Purpose: Whether patients with hypertensive target organ damage (preclinical cardiovascular (CV) disease) are at higher risk of incident diabetes (DM) has never been studied. Methods: We assessed incident DM in 4,176 hypertensive non-diabetic patients (age 58.7±8.9 yrs, 58% male) with ≥1 year follow-up. Left ventricular (LV) hypertrophy was defined as LV mass index (LVMi) ≥51 g/m2.7. Carotid atherosclerosis (CA) was defined as intima-media thickness ≥1.5 mm. Results: During follow-up (4.5±3.5 yrs), DM developed in 393 patients (9.4%), more frequently in those with than without initial LV hypertrophy or CA (OR=1.97 and 1.67, respectively; both p<0.0001). In Cox regression, the presence of either marker of preclinical CV disease increased the chance of incident DM by 62% (HR = 1.62; [95% CI 1.27–2.08]; p<0.0001), a risk that was only marginally increased by the presence of both (HR = 1.64; [95% CI 1.19–2.23]; p=0.002) and that was independent of initial systolic BP (HR = 1.05/5 mmHg; [95% CI 1.02–1.11]; p=0.001), initial BMI (HR = 1.05/kg m-1; [95% CI 1.02–1.08]; p<0.0001), initial fasting plasma glucose (HR = 1.08/mg dL-1; [95% CI 1.07–1.09]; p<0.0001), family history of diabetes (HR = 1.59; [95% CI 1.29–1.96]; p<0.0001) and type and number of anti-hypertensive medications taken during follow-up (not significant). This result was confirmed (HR=1.70 for one of the markers, or 1.93 for both, respectively; both p<0.0001) also after clustering metabolic risk factors in the phenotypes of metabolic syndrome in the Cox model (HR = 2.73; [95% CI 2.21–3.37]; p<0.0001). Conclusions: We provide evidence that initial hypertensive target organ damage (LVH or CA) are significant predictors of new onset DM in a large population of treated hypertensive patients, independently of initial metabolic profile, anti-hypertensive therapy and other significant covariates. This sequence may be attributable to risk factors common to preclinical CVD and DM, but a vascular origin of DM cannot be excluded.