title: Endothelial dysfunction, inflammation and atherosclerosis in chronic kidney disease--a cross-sectional study of predialysis, dialysis and kidney-transplantation patients.
abstract: BACKGROUND
  Cardiovascular morbidity and mortality are high in chronic kidney disease (CKD) patients compared to the general population. Systemic inflammation may contribute to endothelial dysfunction and accelerated atherosclerosis in CKD patients. We assessed the relationship among, endothelial dysfunction, early atherosclerosis and inflammation in predialysis, dialysis and post kidney-transplantation CKD patients.
  
  
  RESULTS
  We studied 76 consecutive CKD patients; 38 predialysis, 18 haemodialysis and 22 kidney-transplant patients. A group of 65 age and gender matched controls were also studied. In both patients and controls, high-sensitivity C-reactive protein (CRP) levels, systemic endothelial function (brachial artery flow mediated dilation, FMD,%) and carotid artery intima-media thickness (IMT, mm) were measured. CKD patients had increased CRP levels (3.7 [1.0-6.0]mg/L vs 1.0 [0.5-2.1]mg/L; p<0.001), reduced FMD (2.2 [1.0-4.0] vs 5.6 [4.4-7.1]; p<0.001) and increased IMT (0.82±0.21 vs 0.67±0.16; p<0.001) values compared to controls. In CKD patients, a significant negative correlation was found between CRP levels and FMD responses (r=-0.51; p<0.001) while a significant positive correlation was found between CRP and IMT values (r=0.50; p<0.001). Increased CRP levels were an independent predictor of both abnormal FMD and IMT after adjusting for age, systolic and diastolic BP and total cholesterol. Compared with predialysis and kidney-transplant patients, haemodialysis subjects had significantly lower FMD and higher CRP and IMT values.
  
  
  CONCLUSIONS
  CKD patients taken together have a higher inflammatory status compared to controls. Abnormal FMD responses and IMT values are more commonly found in dialysis patients. Our findings suggest that endothelial dysfunction and atherosclerotic changes correlate with inflammation.
authors.affiliation: Division of Cardiac and Vascular Sciences, St Georges Hospital and St Georges, University of London, UK.
authors.forename: Alejandro
authors.initials: A
authors.lastname: Recio-Mayoral
authors.forename: Debasish
authors.initials: D
authors.lastname: Banerjee
authors.forename: Chris
authors.initials: C
authors.lastname: Streather
authors.forename: Juan Carlos
authors.initials: JC
authors.lastname: Kaski
mesh_terms: D000368:Aged; D050197:Atherosclerosis / Q000097:blood* / Q000473:pathology*; D002097:C-Reactive Protein / Q000378:metabolism; D002339:Carotid Arteries / Q000473:pathology; D016022:Case-Control Studies; D003430:Cross-Sectional Studies; D042783:Endothelial Cells / Q000166:cytology*; D005260:Female; D005919:Glomerular Filtration Rate; D006801:Humans; D007249:Inflammation / Q000097:blood* / Q000473:pathology*; D007676:Kidney Failure, Chronic / Q000097:blood* / Q000473:pathology* / Q000628:therapy; D016030:Kidney Transplantation; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies
chemical_list: D002097:C-Reactive Protein