Accelerated atherosclerosis, dyslipidemia, and oxidative stress in end-stage renal disease.
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 alpha-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.
Mathur
Surekha
S
Center for Human Nutrition, University of Texas Southwestern Medical Center, Dallas, TX 75390-9073, USA.
Devaraj
Sridevi
S
Jialal
Ishwarlal
I
D001161:Arteriosclerosis / Q000209:etiology*; D006801:Humans; D006949:Hyperlipidemias / Q000209:etiology*; D007676:Kidney Failure, Chronic / Q000150:complications* / Q000378:metabolism*; D018384:Oxidative Stress