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Assessment of Vascular Function in Patients With Chronic Kidney Disease
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Phosphate as a cardiovascular risk factor: effects on vascular and endothelial function.

Kathryn K Stevens1, Rajan K Patel1, Patrick B Mark1

  • 1Renal Unit, Western Infirmary, University of Glasgow, Glasgow, UK.

Lancet (London, England)
|August 28, 2015
PubMed
Summary

High phosphate levels directly impair blood vessel function, contributing to cardiovascular disease risk in chronic kidney disease patients. This study shows phosphate

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Area of Science:

  • Vascular Biology
  • Nephrology
  • Cardiovascular Disease

Background:

  • Hyperphosphatemia is a known risk factor for cardiovascular disease in chronic kidney disease (CKD).
  • The precise mechanisms linking phosphate to cardiovascular complications remain unclear, with possibilities including direct effects, calcification, or FGF23 mediation.
  • This study aimed to elucidate the direct impact of phosphate on endothelial function.

Purpose of the Study:

  • To investigate the direct effects of phosphate on endothelial function in both in vitro and in vivo models.
  • To assess whether phosphate loading impacts endothelial function in healthy volunteers.
  • To explore potential mechanisms underlying phosphate-induced endothelial dysfunction.

Main Methods:

  • Myography was used to assess vasoconstrictor and vasorelaxation responses in isolated rat mesenteric and human resistance vessels exposed to normal or high phosphate conditions.
  • Experiments in rat vessels included assessment with a phosphodiesterase type 5 inhibitor.
  • A cross-over study in healthy volunteers measured endothelial function via flow-mediated dilation (FMD) after phosphate supplementation or binder administration.

Main Results:

  • High phosphate significantly impaired endothelium-dependent vasodilation in both rat and human vessels.
  • In vivo, phosphate loading reduced FMD in healthy volunteers, an effect independent of serum phosphate levels but associated with urinary phosphate and FGF23.
  • Effects in rat vessels were reversible with a phosphodiesterase type 5 inhibitor, suggesting involvement of the NO pathway.

Conclusions:

  • Prolonged phosphate exposure directly causes endothelial dysfunction, potentially contributing to cardiovascular risk in CKD.
  • Both in vitro and in vivo findings demonstrate vascular dysfunction under high phosphate conditions.
  • Disruption of the nitric oxide (NO) pathway may mediate these phosphate-induced vascular effects.