title: Analysis of metabolic parameters as predictors of risk in the RENAAL study.
abstract: OBJECTIVE
  Metabolic factors such as glycemic control, hyperlipidemia, and hyperkalemia are important considerations in the treatment of patients with type 2 diabetes and nephropathy. In the RENAAL (Reduction of End Points in Type 2 Diabetes With the Angiotensin II Antagonist Losartan) study, losartan reduced renal outcomes in the patient population. This post hoc analysis of the RENAAL study reports the effects of losartan on selected metabolic parameters and assesses the relationship between baseline values of metabolic parameters and the primary composite end point or end-stage renal disease (ESRD).
  
  
  METHODS
  Glycemic control (HbA(1c)) and serum lipid, uric acid, and potassium levels were compared between the losartan and placebo groups over time, and baseline levels were correlated with the risk of reaching the primary composite end point (doubling of serum creatinine, ESRD, or death) or ESRD alone.
  
  
  RESULTS
  Losartan did not adversely affect glycemic control or serum lipid levels. Losartan-treated patients had lower total (227.4 vs. 195.4 mg/dl) and LDL (142.2 vs. 111.7 mg/dl) cholesterol. Losartan was associated with a mean increase of up to 0.3 mEq/l in serum potassium levels; however, the rate of hyperkalemia-related discontinuation was similar between the placebo and losartan groups. Univariate analysis revealed that baseline total and LDL cholesterol and triglyceride levels were associated with increased risk of developing the primary composite end point. Similarly, total and LDL cholesterol were also associated with increased risk of developing ESRD.
  
  
  CONCLUSIONS
  Overall, losartan was well tolerated by patients with type 2 diabetes and nephropathy and was associated with a favorable effect on the metabolic profile of this population.
authors.affiliation: Division of Nephrology, Department of Medicine, Columbia University College of Physicians and Surgeons, New York, New York 10032, USA.
authors.forename: Gerald B
authors.initials: GB
authors.lastname: Appel
authors.forename: Jai
authors.initials: J
authors.lastname: Radhakrishnan
authors.forename: Morrell M
authors.initials: MM
authors.lastname: Avram
authors.forename: Ralph A
authors.initials: RA
authors.lastname: DeFronzo
authors.forename: Fernando
authors.initials: F
authors.lastname: Escobar-Jimenez
authors.forename: M M
authors.initials: MM
authors.lastname: Campos
authors.forename: Ellen
authors.initials: E
authors.lastname: Burgess
authors.forename: Darcy A
authors.initials: DA
authors.lastname: Hille
authors.forename: Tania Z
authors.initials: TZ
authors.lastname: Dickson
authors.forename: Shahnaz
authors.initials: S
authors.lastname: Shahinfar
authors.forename: Barry M
authors.initials: BM
authors.lastname: Brenner
mesh_terms: D002784:Cholesterol / Q000097:blood*; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D003404:Creatinine / Q000097:blood; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000453:epidemiology*; D003928:Diabetic Nephropathies / Q000097:blood / Q000453:epidemiology*; D006442:Glycated Hemoglobin / Q000032:analysis; D006801:Humans; D007676:Kidney Failure, Chronic / Q000453:epidemiology*; D012307:Risk Factors; D014280:Triglycerides / Q000097:blood*
chemical_list: D002784:Cholesterol; D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D003404:Creatinine; D006442:Glycated Hemoglobin; D014280:Triglycerides