Novel inflammatory mechanisms of accelerated atherosclerosis in kidney disease

  • Swaminathan S
  • Shah S
  • 45


    Mendeley users who have this article in their library.
  • 49


    Citations of this article.


Objective: Urea undergoes a spontaneous, nonenzymatic transformation to cyanate, the active part of which is isocyanic acid, which can cause modifications of a variety of proteins in a process called carbamylation. We postulated that, in patients with renal disease, the carbamylation of low-density lipoprotein (LDL) is a nontraditional risk factor for cardiovascular disease, and that elevated urea leads to carbamylated LDL (cLDL), which causes vascular injury and leads to atherosclerosis. Results: We showed that carbamylated LDL manifests all of the biological effects relevant to atherosclerosis, including endothelial-cell injury, the expression of adhesion molecules, and vascular smooth muscle cell proliferation. We also developed an enzyme-linked immunosorbent assay to measure carbamylated LDL in patients, and showed that cLDL is markedly elevated in dialysis patients. Conclusions: Our data indicate that cLDL may be an important nontraditional risk factor for atherosclerosis in patients with kidney disease. © 2008 National Kidney Foundation, Inc.

Author-supplied keywords

  • Acute kidney injury
  • Cardiovascular disease
  • Chronic kidney disease
  • Inflammation

Get free article suggestions today

Mendeley saves you time finding and organizing research

Sign up here
Already have an account ?Sign in

Find this document


  • Sundararaman Swaminathan

  • Sudhir V. Shah

Cite this document

Choose a citation style from the tabs below

Save time finding and organizing research with Mendeley

Sign up for free