Vascular toxicity of phosphate in chronic kidney disease: beyond vascular calcification

Circ J. 2014;78(10):2339-46. doi: 10.1253/circj.cj-14-0735. Epub 2014 Jul 31.

Abstract

Chronic kidney disease (CKD) is characterized by high cardiovascular morbidity/mortality, which is linked in part to vascular calcification (VC) and endothelial dysfunction (ED). Hyperphosphatemia, a feature of CKD, is a well-known inducer of VC in preclinical models and is associated with poor outcomes in epidemiological studies. However, it remains to be seen whether lowering phosphate levels in CKD patients reduces VC and the morbidity/mortality rate. Furthermore, it is now clear from preclinical and clinical studies that phosphate is involved in ED. The present article reviews the direct and indirect mechanisms (eg, via fibroblast growth factor 23 and/or parathyroid hormone) by which hyperphosphatemia influence the onset of VC and ED in CKD.

Publication types

  • Review

MeSH terms

  • Animals
  • Endothelium, Vascular / metabolism
  • Humans
  • Hyperphosphatemia* / blood
  • Hyperphosphatemia* / etiology
  • Hyperphosphatemia* / mortality
  • Hyperphosphatemia* / therapy
  • Phosphates / blood*
  • Renal Insufficiency, Chronic* / blood
  • Renal Insufficiency, Chronic* / complications
  • Renal Insufficiency, Chronic* / mortality
  • Renal Insufficiency, Chronic* / therapy
  • Vascular Calcification* / blood
  • Vascular Calcification* / etiology
  • Vascular Calcification* / mortality
  • Vascular Calcification* / therapy

Substances

  • Phosphates