title: Progression of coronary artery calcification in predialysis patients.
abstract: BACKGROUND
  In patients on dialysis coronary artery calcification (CAC) rapidly proceeds due to impaired mineral metabolism and/or exogenous calcium load. Progression has not been assessed in patients with chronic kidney disease not yet requiring dialysis (CKD patients). In this study, rate and determinants of CAC progression have been evaluated in CKD patients who are exposed to minor derangement of mineral metabolism and calcium load.
  
  
  METHODS
  Consecutive patients were enrolled. Exclusion criteria were: symptomatic coronary disease, arrhythmia, myocardial infarction, and diabetes. Serum calcium, phosphorus, parathyroid hormone, homocysteine, C-reactive protein, triglycerides, total cholesterol, high- and low-density lipoprotein cholesterol were serially measured. Fetuin-A was assessed at entry into the study. CAC progression was detected by measuring total calcium score (TCS) with computed tomography. Initial and final scans were obtained. Predictive factors of progression were investigated.
  
  
  RESULTS
  Fifty-three patients had CKD (stage 3-5 CKD; K-DOQI classification) not yet requiring dialysis, and 60 patients had normal renal function (NRF patients). Follow-up lasted 24 +/- 4.2 months (mean +/- SE). Patients with CAC were older with lower serum fetuin-A. TCS increased from 73 +/- 17 to 80 +/- 20 (mean +/- SE; p = NS) in NRF patients, and from 384 +/- 116 to 602 +/- 140 (mean +/- SE; p < 0.01) in CKD patients. Serum phosphorus [OR = 1.97 (1.14-3.41, 95% CI); p = 0.015] was the only variable that was associated with CAC progression. Cardiovascular events occurred in CKD patients with CAC.
  
  
  CONCLUSIONS
  CAC progression was prominent in CKD patients and correlated with serum phosphorus. Fatal and nonfatal cardiovascular events were more frequent in CKD patients. Studies are required to ascertain whether the attainment of serum phosphorus concentration lower than that suggested by current guidelines may reduce CAC progression and ultimately mortality.
authors.affiliation: Department of Nephrology, School of Medicine, University of Naples Federico II, Naples, Italy. domenicorusso51@hotmail.com
authors.forename: Domenico
authors.initials: D
authors.lastname: Russo
authors.forename: Salvatore
authors.initials: S
authors.lastname: Corrao
authors.forename: Ida
authors.initials: I
authors.lastname: Miranda
authors.forename: Carolina
authors.initials: C
authors.lastname: Ruocco
authors.forename: Simona
authors.initials: S
authors.lastname: Manzi
authors.forename: Rosanna
authors.initials: R
authors.lastname: Elefante
authors.forename: Diego
authors.initials: D
authors.lastname: Brancaccio
authors.forename: Mario
authors.initials: M
authors.lastname: Cozzolino
authors.forename: Maria L
authors.initials: ML
authors.lastname: Biondi
authors.forename: Vittorio E
authors.initials: VE
authors.lastname: Andreucci
mesh_terms: D000328:Adult; D002114:Calcinosis / Q000150:complications* / Q000000981:diagnostic imaging; D002908:Chronic Disease; D003324:Coronary Artery Disease / Q000150:complications* / Q000175:diagnosis; D018450:Disease Progression; D005260:Female; D006801:Humans; D007674:Kidney Diseases / Q000150:complications / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D011859:Radiography; D006435:Renal Dialysis