title: Association between biomarkers of inflammation and left ventricular hypertrophy in moderate chronic kidney disease.
abstract: OBJECTIVE
  Left ventricular hypertrophy (LVH) is a predictor for cardiovascular mortality, and it is considered to be a surrogate marker of preclinical cardiovascular disease. This study aimed at evaluating whether fetuin-A plasma levels are decreased in patients with moderate chronic kidney disease (CKD) and their linkage to plasma concentrations of hs-C-reactive protein (CRP), cardiotrophyn-1 (CT-1), tumor necrosis factor-ac (TNF-alpha), propeptide of collagen Type I (PIP) and to LVH.
  
  
  METHODS
  We enrolled 64 moderate CKD and 55 essential hypertensives (EH) with normal renal function as controls. All the patients underwent an echocardiographic examination; plasma samples were obtained to measure routine clinical parameters and the molecules listed above (measured by ELISA).
  
  
  RESULTS
  Among CKD there were 30/64 patients with LVH, and in EH group 14/55 subjects had LVH. Fetuin A was reduced in CKD when compared with EH (p < 0.0001). The comparison between CKD having LVH with those without LVH showed significant differences in plasma levels of fetuin-A (p < 0.002), TNF-alpha (p < 0.01) and hs-CRP (p < 0.001), CT-1 and PIP (p < 0.002). CKD with LVH had lower values of fetuin-A (p < 0.001), and higher values of hs-CRP (p < 0.001) TNF-alpha (p < 0.001), CT-1 (p < 0.001) and PIP (p < 0.001) than EH with LVH. The multivariate analysis of correlation demonstrated that in CKD patients hs-CRP (beta 0.42, p < 0.00006), and systolic blood pressure (beta 0.29, p < 0.02) were independent predictors of LV mass index. The relationship between LV mass index and fetuin-A did not reach statistical significance.
  
  
  CONCLUSIONS
  For the first time in moderate CKD patients, we demonstrate that fetuin-A is decreased and relates to LVH depending on C-reactive protein.
authors.affiliation: Dipartimento di Medicina Interna, Malattie Cardiovascolari e NefroUrologiche, Divisione di Medicina Interna, Nefrologia ed Ipertensione ed Unità Operativa semplice di Malattie Renali ed Ipertensione, Università di Palermo, Italy. sancott@tin.it
authors.forename: S
authors.initials: S
authors.lastname: Cottone
authors.forename: E
authors.initials: E
authors.lastname: Nardi
authors.forename: G
authors.initials: G
authors.lastname: Mulè
authors.forename: A
authors.initials: A
authors.lastname: Vadalà
authors.forename: M C
authors.initials: MC
authors.lastname: Lorito
authors.forename: R
authors.initials: R
authors.lastname: Riccobene
authors.forename: A
authors.initials: A
authors.lastname: Palermo
authors.forename: R
authors.initials: R
authors.lastname: Arsena
authors.forename: M
authors.initials: M
authors.lastname: Guarneri
authors.forename: G
authors.initials: G
authors.lastname: Cerasola
mesh_terms: D000328:Adult; D000704:Analysis of Variance; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000378:metabolism; D016022:Case-Control Studies; D016207:Cytokines / Q000097:blood; D004452:Echocardiography; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000097:blood* / Q000000981:diagnostic imaging; D007249:Inflammation / Q000097:blood; D007676:Kidney Failure, Chronic / Q000097:blood*; D008297:Male; D008875:Middle Aged; D010748:Phosphopeptides / Q000097:blood; D011347:Procollagen / Q000097:blood; D012044:Regression Analysis; D014409:Tumor Necrosis Factor-alpha / Q000097:blood; D000509:alpha-Fetoproteins / Q000378:metabolism
chemical_list: D015415:Biomarkers; D016207:Cytokines; C062121:N-propeptide type I collagen; D010748:Phosphopeptides; D011347:Procollagen; D014409:Tumor Necrosis Factor-alpha; D000509:alpha-Fetoproteins; D002097:C-Reactive Protein; C092073:cardiotrophin 1