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Phosphate Toxicity and Vascular Calcification in Chronic Kidney Disease: A Closer Look Utilizing Transmission

Ying Yang1,2, Ke Yang2,3, Yuxin Xiong1,2

  • 1Department of Endocrinology, the Affiliated Hospital of Yunnan University and the Second People's Hospital of Yunnan Province, Kunming, Yunnan, 650021, China.

Current Protein & Peptide Science
|July 27, 2023
PubMed

Insights

Hyperphosphatemia in chronic kidney disease (CKD) and end-stage renal disease (ESRD) is linked to severe complications. This review explores phosphate toxicity, FGF-23/Klotho axis, and vascular calcification in CKD.

Area of Science:

  • Nephrology
  • Cardiovascular Science
  • Metabolic Disorders

Background:

  • Hyperphosphatemia is a significant complication in chronic kidney disease (CKD) and end-stage renal disease (ESRD), independently associated with vascular calcification, cardiovascular disease, bone-mineral disease, and mortality.
  • The fibroblast growth factor-23 (FGF-23)/Klotho axis is crucial for phosphate homeostasis, with diminished renal Klotho production contributing to elevated phosphate levels in CKD.
  • Associated complications include calciphylaxis, renal tubulointerstitial disease, renal osteodystrophy, and uremic cardiomyopathy.

Purpose of the Study:

  • To review the multifaceted roles of phosphate homeostasis and toxicity in CKD and ESRD.
  • To examine the contribution of the FGF-23/Klotho axis to hyperphosphatemia and its consequences.
  • To explore the ultrastructural remodeling of the thoracic aorta and its relation to vascular calcification, incorporating insights from animal models.

Main Methods:

  • Review of existing literature on hyperphosphatemia, FGF-23, Klotho, and vascular calcification in CKD/ESRD.
  • Incorporation of ultrastructural remodeling data of the thoracic aorta.
  • Utilization of data from nine-week-old male heterozygous (mRen2) 27 (Ren2) rat models and Zucker obese (fa/fa) rat models.

Main Results:

  • Hyperphosphatemia is a key driver of vascular calcification, cardiovascular disease, and mortality in CKD/ESRD.
  • Dysregulation of the FGF-23/Klotho axis contributes to phosphate retention and associated pathologies.
  • Animal models demonstrate aortic remodeling linked to vascular calcification and provide insights into nephrolith formation.

Conclusions:

  • Phosphate homeostasis, toxicity, and the FGF-23/Klotho axis are central to understanding CKD/ESRD progression and complications.
  • Vascular calcification, driven by hyperphosphatemia, involves complex cellular and molecular mechanisms including oxidative stress and inflammation.
  • Further research into these pathways is essential for developing targeted therapies for CKD/ESRD patients.

Keywords:
Aortachronic kidney diseaseendotheliumhyperphosphatemiaultrastructurevascular calcification

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