title: Prevalence, severity and predictors of HOMA-estimated insulin resistance in diabetic and nondiabetic patients with end-stage renal disease.
abstract: BACKGROUND
  Prevalence of insulin resistance (IR) is increased in type 2 diabetes and in end-stage renal disease (ESRD). IR is associated with advanced atherosclerosis and is an independent predictor for cardiovascular disease in diabetes and ESRD patients. We investigated prevalence, severity, predictors and relation to vascular diseases by the homeostasis model assessment (HOMA-IR) in diabetic and nondiabetic ESRD patients.
  
  
  METHODS
  ESRD patients with type 2 diabetes (n = 27) and nondiabetic ESRD patients (n = 35) were included in the study. IR was assessed with the HOMA-IR using fasting glucose and insulin levels. Additionally, serum levels of C-peptide, HbA1c, triglycerides, cholesterol and C-reactive protein and blood pressure were assessed.
  
  
  RESULTS
  Median HOMA-IR was significantly higher in the diabetic ESRD patients than in the nondiabetic ESRD patients (6.3 [range 0.7-61.7] vs. 2.4 [range 0.3-5.7]; p < 0.001). Systolic blood pressure and triglycerides were significantly higher in patients with higher HOMA-IR, whereas HDL cholesterol was significantly lower in those patients. Only nondiabetic patients with increased HOMA-IR had significantly higher C-peptide levels than those with lower HOMA-IR (14.9 + 5.7 vs. 9.0 + 4.3, p = 0.004). Vascular disease prevalence was significantly higher in diabetic patients with higher HOMA-IR than in those with lower HOMA-IR.
  
  
  CONCLUSIONS
  Prevalence and severity of HOMA-IR was greater in diabetic ESRD patients than in those without diabetes. In diabetic patients low HDL cholesterol was the only predictor for higher HOMA-IR, whereas in nondiabetic patients a high C-peptide level was the only predictor for higher HOMA-IR. The prevalence of vascular diseases is associated with higher HOMA-IR in ESRD patients.
authors.affiliation: Second Department of Medicine, General Hospital Linz, Linz-Austria. gerd.bodlaj@akh.linz.at
authors.forename: Gerd
authors.initials: G
authors.lastname: Bodlaj
authors.forename: Jörg
authors.initials: J
authors.lastname: Berg
authors.forename: Robert
authors.initials: R
authors.lastname: Pichler
authors.forename: Georg
authors.initials: G
authors.lastname: Biesenbach
mesh_terms: D000368:Aged; D050197:Atherosclerosis / Q000097:blood / Q000150:complications / Q000453:epidemiology; D001786:Blood Glucose / Q000032:analysis; D001794:Blood Pressure; D002096:C-Peptide / Q000097:blood; D002097:C-Reactive Protein / Q000032:analysis; D002784:Cholesterol / Q000097:blood; D003924:Diabetes Mellitus, Type 2 / Q000097:blood* / Q000453:epidemiology; D003928:Diabetic Nephropathies / Q000097:blood* / Q000150:complications / Q000453:epidemiology; D005215:Fasting / Q000097:blood; D005260:Female; D006442:Glycated Hemoglobin / Q000032:analysis; D006801:Humans; D066298:In Vitro Techniques; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance; D007676:Kidney Failure, Chronic / Q000097:blood* / Q000150:complications / Q000453:epidemiology; D008297:Male; D008875:Middle Aged; D008955:Models, Cardiovascular; D015995:Prevalence; D012720:Severity of Illness Index; D014280:Triglycerides / Q000097:blood
chemical_list: D001786:Blood Glucose; D002096:C-Peptide; D002097:C-Reactive Protein; D002784:Cholesterol; D006442:Glycated Hemoglobin; D007328:Insulin; D014280:Triglycerides; C517652:hemoglobin A1c protein, human