title: Dyslipidemia and the progression of renal disease in chronic renal failure patients.
abstract: Dyslipidemia is a common complication of progressive kidney disease and contributes to the high cardiovascular morbidity and mortality of chronic kidney disease (CKD) patients. Recent evidence also suggests a role for dyslipidemia in the development and progression of renal disease. Experimental studies have demonstrated that lipids may induce glomerular and tubulointerstitial injury, and that lipid-lowering treatments ameliorate renal injury. Various lipid abnormalities have been associated with the development and progression of renal disease in diabetic and nondiabetic patients. Population-based studies and studies of diabetic patients have reported associations of various lipid abnormalities with the development of renal disease. In patients with CKD, lipid abnormalities have also been associated with renal disease progression. Post hoc analyses of some large clinical trials on patients with vascular disease, diabetes, or dyslipidemia, and a meta-analysis of small, prospective, controlled studies on patients with CKD (diabetics and nondiabetics) suggest that statins may slow the progression of kidney disease. It is unclear whether the beneficial renal effects of statins are due to the reduction of serum cholesterol levels and/or their pleiotropic effects. There is also evidence for synergistic renoprotective effects between statins and renin-angiotensin system inhibitors. According to the results of post hoc analysis of several studies, treatment with fibrates does not seem to confer renoprotection, but evidence is scarce. In summary, there is growing evidence that lipid abnormalities may be a risk factor for renal disease, and that statins appear to confer a renoprotective effect.
authors.affiliation: Nephrology Unit, Hospital Clínic, Universitat de Barcelona, Barcelona, Catalonia, Spain. acases@clinic.ub.es
authors.forename: Aleix
authors.initials: A
authors.lastname: Cases
authors.forename: Elisabet
authors.initials: E
authors.lastname: Coll
mesh_terms: D000924:Anticholesteremic Agents / Q000627:therapeutic use; D002986:Clinical Trials as Topic; D018450:Disease Progression; D050171:Dyslipidemias / Q000097:blood / Q000150:complications / Q000188:drug therapy* / Q000503:physiopathology*; D005260:Female; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use; D007676:Kidney Failure, Chronic / Q000097:blood / Q000150:complications / Q000503:physiopathology* / Q000517:prevention & control; D008055:Lipids / Q000097:blood; D008297:Male; D015201:Meta-Analysis as Topic; D012084:Renin-Angiotensin System / Q000502:physiology; D012307:Risk Factors
chemical_list: D000924:Anticholesteremic Agents; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D008055:Lipids