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Abstract: PO1065

Poor Vitamin K Status Associates with Worse Clinical Outcome Independent of Coronary Artery Calcium and Aortic Valve Calcium in ESRD

Session Information

Category: Dialysis

  • 701 Dialysis: Hemodialysis and Frequent Dialysis

Authors

  • Dai, Lu, Division of Renal Medicine and Baxter Novum, Department of Clinical Science, Intervention and Technology, Karolinska Institutet, Stockholm, Sweden
  • Li, Longkai, Division of Renal Medicine and Baxter Novum, Department of Clinical Science, Intervention and Technology, Karolinska Institutet, Stockholm, Sweden
  • Qureshi, Abdul Rashid Tony, Division of Renal Medicine and Baxter Novum, Department of Clinical Science, Intervention and Technology, Karolinska Institutet, Stockholm, Sweden
  • Ripsweden, Jonaz, Division of Medical Imaging and Technology, Department of Clinical Science, Intervention and Technology, Karolinska Institutet, Stockholm, Sweden
  • Brismar, Torkel Bo, Division of Medical Imaging and Technology, Department of Clinical Science, Intervention and Technology, Karolinska Institutet, Stockholm, Sweden
  • Heimburger, Olof, Division of Renal Medicine and Baxter Novum, Department of Clinical Science, Intervention and Technology, Karolinska Institutet, Stockholm, Sweden
  • Barany, Peter F., Division of Renal Medicine and Baxter Novum, Department of Clinical Science, Intervention and Technology, Karolinska Institutet, Stockholm, Sweden
  • Lindholm, Bengt, Division of Renal Medicine and Baxter Novum, Department of Clinical Science, Intervention and Technology, Karolinska Institutet, Stockholm, Sweden
  • Schurgers, Leon J., Department of Biochemistry, Cardiovascular Research School Maastricht, Maastricht University, Maastricht, Netherlands
  • Stenvinkel, Peter, Division of Renal Medicine and Baxter Novum, Department of Clinical Science, Intervention and Technology, Karolinska Institutet, Stockholm, Sweden
Background

Patients with end-stage renal disease (ESRD) are at high risk of vitamin K deficiency and vascular calcification. The association between vitamin K status and vascular calcification is non-affirmative in clinical observations. We investigated the association of vitamin K status with all-cause mortality in ESRD and the modification effect of vascular calcification in this scenario.

Methods

We studied 493 stable ESRD patients (median age 55 years, 66% males) comprising non-dialysis patients (n=321), prevalent peritoneal dialysis (n=122) and hemodialysis patients (n=50). Plasma dephosphorylated-uncarboxylated matrix-Gla protein (dp-ucMGP), a circulating marker of vitamin K deficiency, and other relevant clinical and biochemical data were determined at baseline. A cohort of 553 controls (median 51 age years, 45% males) was referred to estimate vitamin K status in healthy subjects. Vascular calcification was estimated with coronary artery calcium (CAC, n=237) and aortic valve calcium (AVC, n=223) among ESRD patients undergoing cardiac computed tomography scan.

Results

Plasma dp-ucMGP (median 1445 pmol/L) levels were substantially elevated in ESRD patients compared to healthy subjects (median 376 pmol/L). During median 42 months’ follow-up, 92 patients died (19%) and 128 patients (26%) underwent renal transplantation. 1-SD increase of dp-ucMGP associated with increased all-cause mortality (1.19 (1.01-1.40), sub-hazard ratio (95% confidence interval)), with adjustment for age, sex, presence of cardiovascular disease, diabetes, body mass index, inflammation, handgrip strength and dialysis. In subgroup analysis further adjusted for presence of CAC or AVC, dp-ucMGP remained as an independent risk factor of mortality (1.27 (1.03-1.56) and 1.36 (1.05-1.66), respectively). In multivariate linear regression model, increased dp-ucMGP levels were not associated with quantified calcification suggested by CAC (p=0.11, R2=0.30) and AVC (p=0.84, R2= 0.12).

Conclusion

Vitamin K deficiency is evident in ESRD and strongly associated with an increased risk of mortality which is not modified by the presence of vascular calcification. Plasma dp-ucMGP was not an independent risk factor of calcification quantified by CAC and AVC.