Hence, a biological link between hyperglycemia and high BP is highly plausible. The current clinical guideline of the American Diabetes Association for T2D is to reduce glycated hemoglobin below the target of 7.0%. The UKPDS demonstrated that a 10-year intensive glucose control by sulphonylureas or insulin achieved an 11% reduction by tight hyperglycemia control of HbA1c below 7.0% vs. the YC-1 conventional care of HbA1c below 7.9%. Although the intensive hyperglycemia control did not lead to a significant risk reduction in the rate of macro-vascular disease over a 10-year intensive management, it did achieve a 9% reduction in the rate of any diabetes-related end point and risk reduction in microvascular disease. Further tight hyperglycemia control to a level of HbA1c,6.5% may lead to further reduction in the rate of micro- and macro- vascular complications in patients of type 2 diabetes. In this regard, the Outcome Reduction With Initial Glargine Intervention study suggested further tight control of hyperglycemia can achieve an additional risk reduction in diabetes complications when HbA1c was lower than 6.5%, which is safe and able to reduce nephrology risk. The ADVANCE trial demonstrated that reducing HbA1c further to,6.5% is safe and able to further reduce nephrology risk by about 20%. The reduction in albuminuria in the ADVANCE trial may be translated to future reduction in cardiovascular disease. Thus, our data support the notion that intensive hyperglycemia control with a threshold of HbA1c below 6.5% contributes to good BP control in addition to reduced risk of microvascular disease, and potentially reduced risk of macrovascular disease in the long run. This study has several limitations. Firstly, the study was a crosssectional survey and can not establish a causal Argatroban relationship between hyperglycemia and hypertension. Obesity, insulin resis tance and hypertension often appear in clusters and metabolic syndrome is an established risk factor for diabetes. On the other hand, 20% or more of people with hypertension have diabetes, and hypertension is present in up to 60% of patients with T2D. A causal relationship from hyperglycemia to hypertension is biologically plausible.