title: Importance of vascular calcification in kidney transplant recipients.
abstract: BACKGROUND
  Kidney transplantation is the treatment of choice for chronic kidney disease (CKD), but in kidney transplant recipients (KTRs) cardiovascular events are the first cause of death with a functioning graft, ranging from 36 to 55%. The impact of vascular calcification (VC) on morbidity and mortality of KTRs is not appreciated enough nowadays.
  
  
  CONCLUSIONS
  This review summarizes 13 important studies on VC in KTRs, comparing the results with CKD and dialysis populations. We focused on VC evaluation and use of coronary artery calcification (CAC) and aorta calcification (AoC) scores. We also evaluated the influence of traditional and non-traditional progression risk factors.
  
  
  CONCLUSIONS
  VC strongly predicts cardiovascular events and all-cause mortality in KTRs. VC assessment is important in KTRs and based essentially on multislice computed tomography or electron beam computed tomography recognition of lesions. Quantitative measurement of CAC and AoC scores is essential for a correct definition of the calcium burden before and after kidney transplant. Progression of CAC slows down but does not halt after kidney transplant. A variable association of both traditional and non-traditional risk factors is shown. There is a strong association between baseline CAC score and CAC progression. A significant improvement in secondary hyperparathyroidism after transplantation favorably affects the progression of CAC. Low 25(OH)D3 levels are an independent determinant of CAC progression. Diabetes is a risk factor for the presence of CAC in KTRs, but has not been independently associated with CAC progression. The data published on the use of immunosuppressive drugs as progression factors are few and inconclusive.
authors.affiliation: Nephrology, Dialysis and Transplantation Unit, Department of Experimental, Diagnostic and Specialty Medicine, S. Orsola University Hospital, Bologna, Italy.
authors.forename: Giuseppe
authors.initials: G
authors.lastname: Cianciolo
authors.forename: Irene
authors.initials: I
authors.lastname: Capelli
authors.forename: Maria Laura
authors.initials: ML
authors.lastname: Angelini
authors.forename: Chiara
authors.initials: C
authors.lastname: Valentini
authors.forename: Olga
authors.initials: O
authors.lastname: Baraldi
authors.forename: Maria P
authors.initials: MP
authors.lastname: Scolari
authors.forename: Sergio
authors.initials: S
authors.lastname: Stefoni
mesh_terms: D001011:Aorta; D002112:Calcifediol / Q000097:blood; D002135:Calcium-Binding Proteins / Q000378:metabolism; D002318:Cardiovascular Diseases / Q000401:mortality*; D003331:Coronary Vessels; D003920:Diabetes Mellitus / Q000453:epidemiology; D018450:Disease Progression; D016326:Extracellular Matrix Proteins / Q000378:metabolism; D006801:Humans; D006962:Hyperparathyroidism, Secondary / Q000453:epidemiology; D007166:Immunosuppressive Agents; D016030:Kidney Transplantation / Q000401:mortality*; D053244:Osteoprotegerin / Q000378:metabolism; D006435:Renal Dialysis; D051436:Renal Insufficiency, Chronic / Q000378:metabolism / Q000628:therapy; D012307:Risk Factors; D061205:Vascular Calcification / Q000453:epidemiology* / Q000378:metabolism; D060749:alpha-2-HS-Glycoprotein / Q000378:metabolism; D000097568:Matrix Gla Protein
chemical_list: D002112:Calcifediol; D002135:Calcium-Binding Proteins; D016326:Extracellular Matrix Proteins; D007166:Immunosuppressive Agents; D053244:Osteoprotegerin; D060749:alpha-2-HS-Glycoprotein; D000097568:Matrix Gla Protein