P385Correlation between microalbuminuria and arterial wall stiffness is more obvious in patients with never-treated type 2 diabetes than in patients with never-treated essential hypertension

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Microalbuminuria (MAU) has been reported as a predictor of atherosclerotic cardiovascular disease (CVD) in patients with diabetes (DM) or hypertension (HBP). The aim of this study was to evaluate the association between MAU and other predictors of atherosclerosis. We also determined which of 2 aspects of atherosclerosis, arterial thickness or stiffness, more highly correlates with MAU in each DM and HBP.


Total 223 patients with never-treated type 2 DM (109) or essential HBP (114) without overt nephropathy were enrolled. Urinary albumin-to-creatinine ratio (ACR) was assessed before initial treatment to define MAU as ACR≥22 (men), ACR≥31mg/g (women). Arterial stiffness was assessed by brachial-ankle pulse-wave velocity (PWV) and arterial thickness was measured by carotid intima-media thickeness (IMT). Several predictors of CVD, such as hsCRP, left atrial volume index (LAVI) were also assessed.


MAU was observed in 110 patients (52 of DM, 58 of HBP) and 113 patients (57 of DM, 56 of HBP) had normoalbuminuria (NAU, ACR < 22 in men, ACR < 31mg/g in women). There was no significant difference in baseline characteristics. However, levels of hsCRP, IMT, PWV were significantly higher in MAU than in NAU group (2.8 ± 1.4 vs 0.8 ± 0.4mg/L, 0.9 ± 0.2 vs 0.6 ± 0.1mm, 18.1 ± 2.4 vs 14.8 ± 1.5m/sec, p < 0.05). In subgroup analysis, DM-MAU had significantly higher levels of hsCRP, IMT, PWV than DM-NAU group (3.1 ± 0.8 vs 0.9 ± 0.4mg/L, 0.9 ± 0.2 vs 0.6 ± 0.1mm, 18.8 ± 2.8 vs 15.5 ± 1.4m/sec, p < 0.05). In HBP, the results were similar (2.5 ± 1.7 vs 0.7 ± 0.5mg/L, 0.8 ± 0.2 vs 0.5 ± 0.1mm, 17.4 ± 2.2 vs 14.1 ± 1.1m/sec, p < 0.05). In comparison between DM-MAU and HBP-MAU groups, level of IMT was not statistically different, however, levels of PWV and hsCRP were significantly higher in DM-MAU than in HBP-MAU group. There was a positive correlation between levels of MAU and PWV only in DM-MAU group (r=0.43, p < 0.05). Level of hsCRP showed a positive correlation with MAU in MAU-DM and MAU-HBP groups (r=59, r=0.39, p < 0.05).


MAU was strongly associated with increased arterial stiffness, thickness, and hsCRP in both never-treated DM and HBP. Interestingly, DM-MAU demonstrated a higher level of PWV, but not IMT, than HBP-MAU group. And DM-MAU also showed a positive correlation between the levels of MAU and PWV, but not between MAU and IMT. These results could suggest that the correlation between MAU and arterial stiffness is more obvious in early, never-treated DM than in early, never-treated HBP. And in never-treated type 2 DM, MAU is more strongly correlated with arterial stiffness than arterial thickness.

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