title: Insulin resistance, inflammation, and vascular disease in nondiabetic predialysis chronic kidney disease patients.
abstract: BACKGROUND
  Chronic kidney disease (CKD) is associated with high cardiovascular morbidity and mortality, which is not fully explained by traditional risk factors; hence, the interest in nontraditional risk factors such as inflammation and insulin resistance (IR). Though IR is shown in nondiabetic CKD, its association with vascular disease and inflammation in this population is unknown, and is what this study aims to investigate.
  
  
  OBJECTIVE
  IR and inflammation are related to vascular disease in nondiabetic predialysis CKD patients.
  
  
  METHODS
  We studied carotid-artery intima-media thickness (IMT) and endothelial function (brachial artery flow mediated dilation [FMD]) in 35 nondiabetic predialysis patients with stage 3-5 CKD and 35 age- and gender-matched controls. Insulin resistance was measured using the homeostasis model assessment for insulin resistance score (HOMA-IR), inflammation by high-sensitivity CRP (hsCRP), and their relationship with FMD and IMT.
  
  
  RESULTS
  Patients with CKD showed reduced FMD (3.34 ± 2.14% vs. 5.27 ± 1.78%, P<0.001) and increased IMT (0.78 ± 0.22 mm vs. 0.64 ± 0.16 mm, P = 0.003) compared with controls. The CKD patients had a higher HOMA-IR (2.20 ± 1.08 vs. 1.13 ± 0.64, P<0.001) and hsCRP (3.25 ± 5.47 mg/L vs. 1.10 ± 1.85 mg/L [median ± interquartile range], P = 0.02). In the study population, HOMA-IR was directly related to hsCRP. After adjusting for traditional risk factors, high HOMA-IR and hsCRP were significantly related to decreased FMD (adjusted β = -0.44, 95% confidence interval [CI]: -1.55 to -0.08, P = 0.003 and adjusted β = -0.51, 95% CI: -0.51 to -0.15, P = 0.001) and increased IMT (adjusted β = 0.62, 95% CI: 0.54-1.90, P = 0.001 and adjusted β = 0.43, 95% CI: 0.08-0.57, P = 0.011), respectively.
  
  
  CONCLUSIONS
  Subjects with systemic inflammation were more insulin-resistant, and in nondiabetic predialysis CKD, IR and systemic inflammation were independently associated with endothelial dysfunction and atherosclerosis.
authors.affiliation: Renal Medicine and Transplantation Unit, St. George's Hospital NHS Trust, UK. debasish.banerjee@stgeorges.nhs.uk
authors.forename: Debasish
authors.initials: D
authors.lastname: Banerjee
authors.forename: Alejandro
authors.initials: A
authors.lastname: Recio-Mayoral
authors.forename: Nihil
authors.initials: N
authors.lastname: Chitalia
authors.forename: Juan-Carlos
authors.initials: JC
authors.lastname: Kaski
mesh_terms: D000328:Adult; D000368:Aged; D050197:Atherosclerosis / Q000453:epidemiology / Q000503:physiopathology; D015415:Biomarkers / Q000097:blood; D001786:Blood Glucose / Q000032:analysis; D002097:C-Reactive Protein / Q000032:analysis; D002339:Carotid Arteries / Q000000981:diagnostic imaging; D002340:Carotid Artery Diseases / Q000000981:diagnostic imaging / Q000453:epidemiology / Q000503:physiopathology; D016022:Case-Control Studies; D016009:Chi-Square Distribution; D002908:Chronic Disease; D004730:Endothelium, Vascular / Q000503:physiopathology; D005260:Female; D006801:Humans; D007249:Inflammation / Q000097:blood / Q000453:epidemiology* / Q000503:physiopathology; D018836:Inflammation Mediators / Q000097:blood; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance; D007674:Kidney Diseases / Q000097:blood / Q000453:epidemiology* / Q000503:physiopathology; D016014:Linear Models; D008131:London / Q000453:epidemiology; D008297:Male; D008875:Middle Aged; D018570:Risk Assessment; D012307:Risk Factors; D017539:Tunica Intima / Q000000981:diagnostic imaging; D017540:Tunica Media / Q000000981:diagnostic imaging; D014463:Ultrasonography; D014652:Vascular Diseases / Q000097:blood / Q000000981:diagnostic imaging / Q000453:epidemiology* / Q000503:physiopathology; D014664:Vasodilation
chemical_list: D015415:Biomarkers; D001786:Blood Glucose; D018836:Inflammation Mediators; D007328:Insulin; D002097:C-Reactive Protein