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Diabetes Care. 2011 Jan;34(1):156-61. doi: 10.2337/dc10-0788. Epub 2010 Oct 7.

Fetuin-A levels are increased in patients with type 2 diabetes and peripheral arterial disease.

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Department of Medicine II, Medical University of Vienna, Vienna, Austria.



Low levels of fetuin-A, a systemic calcification inhibitor, are linked to mortality in patients on dialysis. In contrast, elevated fetuin-A is associated with cardiovascular events in non-renal patients. We investigated fetuin-A in patients with type 2 diabetes and peripheral arterial disease (PAD).


We studied fetuin-A in 76 patients with PAD and normal glucose metabolism (NGM-PAD) and in 129 patients with PAD and type 2 diabetes (type 2 diabetes-PAD). Additionally, 40 patients with diabetes without any complications (type 2 diabetes-non-PAD) were examined.


Type 2 diabetes-PAD subjects (399 ± 155 μg/ml) had significantly higher fetuin-A levels than type 2 diabetes-non-PAD subjects (247 ± 42; P < 0.001). In NGM-PAD subjects (376 ± 144), fetuin-A was significantly higher than in type 2 diabetes-non-PAD subjects (P < 0.001). Type 2 diabetes-PAD patients with mediasclerosis had lower fetuin-A than subjects without (P < 0.03). Regression analysis in type 2 diabetes-PAD subjects revealed that glycated A1C (P < 0.001) and mediasclerosis (P = 0.004) were the strongest predictors of fetuin-A. Multivariate regression revealed that a 1-SD increase in fetuin-A was associated with an odds ratio (OR) of 2.1 (95% CI 1.1-3.3; P < 0.001) for the prevalence of PAD and an OR of 1.4 (1.0-1.7, P = 0.039) for the prevalence of myocardial infarction.


In contrast to previous findings, fetuin-A was higher in type 2 diabetes-PAD patients than in type 2 diabetes-non-PAD patients. In NGM-PAD patients, fetuin-A was also higher than in type 2 diabetes-non-PAD patients. In type 2 diabetes-PAD patients, fetuin-A was inversely associated with mediasclerosis-the calcification process pathognomonic for diabetic PAD. This association persisted in multivariate regression, which is in line with the calcification inhibition in coronary heart or renal disease.

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