title: Sclerostin blood levels before and after kidney transplantation.
abstract: OBJECTIVE
  Sclerostin is secreted by osteocytes. As a circulating inhibitor of the Wnt-signaling pathway it inhibits bone formation and contributes to the development of osteoporosis. Sclerostin levels are elevated in patients with chronic kidney disease and end-stage renal disease. Since data for patients after kidney transplantation are scarce, we have prospectively measured sclerostin levels before and during the first year after renal transplantation and have examined the association of sclerostin with parameters of bone mineral metabolism and with bone mineral density.
  
  
  METHODS
  Sclerostin levels were measured by ELISA in 42 consecutive renal transplant recipients before and at defined intervals in the first year after transplantation. Bone mineral density was measured by dual energy X-ray absorptiometry.
  
  
  RESULTS
  Pre-transplant serum sclerostin levels were elevated in all patients (61.8 ± 32.3 pmol/l, normal range 20-30 pmol/l). Within 15 days after transplantation and correlating with the improvement of renal function, sclerostin levels dropped to 21.0 ± 14.7 pmol/l and subsequently increased to 23.8 ± 14.9 and 28.0 ± 16.8 pmol/l after 6 and 12 months, respectively (P<0.001). A linear mixed model indicated that pre-transplant sclerostin levels (P<0.001) and time after transplantation (P<0.001) were the most important predictors for the rise of post-transplant sclerostin levels. No correlation was found between post-transplant sclerostin levels and bone mineral density.
  
  
  CONCLUSIONS
  The rapid reduction of elevated serum sclerostin levels shortly after kidney transplantation parallels the improvement of renal function, but contrasts with the more delayed improvement of hyperparathyroidism. The normalization of both hormones could contribute to improved bone health after renal transplantation.
authors.affiliation: Division of Nephrology, University Hospital Zürich, Switzerland.
authors.forename: Marco
authors.initials: M
authors.lastname: Bonani
authors.forename: Daniel
authors.initials: D
authors.lastname: Rodriguez
authors.forename: Thomas
authors.initials: T
authors.lastname: Fehr
authors.forename: Nilufar
authors.initials: N
authors.lastname: Mohebbi
authors.forename: Jens
authors.initials: J
authors.lastname: Brockmann
authors.forename: Markus
authors.initials: M
authors.lastname: Blum
authors.forename: Nicole
authors.initials: N
authors.lastname: Graf
authors.forename: Diana
authors.initials: D
authors.lastname: Frey
authors.forename: Rudolf P
authors.initials: RP
authors.lastname: Wüthrich
mesh_terms: D015502:Absorptiometry, Photon; D048868:Adaptor Proteins, Signal Transducing; D000328:Adult; D000368:Aged; D061067:Antibodies, Monoclonal, Humanized / Q000627:therapeutic use; D015519:Bone Density; D050071:Bone Density Conservation Agents / Q000627:therapeutic use; D019485:Bone Morphogenetic Proteins / Q000097:blood*; D000069448:Denosumab; D005260:Female; D005500:Follow-Up Studies; D005819:Genetic Markers; D006801:Humans; D016030:Kidney Transplantation / Q000009:adverse effects; D008297:Male; D008875:Middle Aged; D010024:Osteoporosis / Q000209:etiology / Q000517:prevention & control; D011446:Prospective Studies; D051436:Renal Insufficiency, Chronic / Q000378:metabolism / Q000601:surgery; D016896:Treatment Outcome
chemical_list: D048868:Adaptor Proteins, Signal Transducing; D061067:Antibodies, Monoclonal, Humanized; D050071:Bone Density Conservation Agents; D019485:Bone Morphogenetic Proteins; D005819:Genetic Markers; C422903:SOST protein, human; D000069448:Denosumab