Abstract: FR-PO146
Sevelamer Use Is Associated with Decreased Vitamin K Levels in Hemodialysis Patients: Results from the Vitamin K Italian (VIKI) Study
Session Information
- Bone and Mineral Metabolism: Phosphorus, FGF23, Vascular Calcification
November 08, 2019 | Location: Exhibit Hall, Walter E. Washington Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Bone and Mineral Metabolism
- 402 Bone and Mineral Metabolism: Clinical
Authors
- Fusaro, Maria, National Research Council – Institute of Clinical Physiology, Pisa, Italy
- Aghi, Andrea, University of Padova, Padova, Italy
- Khairallah, Pascale, Columbia University, New York, New York, United States
- Gallieni, Maurizio, Ospedale San Carlo Borromeo, University of Milano, Milano, Italy
- Cozzolino, Mario, University of Milan, Milan, Italy
- Russo, Domenico, University Federico II, Naples, Italy
- Mereu, Maria cristina Mc, Ospedale NS Bonaria, San Gavino Monreale, Italy
- Ravera, Maura, St Martino Hospital, Genova, Italy
- Tripepi, Giovanni, National Research Council – Institute of Clinical Physiology, Reggio Calabria, Italy
- Nickolas, Tom, Columbia University, New York, New York, United States
Background
Sevelamer (S) is a phosphate binding drug used to treat hyperphosphatemia in patients with CKD. Our aim was to evaluate the hypothesis that the use of (S) could interfere with Vitamin K absorption in hemodialysis (HD) patients of VIKI study.
Methods
We tested this hypothesis in VIKI, a cross-sectional study of 387 hemodialysis patients, we established the prevalence of vitamin K deficiency and to assessed the relationship between vitamin K status, vertebral fractures, vascular calcification. We determined serum concentrations of vitamin 25(OH)D; alkaline phosphatase (ALP); vitamers K1, MK4, MK5, MK6, MK7; osteocalcin (BGP) and Matrix Gla Protein (MGP). We highlighted that MK4 deficiency was the strongest predictor of aortic calcification (OR, 2.82; 95% CI, 1.14–7.01) while vitamin K1 deficiency was the strongest predictor of vertebral fractures fractures (OR: 2.94; 95% CI, 1.38–6.26).
Results
163 of 387 patients (42.1%) were treated with S. There were no differences in levels of 25(OH)D, K1, MK5, MK6 and MK7 among patients treated with and without S. Remarkably, the prevalence of MK4 deficiency was higher in S treated patients (13.5% vs 5.4%, p=0.005). S treated patients also had higher median levels of ALK (89 UI/L vs 77.5 UI/L, p=0.001) and total BGP (210 mcg/L vs 152 mcg/L, p=0.002) and lower median levels of total MGP (16.4 nmol/L vs 20.3 nmol/L, p=0.037). In multivariable logistic regression, the odds ratio of MK4 deficiency (dependent variable) in patients treated with compared to without S was ~3-fold higher (OR: 2.64, 95% CI: 1.25-5.58, p=0.011) after adjustment for confounders of Vitamin K levels, including older age, previous myocardial infarction, type of HD, ALP, PTH, MGP, BGP, cholesterol and albumin.
Conclusion
These data support the hypothesis that S could interfere with MK4 absorption in HD patients. Longitudinal interventional studies are needed to prove the causal nature of these associations.