title: Serum fetuin-A in nondialyzed patients with diabetic nephropathy: relationship with coronary artery calcification.
abstract: BACKGROUND
  Fetuin-A is the most potent circulating inhibitor of calcium phosphorus precipitation and, possibly, an important mediator of insulin resistance.
  
  
  METHODS
  In order to determine the role of fetuin-A in the high coronary artery calcification (CAC) burden seen in nondialyzed individuals with diabetic nephropathy (DN), post-hoc analyses of data collected from a cross-sectional study of 88 patients with type 2 diabetes mellitus was done [age, 40-65 years; normoalbuminuria, N= 30 (Latinos); DN, N= 58 (Latinos and African Americans)].
  
  
  RESULTS
  The serum levels of fetuin-A were significantly higher among Latinos with DN when compared to either African Americans with DN or Latino diabetics with normoalbuminuria. Upon adjusting the data for race/ethnicity, there was a strong, direct relationship between serum fetuin-A levels and the CAC score (r= 0.22, P= 0.038) in the study cohort; however, a strong interaction between the nephropathy status and relationship of serum fetuin-A levels with CAC score was present (DN: r= 0.36, P= 0.006; diabetic controls, r= 0.0, P= 0.98). Among individuals with DN, the significance of the association persisted even after controlling the data for other predictors of CAC (partial r= 0.33, P= 0.018). Furthermore, there was a significant direct relationship between serum fetuin-A and serum triglycerides (partial r= 0.27, P= 0.01) and albumin (partial r= 0.30, P= 0.005), and an inverse relationship with glomerular filtration rate (r=-0.24, P= 0.03).
  
  
  CONCLUSIONS
  This first study in early stages of diabetic chronic kidney disease shows that the role of serum fetuin-A may be far more complex than previously described. During predialysis stage of DN, there is a direct relationship between serum fetuin-A levels and CAC score. The reasons for this association in the presence of nephropathy are unclear, but may be secondary to proatherogenic insulin resistance.
authors.affiliation: Division of Nephrology and Hypertension, Harbor-UCLA Medical Center, Torrance, California 90502, USA. rmehrotra@labiomed.org
authors.forename: Rajnish
authors.initials: R
authors.lastname: Mehrotra
authors.forename: Ralf
authors.initials: R
authors.lastname: Westenfeld
authors.forename: Peter
authors.initials: P
authors.lastname: Christenson
authors.forename: Matthew
authors.initials: M
authors.lastname: Budoff
authors.forename: Eli
authors.initials: E
authors.lastname: Ipp
authors.forename: Junichiro
authors.initials: J
authors.lastname: Takasu
authors.forename: Ajay
authors.initials: A
authors.lastname: Gupta
authors.forename: Keith
authors.initials: K
authors.lastname: Norris
authors.forename: Markus
authors.initials: M
authors.lastname: Ketteler
authors.forename: Sharon
authors.initials: S
authors.lastname: Adler
mesh_terms: D000328:Adult; D000368:Aged; D001798:Blood Proteins / Q000032:analysis*; D002114:Calcinosis / Q000097:blood*; D002908:Chronic Disease; D003327:Coronary Disease / Q000097:blood*; D003430:Cross-Sectional Studies; D003928:Diabetic Nephropathies / Q000097:blood*; D005260:Female; D005919:Glomerular Filtration Rate; D006801:Humans; D008297:Male; D008875:Middle Aged; D060749:alpha-2-HS-Glycoprotein
chemical_list: C556354:AHSG protein, human; D001798:Blood Proteins; D060749:alpha-2-HS-Glycoprotein