title: Low serum fetuin-A concentration predicts poor outcome only in the presence of inflammation in prevalent haemodialysis patients.
abstract: BACKGROUND
  Fetuin-A, a negative acute phase protein that inhibits vascular calcification, has a controversial association with mortality in chronic kidney disease (CKD) patients. Chronic inflammation, which is common in CKD, may promote vascular calcification.
  
  
  METHODS
  We investigated the impact of inflammation on the relationship between serum fetuin-A and mortality (42 months) in 222 prevalent haemodialysis (HD) patients.
  
  
  RESULTS
  Serum fetuin correlated negatively with comorbidity score (assessed by Davies score) and circulating inflammatory markers. Patients with low fetuin-A levels (< median) had higher mortality (Hazard ratio 'HR' 2.2; CI 1.4-3.5, P < 0.001), but this association was lost after adjustment for age, gender, comorbidities score, dialysis vintage and inflammation (CRP > median). In inflamed patients with low fetuin a significantly independent association with mortality (HR 2.3; CI 1.2-4.5, P = 0.01) was observed compared to non-inflamed patients with high fetuin-A, after adjusting for the same variables. Non-inflamed patients with low fetuin-A and inflamed patients with high fetuin-A did not have increased mortality compared to non-inflamed patients with high fetuin-A.
  
  
  CONCLUSIONS
  The results show that low levels of serum fetuin-A are associated with increased mortality in HD patients only in the presence of inflammation. This suggests that coexistence of a low serum fetuin-A level and low-grade inflammation exerts an additive effect on the risk of death in HD patients.
authors.affiliation: Division of Renal Medicine, Department of Clinical Science, Intervention and Technology, Karolinska University Hospital Huddinge, Stockholm, Sweden.
authors.forename: G
authors.initials: G
authors.lastname: Metry
authors.forename: P
authors.initials: P
authors.lastname: Stenvinkel
authors.forename: A R
authors.initials: AR
authors.lastname: Qureshi
authors.forename: J J
authors.initials: JJ
authors.lastname: Carrero
authors.forename: M I
authors.initials: MI
authors.lastname: Yilmaz
authors.forename: P
authors.initials: P
authors.lastname: Bárány
authors.forename: S
authors.initials: S
authors.lastname: Snaedal
authors.forename: O
authors.initials: O
authors.lastname: Heimbürger
authors.forename: B
authors.initials: B
authors.lastname: Lindholm
authors.forename: M E
authors.initials: ME
authors.lastname: Suliman
mesh_terms: D000368:Aged; D015415:Biomarkers / Q000097:blood; D001798:Blood Proteins / Q000032:analysis*; D003430:Cross-Sectional Studies; D005260:Female; D006801:Humans; D007249:Inflammation / Q000097:blood* / Q000401:mortality; D007676:Kidney Failure, Chronic / Q000097:blood* / Q000401:mortality / Q000628:therapy; D008297:Male; D008875:Middle Aged; D006435:Renal Dialysis / Q000401:mortality; D060749:alpha-2-HS-Glycoprotein
chemical_list: C556354:AHSG protein, human; D015415:Biomarkers; D001798:Blood Proteins; D060749:alpha-2-HS-Glycoprotein