuria, and in the group of patients without albuminuria they were not significantly different from the control group. Conclusions. Patients with essential hypertension, regardless of the severity of albuminuria, showed a significant inhibition of fibrinolytic activity of the blood and activation of the last units of blood clotting — fibrin formation. Albuminuria was associated with a more significant activation of fibrin formation and was combined with inhibition of own anticoagulant activity of the blood, as evidenced by the decrease in the content of antithrombin III and protein C.


hypertension; albuminuria; microalbuminuria; plasma hemostasis; thrombophilia


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