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Serum hepcidin predicts uremic accelerated atherosclerosis in chronic hemodialysis patients with diabetic nephropathy

Han Li, Su-Juan Feng, Lu-Lu Su

  • 1Institute of Uro-Nephrology, Beijing Chao-Yang Hospital, Capital Medical University, Beijng 100020, China.

Chinese Medical Journal
|May 13, 2015
PubMed

Insights

Elevated serum hepcidin levels are linked to accelerated atherosclerosis in chronic hemodialysis patients with diabetic nephropathy. This suggests iron metabolism and hepcidin abnormalities may drive this condition.

Area of Science:

  • Nephrology
  • Cardiovascular Medicine
  • Endocrinology

Background:

  • Hepcidin regulates body iron stores and is implicated in anemia of chronic disease.
  • Atherosclerotic cardiovascular disease is a major cause of mortality in chronic hemodialysis (CHD) patients.
  • Diabetic nephropathy (DN) complicates CHD, increasing cardiovascular risk.

Purpose of the Study:

  • To investigate the relationship between serum hepcidin and uremic accelerated atherosclerosis (UAAS) in CHD patients with DN.
  • To compare hepcidin levels in CHD patients with and without DN.

Main Methods:

  • Serum hepcidin-25 levels were measured using liquid chromatography-tandem mass spectrometry in 78 CHD/DN and 86 CHD/non-DN patients.
  • Interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) levels were quantified via ELISA.
  • Common carotid artery intima media thickness (CCA-IMT) was assessed as a marker of atherosclerosis.

Main Results:

  • Serum hepcidin-25 was significantly higher in CHD/DN patients compared to CHD/non-DN patients.
  • Hepcidin-25 positively correlated with ferritin, hs-CRP, TNF-α, and IL-6 in CHD/DN patients.
  • CCA-IMT, hs-CRP, and hepcidin-25 levels were elevated in CHD/DN patients; CCA-IMT correlated with hepcidin, hs-CRP, and LDL-C.

Conclusions:

  • Findings suggest a link between iron metabolism, hepcidin dysregulation, and the development of UAAS in CHD/DN.
  • Abnormalities in hepcidin may contribute to accelerated atherosclerosis in this patient population.
Abstract

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