eGFR was significantly lower in individuals with 1hPG ��155 mg/dl. A greater proportion of individuals with 1hPG ��155 mg/dl were classified into the two lower categories of eGFR (60 to 89 and 30 to 59 ml/min per 1.73 m2) as compared with individuals with 1hPG <155 mg/dl (Table 1). Similar Wortmannin ATM results were observed after excluding from the analysis individuals with IGT (Table 3). In a logistic regression model adjusted for age and gender, individuals with 1hPG ��155 mg/dl showed an increased risk for having CKD (odds ratio [OR] 2.61; 95% confidence interval [CI] 1.01 to 6.77) as compared with individuals with 1hPG <155 mg/dl. When the logistic regression analysis adjusted for age and gender was restricted to individual who had NGT, those with 1hPG ��155 mg/dl still showed a higher risk for having CKD (OR 4.

63 [95% CI 1.43 to 14.93]) as compared with individuals with 1hPG <155 mg/dl. After additional adjustment for a wide range of potential confounders, including BMI, systolic BP, diastolic BP, triglycerides, HDL, and fasting insulin, individuals with 1hPG ��155 mg/dl continued to have higher risk for CKD (OR 3.72 [95% CI 1.02 to 13.58]). These associations were abrogated when the Matsuda ISI or IGF-1 levels were added to the model. Table 3. Anthropometric and clinical characteristics of glucose-tolerant individuals stratified according to 1hPG levels during an OGTT Discussion There is evidence to suggest that individuals with prediabetes, including those with impaired fasting glucose and IGT, not only are at increased risk for developing type 2 diabetes and CVD (1�C3) but also should be considered at increased risk for developing CKD (8).

These findings have led to the hypothesis that type 2 diabetes, CVD, and CKD might have common antecedents of metabolic origin. A number of longitudinal studies have reported that a significant proportion of individuals with NGT at baseline are at risk for both type 2 diabetes (1,2) and CVD (3), indicating that the future risk for these two clinical outcomes is not similar among all individuals with NGT. Two recent studies demonstrated that a cutoff point of 155 mg/dl for the 1hPG during the OGTT can identify individuals who do not have diabetes and are at risk for developing type 2 diabetes (4,5). Moreover, individuals Entinostat with NGT and 1hPG ��155 mg/dl seem to have a worse cardiometabolic risk profile and early signs of vascular atherosclerosis (6,16). In this study, we provide evidence that in a Italian, white cohort, the diagnostic accuracy of the 1hPG levels for detecting individuals who are affected by CKD is superior to that of fasting, 30-minute or 2-hour plasma glucose levels, suggesting that this metabolic parameter may be a useful tool to identify individuals who are at risk for CKD.