title: Novel biomarkers assessing renal function in heart failure: relation to inflammatory status and cardiac remodelling.
abstract: BACKGROUND
  Patients with heart failure (HF) have a significant decline of renal function. We investigate the association between novel biomarkers of renal dysfunction and indices of inflammatory status and cardiac remodeling in patients with HF.
  
  
  METHODS
  We enrolled 79 consecutive patients with HF and 79 healthy subjects, adjusted for age and sex. Serum levels of neutrophil gelatinase-associated lipocalin (NGAL), cystatin-C, b-type natriuretic peptide (BNP), tumor necrosis factor alpha (TNFα) and matrix metalloproteinase-9 (MMP-9) were measured by ELISA. Creatinine clearance was estimated using Cockcroft-Gault formula (eCcl). Left ventricular ejection fraction was determined by echocardiography.
  
  
  RESULTS
  Patients with HF, compared to healthy subjects, had significantly higher NGAL (p=0.007) and cystatin-C levels (p=0.005). In HF patients, NGAL levels were positively correlated with Creatinine levels (r=0.40, p<0.001), TNFa levels (r=0.43, p<0.001), BNP levels (r=0.36, p=0.003), MMP-9 levels (r=0.37, p=0.02) and inversely correlated with left ventricle ejection fraction (r=-0.23, p=0.045). Interestingly, the association between NGAL and MMP-9 levels was independent from confounders such as age, gender, left ventricle ejection fraction, body mass index, TNFα levels, and BNP levels. Moreover, in HF patients, cystatin-C levels were inversely correlated with eCcl (r=-0.21, p=0.04). Cystatin-C levels were not correlated with TNFa, BNP, MMP-9 levels and with left ventricle ejection fraction (p=NS for all).
  
  
  CONCLUSIONS
  NGAL is associated with left ventricle ejection fraction, and biomarkers of inflammation and cardiac remodeling in patients with HF. These findings highlight a possible common pathogenetic mechanism of renal dysfunction, inflammatory process and cardiac dysfunction in HF.
authors.forename: Gerasimos
authors.initials: G
authors.lastname: Siasos
authors.forename: Dimitris
authors.initials: D
authors.lastname: Tousoulis
authors.forename: Stavroula
authors.initials: S
authors.lastname: Michalea
authors.forename: Evangelos
authors.initials: E
authors.lastname: Oikonomou
authors.forename: Manolis
authors.initials: M
authors.lastname: Vavuranakis
authors.forename: Dimitris
authors.initials: D
authors.lastname: Athanasiou
authors.forename: Panagiotis
authors.initials: P
authors.lastname: Tourikis
authors.forename: Nikolaos
authors.initials: N
authors.lastname: Gouliopoulos
authors.forename: Antigoni
authors.initials: A
authors.lastname: Miliou
authors.forename: Konstantinos
authors.initials: K
authors.lastname: Mourouzis
authors.forename: Maria
authors.initials: M
authors.lastname: Limperi
authors.forename: Savvas
authors.initials: S
authors.lastname: Mazaris
authors.forename: Athanasios G
authors.initials: AG
authors.lastname: Papavassiliou
authors.affiliation: University of Athens Medical School, Vas. Sophias 114, Athens, Greece. gsiasos@med.uoa.gr.
authors.forename: Christodoulos
authors.initials: C
authors.lastname: Stefanadis
mesh_terms: D005260:Female; D006333:Heart Failure / Q000097:blood*; D006801:Humans; D007249:Inflammation; D007668:Kidney / Q000473:pathology*; D008297:Male; D011379:Prognosis