Accelerated atherosclerosis, dyslipidemia, and oxidative stress in end-stage renal disease

Surekha Mathur, Sridevi Devaraj, Ishwarlal Jialal

Research output: Contribution to journalArticlepeer-review

48 Scopus citations


Premature atherosclerosis is a major cause of morbidity and mortality in end-stage renal disease patients. Dyslipidemia and increased oxidative stress contribute to premature atherogenesis in these patients. The dyslipidemia of end-stage renal disease consists of both quantitative and qualitative abnormalities in serum lipoproteins. Qualitative changes include hypertriglyceridemia (increased remnant lipoproteins), low high-density lipoprotein-cholesterol, and increased lipoprotein (a). In addition to quantitative changes, lipoproteins in end-stage renal disease undergo compositional and qualitative changes that make them pro-atherogenic, such as various modifications of apolipoprotein B, including oxidation, and modification by advanced glycation end-products. The 3-hydroxy-3- methylglutaryl coenzyme A reductase inhibitors and low-dose fibrates could be effective therapies for lipid disorders. The best evidence for increased oxidative stress in end-stage renal disease is the demonstration of increased plasma F2-isoprostanes. Confirmation of the positive findings with high-dose α-tocopherol in the Secondary Prevention with Antioxidants of Cardiovascular Disease in End-stage Renal Disease Study is urgently needed. Clinical trials with statins and other drugs that improve dyslipidemia also need to be undertaken. These therapies could clearly lead to a reduction in cardiovascular morbidity and mortality in these patients.

Original languageEnglish (US)
Pages (from-to)141-147
Number of pages7
JournalCurrent Opinion in Nephrology and Hypertension
Issue number2
StatePublished - 2002
Externally publishedYes

ASJC Scopus subject areas

  • Nephrology
  • Internal Medicine


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