Wild-type mice normally do not develop atherosclerosis, unless fed cholic acid. Uremia is proinflammatory and increases atherosclerosis 6-10 fold in apolipoprotein -deficent mice. This study examined the effect of uremia on lipoproteins, vascular inflammation, and atherosclerosis in wild-type C57BL/6J mice. Uremia was induced by 5/6 nephrectomy (NX) and increased plasma urea and creatinine concentrations 2.5-4.5 fold; control mice were sham operated. After NX, mice were fed a western-type diet or the same diet with 0.5 % cholic acid. Cholic acid-fed NX mice did not thrive and were sacrificed. In NX mice fed the western-type diet (n=7), the total plasma cholesterol concentration was similar to that in sham mice (n=11), but on gel filtration the LDL/HDL cholesterol ratio was increased. HDL from NX mice contained more serum amyloid A and triglycerides and less cholesterol than HDL from sham mice. Plasma concentrations of sICAM-1 and sVCAM-1 and aortic mRNA expression of ICAM-1 and VCAM-1 did not differ between NX and sham mice. Twenty-six weeks after NX, the average oil-red-O stained area of the aortic root was similar in NX and sham mice fed the western-type diet, while it was increased in cholic acid-fed sham mice. The results suggest that moderate uremia neither induces aortic inflammation nor atherosclerosis in C57BL/6J mice despite increased LDL/HDL cholesterol ratio and altered HDL composition.