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Abstract: PO0535

Plasma Biomarkers of Mineral and Bone Disorder in ADPKD Patients Treated with Tolvaptan

Session Information

Category: Bone and Mineral Metabolism

  • 402 Bone and Mineral Metabolism: Clinical

Authors

  • Bargagli, Matteo, U.O.C. Nefrologia, Fondazione Policlinico Universitario A. Gemelli IRCCS, Rome, Italy
  • Dhayat, Nasser, Division of Nephrology and Hypertension, Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland
  • Anderegg, Manuel, Division of Nephrology and Hypertension, Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland
  • Huynh-do, Uyen, Division of Nephrology and Hypertension, Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland
  • Ferraro, Pietro Manuel, U.O.C. Nefrologia, Fondazione Policlinico Universitario A. Gemelli IRCCS, Rome, Italy
  • Fuster, Daniel G., Division of Nephrology and Hypertension, Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland
Background

Autosomal-dominant polycystic kidney disease (ADPKD) is characterized by a unique bone and mineral phenotype. Patients affected by ADPKD show parathyroid hormone (PTH) resistance, a better-preserved cortical bone mass, higher sclerostin levels, lower bone turnover and total alkaline phosphatase compared to other chronic kidney disease (CKD) aetiologies. To date, the association between tolvaptan administration, plasma biomarkers of mineral and bone disorder (CKD-MBD) and bone mineral density has not been investigated.

Methods

We conducted an analysis of patients enrolled in the Bern ADPKD registry, a prospective observational cohort study. Plasma parameters for CKD-MBD and 24-hour urine analyses were performed at baseline and every 12 months thereafter. DEXA scans were obtained at baseline and after 3 years. Multivariable fixed-effects regression models adjusted for age, sex, BMI, eGFR, urinary sulfate excretion (a marker of acid intake) and NGIA (a marker of alkali intake) were applied to study changes in CKD-MBD parameters and bone mineral density associated with tolvaptan treatment.

Results

A total of 167 participants (56 with and 111 without tolvaptan treatment) were included in the analysis. Median follow-up time was 24.5 months. After adjusting for potential confounders, tolvaptan treatment was associated with a significantly reduced plasma PTH (β -14.84; 95%CI, -28.61 to -1.07; p=0.04), increased total plasma calcium (β 0.05; 95%CI, 0.01 to 0.09; p=0.01), plasma magnesium (β 0.02; 95%CI, 0.00 to 0.04; p=0.03) and femoral but not lumbar bone mineral density (β 0.10; 95%CI, 0.01 to 0.19; p=0.04 and β 0.22; 95%CI, -0.04 to 0.08; p=0.49, respectively). In contrast, tolvaptan treatment was not associated with changes in plasma phosphate, ionized calcium, TmP/GFR, serum intact fibroblast growth factor 23, plasma alkaline phosphatase, blood pH or serum 1,25(OH)2 and 25(OH) vitamin D.

Conclusion

Tolvaptan treatment is associated with changes in mineral metabolism parameters and increased bone mineral density at the femoral neck. Long-term prospective studies are needed to assess the impact of tolvaptan on fracture risk.