title: Progression of coronary artery calcification in renal transplantation and the role of secondary hyperparathyroidism and inflammation.
abstract: OBJECTIVE
  Transplantation should favorably affect coronary calcification (CAC) progression in dialysis; however, changes in CAC score in the individual patient are not reliably evaluated.
  
  
  METHODS
  The authors used special tables of reproducibility limits for each score level to study, by multislice computed tomography and biochemistries, the 2-year changes in CAC in 41 transplant patients (age 48 +/- 13 yr, 25 men, dialysis vintage 4.8 +/- 4.3 yr, underwent transplant 6.2 +/- 5.5 yr prior). Thirty balanced dialysis patients served as controls.
  
  
  RESULTS
  In the study group, Agatston score was stable, and C-reactive protein decreased, whereas fetuin and osteoprotegerin increased. In the control group, Agatston score increased, parathyroid hormone and phosphate decreased, and inflammation markers were persistently twice as high as in the study group. With regard to individual changes, 12.2% transplant patients worsened, compared with 56.6% of patients in dialysis (P < 0.0001). Patients without calcification at entry showed slower progression in transplantation (8.3%) than in dialysis (44.4%; P < 0.034), and the difference was similar to that observed in cases with CAC (17.6% versus 61.9%; P < 0.007). Discriminant analysis indicated parathyroid hormone, the modality of therapy (dialysis or transplantation), and erythrocyte sedimentation rate as the variables most associated with worsening.
  
  
  CONCLUSIONS
  Renal transplantation lowers but does not halt CAC progression. Inflammation and hyperparathyroidism are associated with progression in the populations studied.
authors.affiliation: Department of Clinical Science, University of Rome La Sapienza, Rome, Italy. sandro.mazzaferro@uniroma1.it
authors.forename: Sandro
authors.initials: S
authors.lastname: Mazzaferro
authors.forename: Marzia
authors.initials: M
authors.lastname: Pasquali
authors.forename: Franco
authors.initials: F
authors.lastname: Taggi
authors.forename: Matteo
authors.initials: M
authors.lastname: Baldinelli
authors.forename: Carmina
authors.initials: C
authors.lastname: Conte
authors.forename: Maria Luisa
authors.initials: ML
authors.lastname: Muci
authors.forename: Nicola
authors.initials: N
authors.lastname: Pirozzi
authors.forename: Iacopo
authors.initials: I
authors.lastname: Carbone
authors.forename: Marco
authors.initials: M
authors.lastname: Francone
authors.forename: Francesco
authors.initials: F
authors.lastname: Pugliese
mesh_terms: D000328:Adult; D015415:Biomarkers / Q000097:blood; D001799:Blood Sedimentation; D002114:Calcinosis / Q000097:blood / Q000000981:diagnostic imaging / Q000209:etiology*; D016022:Case-Control Studies; D017023:Coronary Angiography / Q000379:methods; D003324:Coronary Artery Disease / Q000097:blood / Q000000981:diagnostic imaging / Q000209:etiology*; D018450:Disease Progression; D005260:Female; D006801:Humans; D006962:Hyperparathyroidism, Secondary / Q000097:blood / Q000150:complications*; D007249:Inflammation / Q000097:blood / Q000150:complications*; D007674:Kidney Diseases / Q000097:blood / Q000150:complications / Q000601:surgery / Q000628:therapy*; D016030:Kidney Transplantation; D008297:Male; D008875:Middle Aged; D006435:Renal Dialysis; D012307:Risk Factors; D012720:Severity of Illness Index; D013997:Time Factors; D014057:Tomography, X-Ray Computed; D016896:Treatment Outcome
chemical_list: D015415:Biomarkers