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Abstract: SA-PO879

Bone Phenotype in ADPKD Patients with ESRD

Session Information

  • Mineral Disease: CKD-Bone
    November 04, 2017 | Location: Hall H, Morial Convention Center
    Abstract Time: 10:00 AM - 10:00 AM

Category: Mineral Disease

  • 1203 Mineral Disease: CKD-Bone


  • Evenepoel, Pieter, University Hospitals Leuven, Leuven, Belgium
  • Claes, Kathleen, University Hospitals Leuven, Leuven, Belgium
  • Bammens, Bert, University Hospitals Leuven, Leuven, Belgium
  • Cavalier, Etienne, University of Liege, CHU Sart-Tilman, Liege, Belgium
  • Meijers, Bjorn, University Hospitals Leuven, Leuven, Belgium
  • Stenvinkel, Peter, Karolinska University Hospital Huddinge, Stockholm, Sweden
  • Jankowska, Magdalena, Medical University of Gdansk, Gdansk, Poland
  • D'Haese, Patrick C., University Antwerp, Edegem, Belgium

Autosomal dominant polycystic kidney disease (ADPKD) is among the most common hereditary nephropathies and arises as the consequence of mutations in one of two genes, pkd1 or pkd2. PKD1 and PKD2 proteins form a complex on the primary cilium and are thought to play a role in mechanosensation in various cells including osteocytes. Preliminary data showed increased sclerostin levels suggesting impaired mechanosensation in ADPKD patients with end stage renal disease (ESRD). A bone phenotype of reduced bone mass and turnover has been reported in mice with targeted disruption of pkd1 and normal kidney function. The aim of the present post-hoc analysis was to compare the bone phenotype between ADPKD patients with ESRD to non-ADPKD controls.


Laboratory parameters of mineral metabolism including FGF23 (Kainos) and sclerostin (Tecomedical), bone turnover markers (all IDS iSYS) and bone mineral density (BMD, by dual energy x-ray absorptiometry, DXA) were assessed in 518 renal transplant candidates (ADPKD, n=99), with also bone biopsy data available in a subset of patients (n=71).


Circulating sclerostin levels were significantly higher in ADPKD patients (2.20 vs 1.84 ng/L, p=0.001). Circulating levels of bone alkaline phosphatase (17.4 vs 22.6 ng/mL, p<0.0001) and tartrate-resistant acid phosphatase 5b (4.65 vs 5.46 U/L, p=0.006) were significantly lower in ADPKD, as were histomorphometric parameters of bone formation (e.g. Ob.Pm/T.Pm p=0.04). Associations remained after adjustment for classical determinants (e.g. PTH, age, gender) in regression analysis. Histomorphometric parameters of bone mineralization were numerically higher in ADPKD (e.g. O.Pm/B.Pm, p=0.06). DXA showed better preserved BMD in skeletal sites rich in cortical bone (Z-score radius 1/3 -0.04 vs -0.14, p<0.0001; femoral neck -0.72 vs -1.02, p=0.01).


Our data confirm a distinct bone phenotype in ADPKD patients with ESRD, characterized by high sclerostin levels, depressed bone turnover and preserved areal bone mineral density in skeletal sites rich in cortical bone.