Key result
Type 2 diabetes patients with macrovascular disease had significantly higher thrombin generation (AUC 3464 vs 3091 nM; P=0.01) than those without macrovascular disease.
Why the study?
Is thrombin generation altered in patients with type 2 diabetes mellitus depending on albuminuria stage and presence of macrovascular disease?
Cross-Sectional (n=160)
Is thrombin generation altered in patients with type 2 diabetes mellitus depending on albuminuria stage and presence of macrovascular disease?
Patients with type 2 diabetes and macrovascular disease exhibit earlier and higher thrombin generation, suggesting hypercoagulability may contribute to macrovascular complications in diabetic nephropathy.
Elevated thrombin generation may signal thrombotic risk in type 2 diabetes with macrovascular disease; hypothesis-generating and requires prospective validation.
BACKGROUND: Albuminuria is an indicator of cardiovascular morbidity and mortality in patients with type 2 diabetic mellitus (T2DM). MATERIALS AND METHODS: In our cross-sectional study, we measured thrombin generation (TG), a key process in haemostasis and a tool to detect an individual's coagulation potential, in normo-, micro- and macroalbuminuria in T2DM with and without macrovascular disease (MVD). The TG-assay was performed, and the TG-curve [including the lag phase, peak thrombin and area under the curve (AUC)] was analysed. RESULTS: A total of 160 patients (62 women; mean age ± SD: 67 ± 11 years) with T2DM and normo-, micro- or macroalbuminuria were investigated. Of those, 90 (56%) patients had normoalbuminuria, 40 (25%) microalbuminuria and 30 (19%) macroalbuminuria. The AUC between the groups of patients with normo-, micro- and macroalbuminuria was statistically significantly different [3297 (2785; 3764) vs. 3222 (2381; 3678) vs. 3726 (3153; 4235) nM Thrombin; P = 0AE019]. T2DM patients with MVD (n = 121) had a significantly shorter lag phase [12 (9; 16) vs. 20 (15; 25) min; P < 0AE001], a significantly higher peak thrombin [233 (130; 339) vs. 133 (82; 187) nM; P < 0AE001] and a significantly higher AUC [3464 (2969; 3868) vs. 3091 (2384; 3619) nM Thrombin; P = 0AE01] than T2DM patients without MVD (n = 39), indicating an earlier and higher thrombin generation. CONCLUSION: Our results support the hypothesis that TG may be involved in the pathogenesis of MVD in diabetic nephropathy as for the first time, we could show that patients with T2DM in different stages of diabetic nephropathy had disturbances in thrombin generation.
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Ay et al. (2011) conducted a cross-sectional in Type 2 diabetes mellitus (n=160). Macrovascular disease vs. No macrovascular disease was evaluated on Thrombin generation area under the curve (AUC) (p=0.01). Type 2 diabetes patients with macrovascular disease had significantly higher thrombin generation (AUC 3464 vs 3091 nM; P=0.01) than those without macrovascular disease.
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