Review
Copyright ©The Author(s) 2015.
World J Transplant. Dec 24, 2015; 5(4): 222-230
Published online Dec 24, 2015. doi: 10.5500/wjt.v5.i4.222
Table 1 Summary of findings of prospective studies that investigated the progression of coronary artery calcium and aortic calcium after kidney transplantation, and studies that assessed the prognostic significance of coronary artery calcium after transplantation; all imaging studies were performed with cardiac computed tomography
Ref.SizeFollow-upMain findings
Risk factors associated with vascular calcification progression in KTR
Maréchal et al[56], 2012281 enrolled, 197 analyzed4.4 yrCAC increase: 11%/yr
AoC increase: 4%/yr
Risk factors for CAC progression: Baseline CAC, history of CVD, statin use, 25OH vit D levels
Risk factors for AoC progression: Baseline AoC, higher pulse pressure, statin therapy, older age, serum phosphate level, use of aspirin, and male sex
Mazzaferro et al[55], 200941 KTR compared to 31 matched dialysis patients2 yrKTR blunts but does not halt CAC progression (12.2% vs 56.6% CAC progression in KTR vs dialysis patients)
Factors associated with CAC progression: Parathyroid hormone serum levels, modality of renal replacement therapy (dialysis vs transplantation), erythrocyte sedimentation rate
Seyahi et al[57], 2012150 prevalent KTR without history of CVD2.8 yrBaseline CAC prevalence 35.3% (mean CAC: 60 ± 174)
Follow-up: CAC prevalence 64.4% (mean CAC: 94 ± 245)
Individual CAC progression: 28%-38%
Median annualized CAC progression 11 Agatston Units
Factors associated with CAC progression: Baseline CAC, high triglyceride levels, biphosphonate therapy
Prognostic relevance of vascular calcification in KTR
Roe et al[61], 2010112 asymptomatic incident KTR without history of CVD6 yrMedian CAC at study inception 70 (33% of patients had no CAC)
CAC was associated with increased risk of the composite endpoint of coronary artery bypass surgery, percutaneous intervention or myocardial infarction, cerebrovascular accident or peripheral arterial disease (revascularization or amputation), and all-cause mortality. Per 100 unit increase in CAC: HR = 1.05, 95%CI: 1.00-1.11; P = 0.045
Nguyen et al[62], 2010281 enrolled2.3 yrCAC independent predictor of the composite endpoint of cardiovascular death, myocardial infarction, stroke or transient ischemic attack and revascularization. For a 2.72 fold increase in CAC, HR = 1.40, 95%CI: 1.12-1.75, for a 2.72-fold increase in CAC, P < 0.0031