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Chinese Journal of Kidney Disease Investigation(Electronic Edition) ›› 2013, Vol. 02 ›› Issue (02): 76-79. doi: 10.3877/cma.j.issn.2095-3216.2013.02.005

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Relationship between secondary hyperparathyroidism and cardiovascular calcification in chronic kidney disease patients and its clinical implication

Shan LIN1,(), Jun-ya JIAN1   

  1. 1.Department of Nephrology, Tianjin Medical University General Hospitol, Tianjin 300052, China
  • Online:2013-04-15 Published:2024-12-06
  • Contact: Shan LIN

Abstract:

Secondary hyperparathyroidism (SHPT) is often accompanied by cardiovascular calcification in chronic kidney disease (CKD) patients. Through its effects on calcium and phosphorus metabolism, SHPT can indirectly cause or aggravate vascular calcification. However, the direct effects of parathyroid hormone (PTH) on cardiovascular calcification are biphasic. Physiological dose of PTH inhibits vascular smooth muscle cells (VSMC) proliferation and calcification while supraphysiological dose of PTH promotes these processes by increasing inflammatory mediators such as IL-6, RAGE or by promoting transcription of the calcification gene. Therefore, prevention of SHPT is important for intervention in the cardiovascular calcification. It has been found that parathyroidectomy, dietary phosphorus restriction, use of phosphate binders, active vitamin D and/or its analogs may effectively improve SHPT, but their effects on vascular calcification still remains unclear yet. Recently, cinacalcet, the only drug of calcimimetics, has been found to slow down the progression of cardiovascular calcification in dialysis patients, which provides important evidence for prevention of the cardiovascular calcification with anti-SHPT drugs in CKD patients.

Key words: Secondary hyperparathyroidism, Calcification, Cardiovascular, Parathyroid hormone

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