Elevated cardiac markers in chronic kidney disease as a consequence of hyperphosphatemia-induced cardiac myocyte injury

Shu Wang, Ling Qin, Tianfu Wu, Bingqing Deng, Yuerun Sun, Dayong Hu, Chandra Mohan, Xin J. Zhou, Ai Peng

Research output: Contribution to journalArticlepeer-review

16 Scopus citations


Background: Elevated cardiac markers (CMs) and hyperphosphatemia are commonly encountered in patients with chronic kidney diseases (CKD), but the causal relationship between them has not been established.

Material/Methods: We enrolled 151 patients with different kidney functions in a cross-sectional study to explore the relationship of serum phosphorus with CMs, including cardiac troponin T (cTnT), myoglobin (MYO), creatine kinaseMB (CK-MB), and brain natriuretic peptide (BNP). Then, the effect of reducing phosphorus levels on CMs by taking phosphate binder for 3 months was prospectively observed in 64 hemodialysis patients. Finally, human cardiomyocytes were exposed to different concentrations of inorganic phosphorus to examine its underlying mechanism.

Results: 1) Serum phosphorus and CMs gradually increased as the glomerular filtration rate declined in CKD patients (p<0.01). 2) Elevation of CMs was much greater and cardiac structure and function were worse in CKD patients who had higher serum phosphorus concentrations (p<0.05). 3) Serum phosphorus level positively correlated with cTnT, MYO, and BNP in CKD patients (p<0.001). 4) In hemodialysis patients, the reduction of cTnT, MYO, and CK-MB was synchronous with the pharmacologically-induced decline of serum phosphorus level. However, levels of serum Fibroblast growth factor 23 (FGF23) had no statistical decrease. 5) Simulated hyperphosphatemia inhibited proliferation of human cardiomyocytes in a timeand concentration-dependent manner.

Conclusions: Hyperphosphatemia may induce myocardial damage in CKD patients, possibly through triggering apoptosis of human cardiomyocytes, and this could account for the elevated cardiac markers in CKD patients.

Original languageEnglish (US)
Pages (from-to)2043-2053
Number of pages11
JournalMedical Science Monitor
StatePublished - Oct 25 2014


  • Apoptosis
  • Biological markers
  • Fibroblast growth factors
  • Hyperphosphatemia
  • Renal insufficiency chronic
  • Troponin T

ASJC Scopus subject areas

  • Medicine(all)


Dive into the research topics of 'Elevated cardiac markers in chronic kidney disease as a consequence of hyperphosphatemia-induced cardiac myocyte injury'. Together they form a unique fingerprint.

Cite this