title: Relationship between serum sclerostin, bone metabolism markers, and bone mineral density in maintenance hemodialysis patients.
abstract: BACKGROUND
  Sclerostin, which is secreted exclusively by osteocytes, is a negative regulator of bone formation. The role of sclerostin in chronic kidney disease-mineral and bone disorder is not well known. In the present study, we examined the relationship between serum sclerostin levels, bone turnover markers, and bone mineral density (BMD) of the radius in maintenance hemodialysis patients.
  
  
  METHODS
  This was a cross-sectional study that analyzed sclerostin, bone alkaline phosphatase (a bone formation marker), and tartrate-resistant acid phosphatase 5b (a bone resorption marker) in stored serum samples from 181 hemodialysis patients (age, 68 ± 11 y; 105 males and 76 females; hemodialysis duration, 6.9 ± 5.9 y). The BMD in the distal one-third of the radius and in the ultradistal radius, which are enriched with cortical and cancellous bone, respectively, was examined by dual-energy x-ray absorptiometry.
  
  
  RESULTS
  Serum sclerostin was 125 ± 53 pmol/L (mean ± SD). Serum sclerostin correlated significantly and negatively with serum bone alkaline phosphatase and tartrate-resistant acid phosphatase 5b (r = -0.265, P < .001; r = -0.218, P < .01, respectively). The BMD in the distal one-third of the radius and in the ultradistal radius both correlated significantly and positively with serum sclerostin levels (r = 0.454, P < .0001; r = 0.329, P < .0001, respectively). In multiple regression analysis, serum sclerostin was associated significantly and independently with BMD of both parts of the radius (β = 0.200, P < .001; β = 0.218, P < .05), after adjustment for age, hemodialysis duration, and bone metabolism markers.
  
  
  CONCLUSIONS
  Serum sclerostin was associated significantly, independently, and positively with BMD of both cortical and cancellous bone. Sclerostin is considered to be one of the factors associated with chronic kidney disease-mineral and bone disorder in hemodialysis patients.
authors.affiliation: Department of Nephrology, Department of Metabolism, Endocrinology, and Molecular Medicine, Osaka City University Graduate School of Medicine, Kidney Center, Shirasagi Hospital, Osaka 545-8585, Japan.
authors.forename: Eiji
authors.initials: E
authors.lastname: Ishimura
authors.forename: Senji
authors.initials: S
authors.lastname: Okuno
authors.forename: Mitsuru
authors.initials: M
authors.lastname: Ichii
authors.forename: Kyoko
authors.initials: K
authors.lastname: Norimine
authors.forename: Tomoyuki
authors.initials: T
authors.lastname: Yamakawa
authors.forename: Shigeichi
authors.initials: S
authors.lastname: Shoji
authors.forename: Yoshiki
authors.initials: Y
authors.lastname: Nishizawa
authors.forename: Masaaki
authors.initials: M
authors.lastname: Inaba
mesh_terms: D000135:Acid Phosphatase / Q000097:blood; D048868:Adaptor Proteins, Signal Transducing; D000368:Aged; D000369:Aged, 80 and over; D000469:Alkaline Phosphatase / Q000097:blood; D015415:Biomarkers / Q000097:blood; D015519:Bone Density / Q000502:physiology*; D019485:Bone Morphogenetic Proteins / Q000097:blood*; D001862:Bone Resorption / Q000097:blood*; D001842:Bone and Bones / Q000378:metabolism*; D003430:Cross-Sectional Studies; D005260:Female; D005819:Genetic Markers; D006801:Humans; D007527:Isoenzymes / Q000097:blood; D007676:Kidney Failure, Chronic / Q000097:blood / Q000628:therapy*; D008297:Male; D008875:Middle Aged; D006435:Renal Dialysis; D000071681:Tartrate-Resistant Acid Phosphatase
chemical_list: D048868:Adaptor Proteins, Signal Transducing; D015415:Biomarkers; D019485:Bone Morphogenetic Proteins; D005819:Genetic Markers; D007527:Isoenzymes; C422903:SOST protein, human; D000469:Alkaline Phosphatase; D000135:Acid Phosphatase; D000071681:Tartrate-Resistant Acid Phosphatase