title: Impact of dyslipidemia in end-stage renal disease.
abstract: Heart disease is a major cause of morbidity and mortality among patients with renal failure. Premature atherosclerotic coronary heart disease is driven by multiple risk factors, including dyslipidemia and oxidative stress. In the nondialysis population, there is overwhelming evidence that treatment of dyslipidemia can significantly improve cardiovascular outcomes. Accumulating data indicate that dialysis patients have atherogenic lipid abnormalities. Although LDL cholesterol (LDL-C) levels in patients who undergo hemodialysis are normal or near normal, increased oxidized LDL-C, triglycerides, and lipoprotein (a) [Lp(a)]; decreased HDL cholesterol (HDL-C); and triglyceride-rich VLDL have been noted. Patients who receive peritoneal dialysis have a more atherogenic lipid profile with increased LDL-C, apolipoprotein B, oxidized LDL-C, triglycerides, and Lp(a) and decreased HDL-C. Furthermore, the LDL particles of peritoneal dialysis patients are small and dense. However, there is a dearth of information regarding the goals, efficacy, and safety of dyslipidemia treatment among dialysis patients. Given the strong evidence of risk reduction and the benefits of lipid-lowering treatment in the nondialysis population, the emerging consensus is that dialysis patients should be treated aggressively for dyslipidemia to an LDL-C goal below 100 mg/dl. Although physicians and patients may be reluctant to add medications because of concerns about polypharmacy, potential decreased compliance, and increased cost, the use of agents such as sevelamer that can serve multiple functions, including phosphate control, lipid lowering (decreased LDL-C and total cholesterol), and anti-inflammatory effects (decreased high-sensitivity C-reactive protein), should be explored and considered for patients who would benefit from such treatment.
authors.affiliation: Department of Medicine, McGill University, Montreal, Quebec, Canada. sarah.prichard@muhc.mcgill.ca
authors.forename: Sarah S
authors.initials: SS
authors.lastname: Prichard
mesh_terms: D003327:Coronary Disease / Q000097:blood / Q000209:etiology*; D006801:Humans; D006949:Hyperlipidemias / Q000097:blood / Q000188:drug therapy / Q000209:etiology*; D000960:Hypolipidemic Agents / Q000627:therapeutic use; D007676:Kidney Failure, Chronic / Q000097:blood / Q000150:complications* / Q000628:therapy; D008055:Lipids / Q000097:blood*; D006435:Renal Dialysis; D012307:Risk Factors
chemical_list: D000960:Hypolipidemic Agents; D008055:Lipids