 Design and methods We plan to recruit sixty statin naive patients with diabetes mellitus type-2 andor obesity BMI 25 kgm2 andor hypertension RR 14090 mmHg. Patients with KDOQI stage 5 chronic kidney disease Cockcroft-Gault clearance of less than 15mlmin1.73m2 and patients who use any vitamin preparation or statins in the last three months will be excluded from the study. Because of the documented influence of ACE-inhibitors on oxidative stress we will stratify patients for prior ACE-inhibitor use during randomization. All included patients are randomized to treatment with simvastatin 40 mg daily or atorvastatin 10 mg daily in order to achieve a comparable lipid reduction. Established parameters of oxidative stress, such as oxidized LDL, malondealdehyde will be measured 14-18 in plasma on inclusion, one week, six weeks and three months after the inclusion. Primary end point of the study will be the absolute difference between oxidized LDL reduction between the two groups. We also plan to measure endothelial function parameters such as soluble Vascular Adhesion Molecule sVCAM and von Willebrand factor. In addition parameters of inflammation such as high sensitive c-reactive protein, TNF-alfa and Interleuking-6 will also be measured to investigate whether there is any correlation between eventual oxidative stress lowering and endothelial function and inflammation. The inhibitory effect of HDL to prevent oxidation of LDL will be determined by measurement of lipid peroxides formed during in vitro oxidation of LDL co-incubated with HDL. The anti-inflammatory properties of HDL will be tested by measurement of the HDL capacity to inactivate oxidized palmitoyl-2-arachidonoyl-sn-glycero-3-phosphorylcholine ox-PAPC. For this measurement we will use a cell-free assay that has been developed by Navab and co-workers 19. Collections of 24 hours of urine at the beginning and after one week, and three months will be used to measure urine F2-isoprostane levels 20-24. 