ASN's Mission

ASN leads the fight to prevent, treat, and cure kidney diseases throughout the world by educating health professionals and scientists, advancing research and innovation, communicating new knowledge, and advocating for the highest quality care for patients.

learn more

Contact ASN

1401 H St, NW, Ste 900, Washington, DC 20005

email@asn-online.org

202-640-4660

The Latest on Twitter

Kidney Week

Abstract: TH-PO585

Bone Phenotype in Patients with ESKD Treated with Proton Pump Inhibitors

Session Information

Category: Bone and Mineral Metabolism

  • 402 Bone and Mineral Metabolism: Clinical

Authors

  • Evenepoel, Pieter, University Hospitals Leuven, Leuven, Belgium
  • Claes, Kathleen, University Hospital Gasthuisberg, Leuven, Belgium
  • Bammens, Bert, University Hospitals Leuven, Leuven, Belgium
  • Meijers, Björn Ki, UZ Leuven, Leuven, Belgium
  • Cavalier, Etienne, University of Liege, CHU Sart-Tilman, Liege, Belgium
  • Behets, Geert J., University of Antwerp, Antwerp (Wilrijk), Belgium
  • D'Haese, Patrick C., University Antwerp, Edegem, Belgium
  • Kuypers, Dirk R., University Hospitals Leuven, Leuven, Belgium
Background

Proton pump inhibitors (PPIs) are suspected of having a negative impact on the skeleton and possibly increasing the risk of osteoporosis in the general population and patients with chronic kidney disease. Underlying pivotal pathophysiological mechanisms include calcium malabsorption, gastrin-mediated parathyroid gland stimulation, vitamin B12 deficiency, and impaired function of osteoblasts and osteoclasts. The present cohort study aimed to map the impact of PPI use on the bone phenotype in end stage kidney disease (ESKD) patients.

Methods

Bone mineral density (BMD, by dual energy x-ray absorptiometry, DXA) both at the lumbar spine and hip (total hip and femoral neck) and bone turnover markers (BTMs; bone alkaline phosphatase, tartrate-resistant acid phosphatase 5b, procollagen type I N-terminal propeptide) were assessed in 308 patients with ESKD (53.7 ± 13.1 yrs, male 64%), with bone histomorphometry data available in 69 patients. On-hundred and three patients (33%) were treated with PPIs (cases). Laboratory parameters of mineral metabolism including calcium, phosphate, magnesium, parathyroid hormone (PTH), fibroblast growth factor 23 (FGF23) and sclerostin, parameters of inflammation (C-reactive protein, Interleukin-6), vitamin B12 levels, and nonphosphorylated-uncarboxylated isoform of MGP (dp-ucMGP), as a proxy of vitamin K status were assessed in all patients.

Results

ESKD patients on PPI therapy showed lower BMD at the hip, while BTMs and bone histomorphometry were not different from controls. PPI users, furthermore, were characterized by older age, more cardiovascular morbidity, lower serum magnesium, lower phosphate and FGF23, and higher serum dp-ucMGP levels and parameters of inflammation. PTH and vitamin B12 levels did not differ between PPI users and non-users. PPI use associated with BMD at the femoral neck, independent of classical (age, gender, BMI) and non-classical (vitamin K status, cardiovascular disease, inflammation) determinants.

Conclusion

PPI use in patients with ESKD independently associated with low BMD at the hip. Our data argue against an important role of PTH, vitamin B12 or dysfunctional osteoblast and osteoclast in the pathophysiology of PPI-related osteoporosis in ESKD. The link between PPI use and poor vitamin K status needs further investigation.