title: Fenofibrate reduces progression to microalbuminuria over 3 years in a placebo-controlled study in type 2 diabetes: results from the Diabetes Atherosclerosis Intervention Study (DAIS).
abstract: BACKGROUND
  Microalbuminuria is an early marker of diabetic nephropathy and an independent risk factor for cardiovascular disease. In the Diabetes Atherosclerosis Intervention Study (DAIS), treatment of people with type 2 diabetes with micronized fenofibrate for an average of 38 months reduced the progression of angiographically evaluated coronary artery disease and improved lipoprotein level abnormalities compared with placebo. The aim of this analysis is to study the influence of the treatment on changes in urinary albumin excretion.
  
  
  METHODS
  Microalbuminuria was measured on 2 to 3 occasions by using timed overnight samples at baseline and yearly thereafter in 314 DAIS participants (77 women, 237 men; average age, 56 years); all except 3 participants had either a normal albumin excretion rate (<20 microg/min; n = 214) or microalbuminuria (albumin, 20 to 200 microg/min; n = 97) before randomization. Tabulated shifts (between normal, microalbuminuria, and macroalbuminuria) from baseline to last observed values were compared between treatment groups by means of chi-square or Fisher's exact test.
  
  
  RESULTS
  Fenofibrate significantly reduced the worsening of albumin excretion (fenofibrate, 8% versus placebo, 18%; P < 0.05). This effect was caused mostly by reduced progression from normal albumin excretion to microalbuminuria: 3 of 101 participants in the fenofibrate group versus 20 of 113 participants in the placebo group (P < 0.001). Overall, changes in albumin excretion were independent of age or changes in lipid or creatinine levels, weight, or blood pressure.
  
  
  CONCLUSIONS
  Improvement in lipid profiles with fenofibrate in patients with type 2 diabetes was associated with reduced progression from normal albumin excretion to microalbuminuria.
authors.affiliation: Department of Clinical Research and Medical Affairs, Fournier Pharma, Daix, France. jc.ansquer@fr.fournierpharma.com
authors.forename: Jean-Claude
authors.initials: JC
authors.lastname: Ansquer
authors.forename: Christelle
authors.initials: C
authors.lastname: Foucher
authors.forename: Stephanie
authors.initials: S
authors.lastname: Rattier
authors.forename: Marja-Riitta
authors.initials: MR
authors.lastname: Taskinen
authors.forename: George
authors.initials: G
authors.lastname: Steiner
mesh_terms: D000419:Albuminuria / Q000453:epidemiology / Q000517:prevention & control*; D047228:Angiotensin II Type 1 Receptor Blockers / Q000627:therapeutic use; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D000959:Antihypertensive Agents / Q000627:therapeutic use; D001794:Blood Pressure; D015992:Body Mass Index; D003404:Creatinine / Q000097:blood; D003924:Diabetes Mellitus, Type 2 / Q000150:complications*; D003928:Diabetic Nephropathies / Q000453:epidemiology / Q000517:prevention & control*; D018450:Disease Progression; D004311:Double-Blind Method; D005260:Female; D011345:Fenofibrate / Q000008:administration & dosage / Q000627:therapeutic use*; D005340:Fibrinogen / Q000032:analysis; D005500:Follow-Up Studies; D006442:Glycated Hemoglobin / Q000032:analysis; D006710:Homocysteine / Q000097:blood; D006801:Humans; D006949:Hyperlipidemias / Q000150:complications / Q000188:drug therapy*; D006973:Hypertension / Q000150:complications / Q000188:drug therapy; D000960:Hypolipidemic Agents / Q000008:administration & dosage / Q000627:therapeutic use*; D015994:Incidence; D008297:Male; D008875:Middle Aged; D008954:Models, Biological; D012907:Smoking / Q000453:epidemiology; D016896:Treatment Outcome
chemical_list: D047228:Angiotensin II Type 1 Receptor Blockers; D000806:Angiotensin-Converting Enzyme Inhibitors; D000959:Antihypertensive Agents; D003404:Creatinine; D011345:Fenofibrate; D005340:Fibrinogen; D006442:Glycated Hemoglobin; D006710:Homocysteine; D000960:Hypolipidemic Agents