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OBJECTIVE- To examine uric acid (UA) as a possible predictor of the progression of coronary artery calcification (CAC) using data from the prospective Coronary Artery Calcification in Type 1 Diabetes (CACTI) Study.
RESEARCH DESIGN AND METHODS- CAC was measured by electron beam tomography at the baseline and at a follow-up 6.0 ± 0.5 years later. The study population included 443 participants with type 1 diabetes and 526 control subjects who were free of diagnosed coronary artery disease at baseline. The presence of renal disease was defined by the presence of albuminuria and/or low glomerular filtration rate.
RESULTS- In subjects without renal disease, serum UA predicted CAC progression (odds ratio 1.30 [95% CI 1.07-1.58], P = 0.007) independent of conventional cardiovascular risk factors including diabetes and the presence of metabolic syndrome.
CONCLUSIONS- Serum UA levels predict the progression of coronary atherosclerosis and may be useful in identifying who is at risk for vascular disease in the absence of significant chronic kidney disease.
Diabetes Care 33:2471-2473, 2010
Elevated serum uric acid (UA) is associated with kidney disease, but it has also been linked to endothelial dysfunction and development of hypertension irrespective of renal involvement (1). UA may contribute to the atherosclerotic process through induction of endothelial dysfunction (2) and inflammation (3).
Serum UA levels have been correlated with negative cardiovascular outcomes in the general population (4) and type 2 diabetic subjects (5) and predict the progression of diabetic nephropathy (6) in type 1 diabetic subjects. The objective of this study was to evaluate UA levels as a predictor of subclinical atherosclerosis progression in the Coronary Artery Calcification in Type 1 Diabetes (CACTI) Study.
RESEARCH DESIGN AND METHODS- Of the 1,416 individuals asymptomatic for coronary artery disease (CAD) enrolled at baseline, 1,022 had data on coronary artery calcification (CAC) progression. Subjects with coronary events during follow-up (n = 18) and incomplete information about covariates (n = 35) were excluded, resulting in 969 subjects. Clinical and laboratory evaluations were performed as previously described (7). CAC was measured twice and averaged at the baseline and at follow-up 6.0 ± 0.5 years later. CAC progressors were defined as participants whose square root-transformed CAC volume (CVS) increased by ≥2.5 mm (8). Serum UA levels were measured at baseline on the clinical...