P1642CORONARY ARTERY CALCIFICATION AMONG RENAL TRANSPLANT RECIPIENTS
Authors: Osama Mohamed , Mahmoud Medhat , El Deeb Salem , Elmowafy Ahmed , Sheashaa Hussein , Donia Ahmed , Refaie Ayman , Fouda Ashraf 
Published: June 2020

Background and Aims

Bone-mineral disease and vascular calcification are common complications in hemodialysis. The harmony between parathyroid hormone, calcium and phosphorus is impaired during hemodialysis and it supposed to be reversed by kidney transplantation but it is not known if the effect on vascular calcification will be reversed. Our aim is to study renal transplantation effect on hemodialysis associated vascular calcification and the risk factors for development and progression of vascular calcification.

Method

Transplant registry in Mansoura Urology and Nephrology Center, Egypt was reviewed for kidney transplant recipients (KTRs) who received renal allo-transplantation between January 2016 and December 2017 (149 KTRs). Patients were divided according to the presence of vascular calcification using non-contrast CT into 2 groups. Group I: 58 KTRs with pre-transplant vascular calcification, Group II: 91 KTRs without pre-transplant vascular calcification. Group I then were subdivided into 3 groups according to Agatston score (coronary calcium score) to 3 groups: Mild calcification (11-100), Moderate calcification (101-400), Severe calcification (&gt;400). All patients were screened for coronary vascular calcification 2 years after transplantation using multi-slice coronary CT. Patients with detectable CAC at baseline and a CAC score change was ≥25% and patient with CAC score of 0 and follow up ≥ 4 were considered as progressors.

Results

The recipients` age in both group ranged from 18 years to 55 years. Older age is associated with higher incidence of vascular calcification (p value: 0.048) with male predominance and mean body mass index is 32.5±2.3.

Majority of patients underwent hemodialysis before transplantation (90%). The longer hemodialysis duration, the more severe the degree of vascular calcification (p value: 0.003). There was no difference among both groups regarding CKD bone-mineral biomarkers except for intact PTH which was higher among vascular calcification patients (p value: 0.023).

The majority of our patients received induction therapy; Basiliximab and received tacrolimus based immunosuppressive regimen. There was no significant difference regarding rejection episodes or post-transplant medical disorders. Presence of vascular calcification did not affect graft outcome over 2 years.

Despite significant improvement in CKD-bone disease biomarkers (p value: 0.001; calcium, phosphorus, alk. phosphatase and intact PTH changes), Vascular calcification incidence increased after transplantation from 38.9% to 40.9% especially for severe form with rise of median agatston score from 258.85 (21,813) to 354.55(20, 1198.8). Patients were divided according to progression into 2 groups: progressors (59 KTRs) and non-progressors (90 KTRs). On comparison of both groups, there were 3 independent risk factors for CAC progression: pre-transplant Calcium score (Figure 1), dialysis duration (Figure 2) and pre-transplant PTH level (Figure 3) with significant p value: &lt;0.001, &lt;0.001 and 0.05 respectively. Pre-emptive transplantation is inversely proportional in determining CAC progression with p value: 0.02. ROC curve analyses were performed to evaluate the discriminatory power of the three parameters.

Conclusion

Baseline CAC, duration of dialysis and pre-transplant serum PTH level are factors associated CAC progression. Renal transplantation does not stop or reverse CAC. Progression of CAC is the usual evolution pattern of CAC in renal transplant recipients. Very important was the finding that the follow-up calcium Score was significantly related to the baseline score., which emphasizes the importance of primary prevention of CAC development.