 Methods: We plan to recruit sixty statin naive patients, with diabetes mellitus type 2 andor obesity BMI 25 andor hypertension RR14090 mmHg. Patients with KDOQI stage 5 chronic kidney disease Cockcroft-Gault clearance of less than 15 mlmin1.73m2, patients who use any vitamin preparation, or statins in the last three months and patients with LDL cholestrerol 2.5 mmoll will be excluded from the study. Because of the influence of angiotensin-converting enzyme inhibitors ACE-inhibitors on oxidative stress, patients will be stratified for prior ACE-inhibitor use during randomization. All included patients are randomized to treatment with simvastatin 40 mg daily or atorvastatin 10 mg daily to achieve a comparable lipid reduction. Established parameters of oxidative stress such as oxidized LDL, malondealdehyde and isoprostane will be measured in plasma on inclusion, one week, six weeks and three months after inclusion. 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, interleukin-6 and myeloperoxidase will be measured to investigate whether there is any correlation between 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 inflammatory 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. Collections of 24 hours of urine at the beginning and after one week, six weeks and three months will be used to measure urine F2-isoprostane levels. 