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Abstract: PO0593

Hyperphosphatemia Is Associated with Vasoconstriction and Endothelial Cell Dysfunction in Hemodialysis Patients

Session Information

Category: Bone and Mineral Metabolism

  • 402 Bone and Mineral Metabolism: Clinical

Authors

  • Jung, Jinwoo, The University of Texas Southwestern Medical Center, Dallas, Texas, United States
  • Sambandam, Kamalanathan K., The University of Texas Southwestern Medical Center, Dallas, Texas, United States
  • Shastri, Shani, The University of Texas Southwestern Medical Center, Dallas, Texas, United States
  • Van Buren, Peter N., The University of Texas Southwestern Medical Center, Dallas, Texas, United States
Background

Hyperphosphatemia is associated with increased mortality in hemodialysis (HD) patients. High phoshate (Ph) causes vascular structural changes including medial calcification. While there is in vitro evidence that high Ph can induce endothelial cell dysfunction (ECD), little is known about the relationship between Ph and vasoconstriction or ECD in HD patients.

Methods

We studied hypertensive HD patients with the following outcome data: pre-HD systolic blood pressure (BP), total peripheral resistance index (TPRI) obtained with non-invasive cardiac output monitor, and serum levels of endothelin-1 (ET-1) and asymmetric dimethylarginine (ADMA). The most recent pre-HD serum Ph was the predictor variable. We conducted correlation and multivariate linear regression analyses while controlling for other clinical variables.

Results

Among the 60 participants, the mean age was 50 years. There were 62% male, 58% Black, and 60% with diabetes. Serum Ph had significant correlations with systolic BP, TPRI, ET-1, and ADMA (Figure 1). Multivariate regression analysis showed independent associations for Ph with all outcomes except ADMA (Figure 2), but PTH did have an independent association with ADMA.

Conclusion

Hyperphosphatemia is independently associated with vasoconstriction in HD patients. Serum Ph is also associated with ECD, but this is in part confounded by PTH. These data show the adverse cardiovascular consequences of hyperphosphatemia extend beyond vascular calcification. Further human studies are needed to determine 1) if lowering Ph improves endothelial function in HD patients and 2) if pharmacologic therapy aimed at improving ECD reduces the cardiovascular burden associated with hyperphosphatemia.

Funding

  • NIDDK Support