Patients dialyzed due to
diabetic nephropathy are at a higher risk of death due to cardiovascular complications than dialyzed non-diabetic patients. Disturbances in hemostasis may play a role in the vascular
complications of diabetes mellitus. It has been postulated that TAFI-
thrombin activatable fibrinolysis inhibitor, which couples two opposite systems: coagulation and fibrinolysis, may be involved in the mechanism of vascular endothelial damage in diabetic patients. We assessed: TAFI and TAFIa, markers of ongoing coagulation:
thrombin-
antithrombin complexes,
prothrombin fragments 1+2, a marker of ongoing fibrinolysis:
plasmin-
antiplasmin complexes in diabetic and non-diabetic patients on
hemodialyses-HD,
peritoneal dialyses-
CAPD, patients with
chronic renal failure with and without
diabetic nephropathy on
conservative treatment. Both groups of dialyzed diabetic patients have a higher concentration of markers of ongoing coagulation and TAFI activity when compared to dialyzed non-diabetic patients. Linear regression analysis showed that TAFI concentration was directly related to
albumin in HD and
CAPD patients without
diabetic nephropathy, whereas TAFIa correlated with
triglycerides,
fibrinogen and leukocytes count in this group. When evaluated separately (HD,
CAPD), significant correlations between TAFIa and
triglycerides and
fibrinogen were found only in diabetic
CAPD patients. Multivariate analysis showed no correlation between TAFI and other parameters studied. In conclusion, elevated circulating TAFI and TAFIa might be a new link in the pathogenesis of impaired fibrinolysis in
diabetic nephropathy, and thus
atherosclerosis progression, particularly in
CAPD patients. Hypercoagulable state observed in diabetic patients on
conservative treatment and maintained on dialyses may contribute to the higher cardiovascular mortality in this population. In these patients there is also evidence of endothelial injury, and probably secondary activation of the coagulation cascade.