Fibrinolysis in insulin-dependent diabetic patients with and without nephropathy

Objective: To investigate possible contributions from fibrinolytic disturbances to susceptibility for cardiovascular complications in insulin-dependent diabetic patients with nephropathy.

Design: Cross-sectional study.

Setting: Outpatient diabetic clinic in a tertiary hospital.

Subjects: Insulin-dependent diabetic patients without diabetic nephropathy (normoalbuminuria, n = 17), patients with incipient diabetic nephropathy (n = 19), and patients with diabetic nephropathy (n = 13). Non-diabetic subjects served as a control group (n = 14).

Results: Tissue-type plasminogen activator antigen and plasminogen activator inhibitor type 1 were lower in diabetic patients, irrespective of the level of albuminuria. Tissue-type plasminogen activator activity measured in acidified plasma by bioimmunoassay was increased in normoalbuminuria, while the level in diabetic nephropathy was not different from a non-diabetic control level, and was significantly lower than in the normoalbuminuric group. D-Dimer and soluble fibrin were elevated in the pooled group of diabetic patients and were not influenced by presence of nephropathy. The level of plasmin-α₂-antiplasmin complexes was elevated to the same extent in each group of insulin-dependent diabetic patients.

Conclusion: The data suggest increased fibrinogen turnover in insulin-dependent diabetes mellitus, irrespective of the presence of nephropathy. In normoalbuminuric patients, an increase in plasminogen activation could be explained by increased activity of tissue plasminogen activator, while other explanations, e.g. fibrin accumulation, probably connected to developing atherogenesis, could be hypothesized in patients with nephropathy.