title: A1C and survival in maintenance hemodialysis patients.
abstract: OBJECTIVE
  The optimal target for glycemic control has not been established in diabetic dialysis patients.
  
  
  METHODS
  To address this question, the national database of a large dialysis organization (DaVita) was analyzed via time-dependent survival models with repeated measures.
  
  
  RESULTS
  Of 82,933 patients undergoing maintenance hemodialysis (MHD) in DaVita outpatient clinics over 3 years (July 2001 through June 2004), 23,618 diabetic MHD patients had A1C measurements at least once. Unadjusted survival analyses indicated paradoxically lower death hazard ratios (HRs) with higher A1C values. However, after adjusting for potential confounders (demographics, dialysis vintage, dose, comorbidity, anemia, and surrogates of malnutrition and inflammation), higher A1C values were incrementally associated with higher death risks. Compared with A1C in the 5-6% range, the adjusted all-cause and cardiovascular death HRs for A1C > or = 10% were 1.41 (95% CI 1.25-1.60) and 1.73 (1.44-2.08), respectively (P < 0.001). The incremental increase in death risk for rising A1C values was monotonic and robust in nonanemic patients (hemoglobin > 11.0 g/dl). In subgroup analyses, the association between A1C > 6% and increased death risk was more prominent among younger patients, those who had undergone dialysis for > 2 years, and those with higher protein intake (> 1 g x kg(-1) x day(-1)), blood hemoglobin (> 11 g/dl), or serum ferritin values (> 500 ng/ml).
  
  
  CONCLUSIONS
  In diabetic MHD patients, the apparently counterintuitive association between poor glycemic control and greater survival is explained by such confounders as malnutrition and anemia. All things equal, higher A1C is associated with increased death risk. Lower A1C levels not related to malnutrition or anemia appear to be associated with improved survival in MHD patients.
authors.affiliation: Harold Simmons Center for Kidney Disease Research and Epidemiology, Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, Torrance, California 90509-2910, USA. kamkal@ucla.edu
authors.forename: Kamyar
authors.initials: K
authors.lastname: Kalantar-Zadeh
authors.forename: Joel D
authors.initials: JD
authors.lastname: Kopple
authors.forename: Deborah L
authors.initials: DL
authors.lastname: Regidor
authors.forename: Jennie
authors.initials: J
authors.lastname: Jing
authors.forename: Christian S
authors.initials: CS
authors.lastname: Shinaberger
authors.forename: Jason
authors.initials: J
authors.lastname: Aronovitz
authors.forename: Charles J
authors.initials: CJ
authors.lastname: McAllister
authors.forename: David
authors.initials: D
authors.lastname: Whellan
authors.forename: Kumar
authors.initials: K
authors.lastname: Sharma
mesh_terms: D000328:Adult; D000368:Aged; D015415:Biomarkers / Q000097:blood*; D002318:Cardiovascular Diseases / Q000401:mortality; D015331:Cohort Studies; D015897:Comorbidity; D003928:Diabetic Nephropathies / Q000401:mortality / Q000628:therapy*; D005260:Female; D006442:Glycated Hemoglobin / Q000032:analysis*; D006801:Humans; D007676:Kidney Failure, Chronic / Q000401:mortality / Q000628:therapy; D008297:Male; D008875:Middle Aged; D006435:Renal Dialysis / Q000401:mortality*; D012307:Risk Factors; D016019:Survival Analysis; D013997:Time Factors
chemical_list: D015415:Biomarkers; D006442:Glycated Hemoglobin