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Supplementary Material for: Long-Term Progression of Coronary Artery Calcification Is Independent of Classical Risk Factors, C-Reactive Protein, and Parathyroid Hormone in Renal Transplant Patients

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posted on 2017-07-12, 13:39 authored by Gulcicek S., Zoccali C., Olgun D.Ç., Tripepi G., Alagoz S., Yalın S.F., Trabulus S., Altiparmak M.R., Seyahi N.

Aims: Compared to the general population, mortality is significantly increased in renal transplant recipients. In the general population, coronary artery calcification (CAC) and its evolution over time are associated with cardiovascular and all-cause mortality, and the study of this biomarker could provide useful information for describing the long-term progression of coronary heart disease in renal transplant recipients. Methods: We followed up a cohort of 113 renal transplant patients by performing three multi-detector computed tomography studies over 83.6 ± 6.8 months. Data analysis was performed by logistic regression analysis and by mixed linear modelling. Results: Progression was observed in 34.5% of patients. Baseline CAC and time-to-transplantation were the sole variables that predicted CAC evolution over time. Neither classical nor nontraditional risk factors, biomarkers of renal function (GFR) and kidney damage (albuminuria) or biomarkers of bone mineral disorder (BMD), such as serum phosphorus, calcium, and PTH, were associated with the long-term progression of coronary calcification. Serum triglycerides predicted CAC progression only in logistic regression analysis, while in addition to baseline CAC, time to transplantation was the sole variable predicting CAC progression when the data were analyzed by mixed linear modelling. These data suggested that, in addition to the background calcification burden, other unmeasured factors play major roles in promoting the evolution of coronary calcification in the transplant population. Conclusion: CAC progression continued over the long-term follow-up of renal transplant patients. This phenomenon was unaccounted for by classical and nontraditional risk factors, as well as by biomarkers of renal dysfunction and renal damage.

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