Haemostatic Changes in Patients with Diabetic Nephropathy due to Proteinuria

OBJECTIVE: It is known that diabetes may cause to hypercoagulability. The pathogenetic mechanism of coagulation activation is not completely clear and the origin is multifactorial. While chronic hyperglycemia is considered to be the main underlying pathology, there are various comments on the association between glycemic control and haemostatic disorders. In this study, we have aimed to compare patients with diabetic nephropathy and patients with idiopathic nephrotic syndrome with respect to haemostatic differences.

MATERIAL and METHODS: We compared 10 newly diagnosed idiopathic nephrotic syndrome patients with 10 normoalbuminuric, 10 microalbuminuric and 10 macroalbuminuric Type II diabetic patients in terms of haemostatic disorders. We included 12 healthy controls in the study. In all groups, protein C activity, free protein S, Antithrombin III, Factor VII, VIII, IX, XI, plasminogen, fibrinogen and platelet count were evaluated.

RESULTS: Antithrombin III levels of patients with nephrotic syndrome were significantly lower than the control group and macroalbuminuric diabetics but fibrinogen levels were significantly higher than controls. Fibrinogen levels of microlalbuminuric diabetics were significantly higher than controls. Other haemostatic parameters were all in normal range in all patient groups.

CONCLUSIONS: These findings suggest that the mechanism of hypercoagulation works in a different pathway than the hypercoagulation in nephrotic patients.