title: The relation of calcium-phosphorus metabolism-related indexes with cardiac damages.
abstract: To observe and analyze the relation of calcium-phosphorus metabolism-related indexes with cardiac damage-related indexes in patients with chronic kidney disease (CKD) and to explore the roles of calcic and phosphor metabolization in cardiac damage and provide references for prevention of cardiovascular events in CKD patients.
  
  
  
  A total of 98 inpatients, from Urology Department, who were not undergoing dialysis treatment and diagnosed with stages 3, 4, and 5 CKD according to K/DOQI guide were recruited. We measured the calcium-phosphorus metabolism-related indexes (including serum calcium (Ca), the serum phosphate (Pi), the intact parathyroid hormone (iPTH), the β-collagen-specific sequences (β-CTX), the total N-terminal propeptide of type I procollagen (TPINP), the N-terminal-mid fragment of osteocalcin (N-MID), the cardiac damage-related indexes (including left ventricular end diastolic diameter (LVEDD), the interventricular septal thickness (IVST), the left ventricular posterior wall thickness (LVPWT), the ejection fraction (EF), the blood flow velocity at mitral diastolic late phase (A) and mitral diastolic early phase (E) via echocardiography. Then, we conducted a correlation analysis employing these two types of indexes.
  
  
  
  We found an escalating trend in the level of calcium-phosphorus metabolism-related indexes from stage 3 to stage 5 CKD. The difference between stage 3 and 5 is statistically significant (p < 0.05) while that between stage 3 and 4 is not (p > 0.05). Among 98 CKD patients, the myocardial hypertrophy accounted for 35.9% (n = 36), the diastolic dysfunction accounted for 72.1% (n = 70), and systolic dysfunction accounted for 27.5% (n = 27). Levels of β-CTX, N-MID, TP1NP, Pi, and iPTH are positively associated with the myocardial hypertrophy and yet negatively associated with cardiac systolic (EF) and diastolic function (A/E value).
  
  
  
  Calcium-phosphorus metabolism disorder in the context of kidney dysfunction may contribute to the damages of cardiac structure and functions.
authors.affiliation: Department of Urology, Central Hospital, Xu Zhou, Jiangsu Province, China. wuling001@sina.com.
authors.forename: L
authors.initials: L
authors.lastname: Wu
authors.forename: Y-H
authors.initials: YH
authors.lastname: Bai
authors.forename: T
authors.initials: T
authors.lastname: Chen
authors.forename: L
authors.initials: L
authors.lastname: Zhang
authors.forename: Y-R
authors.initials: YR
authors.lastname: Wang
authors.forename: H
authors.initials: H
authors.lastname: Zhu
authors.forename: Y-X
authors.initials: YX
authors.lastname: Jiao
authors.forename: L
authors.initials: L
authors.lastname: Sun
mesh_terms: D002118:Calcium / Q000378:metabolism*; D006801:Humans; D009206:Myocardium / Q000473:pathology*; D010281:Parathyroid Hormone / Q000097:blood; D010758:Phosphorus / Q000378:metabolism*; D051436:Renal Insufficiency, Chronic / Q000097:blood / Q000378:metabolism*
chemical_list: D010281:Parathyroid Hormone; D010758:Phosphorus; D002118:Calcium