title: Serum lipids and the progression of nephropathy in type 1 diabetes.
abstract: OBJECTIVE
  Dyslipidemia contributes to the progression of microvascular disease in diabetes. However, different lipid variables may be important at different stages of nephropathy. This study examines the pattern of dyslipidemia associated with the progression of nephropathy in patients with type 1 diabetes.
  
  
  METHODS
  A total of 152 patients with type 1 diabetes were recruited in order to represent various phases of nephropathy. Patients were followed for 8-9 years, during which time they received standard care. Renal progression was defined a priori as a doubling in albumin excretion (in patients with normo- or microalbuminuria) or a decline in creatinine clearance (in those with macroalbuminuria). A panel of lipid variables was determined and correlated with indexes of progression.
  
  
  RESULTS
  In patients with normoalbuminuria (n = 66), progression was associated with male sex (P < 0.05), borderline albuminuria (P = 0.02), and LDL-free cholesterol (P = 0.02). In patients with microalbuminuria (n = 51), progression was independently associated with triglyceride content of VLDL and intermediate-density lipoprotein (both P < 0.05). In patients with macroalbuminuria (n = 36), a significant decline in the renal function (>3 ml x min(-1) x year(-1)) was independently associated with poor glycemic control, hypertension, and LDL size (P < 0.05). When all patients with progressive nephropathy were analyzed together, only LDL cholesterol was predictive on multivariate analysis (P < 0.05), which masked the importance of triglyceride enrichment in microalbuminuria.
  
  
  CONCLUSIONS
  Lipid variables are associated with progression of diabetic kidney disease, but the relationship is not the same at all stages. This finding has implications for the design of renoprotective strategies and the interpretation of clinical trials in type 1 diabetes.
authors.affiliation: The Baker Heart Research Institute, Melbourne, Australia.
authors.forename: Merlin C
authors.initials: MC
authors.lastname: Thomas
authors.forename: Milla
authors.initials: M
authors.lastname: Rosengård-Bärlund
authors.forename: Vashti
authors.initials: V
authors.lastname: Mills
authors.forename: Mats
authors.initials: M
authors.lastname: Rönnback
authors.forename: Stephen
authors.initials: S
authors.lastname: Thomas
authors.forename: Carol
authors.initials: C
authors.lastname: Forsblom
authors.forename: Mark E
authors.initials: ME
authors.lastname: Cooper
authors.forename: Marja-Riitta
authors.initials: MR
authors.lastname: Taskinen
authors.forename: Giancarlo
authors.initials: G
authors.lastname: Viberti
authors.forename: Per-Henrik
authors.initials: PH
authors.lastname: Groop
mesh_terms: D000328:Adult; D000419:Albuminuria / Q000378:metabolism*; D000959:Antihypertensive Agents / Q000627:therapeutic use; D001055:Apolipoproteins B / Q000097:blood; D003404:Creatinine / Q000652:urine*; D003922:Diabetes Mellitus, Type 1 / Q000097:blood* / Q000150:complications; D003928:Diabetic Nephropathies / Q000097:blood* / Q000209:etiology; D018450:Disease Progression; D050171:Dyslipidemias / Q000150:complications* / Q000188:drug therapy; D005260:Female; D006801:Humans; D006973:Hypertension / Q000188:drug therapy; D000960:Hypolipidemic Agents / Q000627:therapeutic use; D008137:Longitudinal Studies; D008297:Male; D014280:Triglycerides / Q000097:blood
chemical_list: D000959:Antihypertensive Agents; D001055:Apolipoproteins B; D000960:Hypolipidemic Agents; D014280:Triglycerides; D003404:Creatinine