title: ACE-I/ARB treatment in type 1 diabetes patients with albuminuria is associated with lower odds of progression of coronary artery calcification.
abstract: OBJECTIVE
  The objective of this study was to determine whether baseline albuminuria predicts coronary artery calcification (CAC) progression in subjects with type 1 diabetes and whether angiotensin-converting enzyme inhibitor (ACE-I) or angiotensin II type I receptor blocker (ARB) treatment is associated with lower odds of CAC progression.
  
  
  METHODS
  In 2000-2002, the Coronary Artery Calcification in Type 1 Diabetes study enrolled 652 subjects with type 1 diabetes who were between 19 and 56 years old and had no known history of coronary artery disease (CAD). In this analysis, CAC progression over 2.5+/-0.4 years was evaluated in 478 subjects (age=37+/-9 years; male=45%; diabetes duration=23+/-9 years) at a follow-up visit. Albuminuria was defined by American Diabetes Association criteria, and microalbuminuria and macroalbuminuria were combined for the analysis. Logistic regression was used to evaluate the relationship between baseline categorical presence of albuminuria and CAC progression.
  
  
  RESULTS
  At baseline, of the 478 subjects, 157 (33%) were on ACE-I/ARB treatment and 83 (17%) had albuminuria, with 114 (24%) having CAC progression at follow-up. In backward logistic regression, presence of albuminuria at baseline predicted progression of CAC among subjects not treated with ACE-I/ARB [odds ratio=4.06; 95% confidence interval (CI)=1.45-11.35; P=.008]. Among the subjects with albuminuria, the odds of progression was 62% lower (95% CI=88% decrease to 23% increase; P=.106) in those treated with ACE-I/ARB.
  
  
  CONCLUSIONS
  Albuminuria is a significant independent risk factor for CAC progression in young type 1 diabetes patients asymptomatic for CAD, and ACE-I/ARB treatment is associated with substantially lower odds of CAC progression.
authors.affiliation: Barbara Davis Center for Childhood Diabetes, University of Colorado Health Sciences Center, Aurora, CO, USA. david.maahs@uchsc.edu
authors.forename: David M
authors.initials: DM
authors.lastname: Maahs
authors.forename: Janet K
authors.initials: JK
authors.lastname: Snell-Bergeon
authors.forename: Gregory L
authors.initials: GL
authors.lastname: Kinney
authors.forename: R Paul
authors.initials: RP
authors.lastname: Wadwa
authors.forename: Satish
authors.initials: S
authors.lastname: Garg
authors.forename: Lorraine G
authors.initials: LG
authors.lastname: Ogden
authors.forename: Marian
authors.initials: M
authors.lastname: Rewers
mesh_terms: D000328:Adult; D000419:Albuminuria / Q000188:drug therapy*; D057912:Angiotensin II Type 2 Receptor Blockers; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use*; D000959:Antihypertensive Agents / Q000627:therapeutic use; D002114:Calcinosis / Q000503:physiopathology* / Q000517:prevention & control; D003327:Coronary Disease / Q000503:physiopathology* / Q000517:prevention & control; D003922:Diabetes Mellitus, Type 1 / Q000150:complications / Q000188:drug therapy*; D003925:Diabetic Angiopathies / Q000503:physiopathology* / Q000517:prevention & control; D018450:Disease Progression; D005260:Female; D006801:Humans; D006973:Hypertension / Q000188:drug therapy; D008297:Male; D008875:Middle Aged; D012044:Regression Analysis