title: The effect of omega-3 fatty acids on the atherogenic lipoprotein phenotype in patients with nephrotic range proteinuria.
abstract: OBJECTIVE
  Patients with nephrotic range proteinuria are known to have an increased risk of cardiovascular disease partly due to possessing the atherogenic lipoprotein phenotype. The aim of this study was to examine the effect of high dose omega-3 fatty acids on atherogenic triglyceride rich lipoproteins in patients with nephrotic range proteinuria, comparing their effect on lipoprotein profiles in age and sex matched controls.
  
  
  METHODS
  17 patients with nephrotic range proteinuria and 17 age and sex matched controls were studied. Fasting lipids and lipoproteins were measured before and after 8 weeks treatment with 4 g daily of omega-3 fatty acids (Omacor®).
  
  
  RESULTS
  In patients with proteinuria treatment reduced plasma triglyceride by a mean of 0.45 mmol/l (95%CI 0.16 - 0.74, p = 0.005) and plasma very low density lipoprotein cholesterol by a mean of 0.38 (95%CI 0.01 - 0.75, p = 0.04). LDL III concentration fell from 178.8 mg/dl (61.6 - 231.0) to 96.1 mg/dl (49.3 - 204.5), p = 0.05. In patients treatment altered the LDL profile so that LDLIII which was the major subfraction present at baseline was reduced from 49.9% to 29.8% (p = 0.01). Remnant lipoproteins (RLP) also fell with a mean reduction of 3.5 mg/dl in RLP-Cholesterol (95%CI 0.1 - 6.9, p = 0.05) and 12.4 mg/dl in RLP-triglyceride (95%CI 2.6 - 22.2, p = 0.03). There was however a 0.6 mmol/l rise in LDL-C (p = 0.06) in the patients. Treatment did not alter HDL-C.
  
  
  CONCLUSIONS
  In patients with nephrotic range proteinuria, omega-3 fatty acids reduced triglyceride rich lipoproteins, LDL III and remnant lipoproteins. A tendency to an increase in LDL-C was observed but this was offset by an alteration in the distribution of the LDL profile towards lighter, larger LDL particles. We propose that treatment with omega-3 fatty acids in conjunction with a statin may be the ideal therapy in these patients.
authors.affiliation: Institute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow Royal Infirmary, Glasgow, UK. samira.bell@nhs.net
authors.forename: Samira
authors.initials: S
authors.lastname: Bell
authors.forename: Josephine
authors.initials: J
authors.lastname: Cooney
authors.forename: Christopher J
authors.initials: CJ
authors.lastname: Packard
authors.forename: Muriel J
authors.initials: MJ
authors.lastname: Caslake
authors.forename: Christopher J
authors.initials: CJ
authors.lastname: Deighan
mesh_terms: D000368:Aged; D050197:Atherosclerosis / Q000097:blood / Q000150:complications / Q000188:drug therapy*; D015415:Biomarkers / Q000097:blood; D019587:Dietary Supplements; D004281:Docosahexaenoic Acids / Q000627:therapeutic use*; D004338:Drug Combinations; D015118:Eicosapentaenoic Acid / Q000627:therapeutic use*; D005260:Female; D006801:Humans; D000960:Hypolipidemic Agents / Q000627:therapeutic use*; D008074:Lipoproteins / Q000097:blood*; D008297:Male; D008875:Middle Aged; D009401:Nephrosis / Q000097:blood / Q000150:complications / Q000188:drug therapy*; D010641:Phenotype; D011507:Proteinuria / Q000097:blood / Q000150:complications / Q000188:drug therapy*; D012606:Scotland; D013997:Time Factors; D016896:Treatment Outcome
chemical_list: D015415:Biomarkers; D004338:Drug Combinations; D000960:Hypolipidemic Agents; D008074:Lipoproteins; D004281:Docosahexaenoic Acids; D015118:Eicosapentaenoic Acid; C405603:Omacor