OBJECTIVE: Both arterial stiffness and proteinuria are important markers for organ damage in hypertension. This study was planed to investigate the association between arterial stiffness and inflammation and to define the influences of proteinuria on arterial stiffness and inflammation in non-diabetic hypertension. METHODS: We enrolled 205 patients (mean age 41 +/- 8 years, 66 women) with essential hypertension noted for less than 5 years in this study. They did not have diabetes mellitus or any overt cardiac, vascular, or renal complications. Stiffness index (SI) derived from digital volume pulse was used for assessment of arterial stiffness. High-sensitivity C-reactive protein (hsCRP) was measured in each patient during enrollment. Left ventricular hypertrophy (LVH) was documented by electrocardiography and proteinuria was assessed by measuring 24-h urine protein. RESULTS: SI was significantly correlated with hsCRP (r = 0.166, p = 0.017). LVH was noted in 34 patients (17%). SI was significantly higher in patients with LVH (8.03 +/- 1.74 vs 7.19 +/- 1.19 m/s, p = 0.001). Proteinuria was noted in three patients with LVH. SI was gradually increased among patients without LVH, with LVH but not proteinuria, and with LVH and proteinuria (7.19 +/- 1.19, 7.68 +/- 1.21, 11.75 +/- 2.51 m/s respectively; p<0.001). HsCRP was also gradually increased among patients without LVH, with LVH but not proteinuria, and with LVH and proteinuria (0.20 +/- 0.24, 0.30 +/- 0.59, 1.56 +/- 1.58 mg/dl respectively; p<0.001). CONCLUSIONS: SI was significantly correlated with hsCRP. Arterial stiffness and inflammation were increased in association with proteinuria in non-diabetic essential hypertension.
OBJECTIVE: Both arterial stiffness and proteinuria are important markers for organ damage in hypertension. This study was planed to investigate the association between arterial stiffness and inflammation and to define the influences of proteinuria on arterial stiffness and inflammation in non-diabetic hypertension. METHODS: We enrolled 205 patients (mean age 41 +/- 8 years, 66 women) with essential hypertension noted for less than 5 years in this study. They did not have diabetes mellitus or any overt cardiac, vascular, or renal complications. Stiffness index (SI) derived from digital volume pulse was used for assessment of arterial stiffness. High-sensitivity C-reactive protein (hsCRP) was measured in each patient during enrollment. Left ventricular hypertrophy (LVH) was documented by electrocardiography and proteinuria was assessed by measuring 24-h urine protein. RESULTS: SI was significantly correlated with hsCRP (r = 0.166, p = 0.017). LVH was noted in 34 patients (17%). SI was significantly higher in patients with LVH (8.03 +/- 1.74 vs 7.19 +/- 1.19 m/s, p = 0.001). Proteinuria was noted in three patients with LVH. SI was gradually increased among patients without LVH, with LVH but not proteinuria, and with LVH and proteinuria (7.19 +/- 1.19, 7.68 +/- 1.21, 11.75 +/- 2.51 m/s respectively; p<0.001). HsCRP was also gradually increased among patients without LVH, with LVH but not proteinuria, and with LVH and proteinuria (0.20 +/- 0.24, 0.30 +/- 0.59, 1.56 +/- 1.58 mg/dl respectively; p<0.001). CONCLUSIONS: SI was significantly correlated with hsCRP. Arterial stiffness and inflammation were increased in association with proteinuria in non-diabetic essential hypertension.