4.6 Article

Evolution of large-vessel arteriopathy in paediatric patients with chronic kidney disease

Journal

NEPHROLOGY DIALYSIS TRANSPLANTATION
Volume 23, Issue 8, Pages 2552-2557

Publisher

OXFORD UNIV PRESS
DOI: 10.1093/ndt/gfn083

Keywords

atherosclerosis; chronic kidney disease; hypertension; paediatrics; risk factors

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This observational study was designed to verify the hypothesis that the treatment modality significantly affects the evolution of CKD-associated arteriopathy. Patients. Paediatric patients (mean age 13.8 +/- 4.2 years) with chronic kidney disease (CKD) stages 3-5, including 24 patients with mean GFR 54 +/- 21 ml/min/1.73 m(2) (CKD group) and 32 patients in end-stage renal disease, of whom 19 received a renal allograft (D-Rtx) and 13 remained on dialysis (D-D). Methods. Sonography of the common carotid artery was performed at baseline and after 12 months. Intima-media thickness (IMT) and the cross-sectional areas of the vessel wall (WCSA) and lumen (LCSA) were measured and normalized to age (SDS). Results. At baseline IMT-SDS and WCSA-SDS were increased above normal, and were significantly higher in D than in CKD patients (P < 0.001). IMT-SDS increased over time in CKD and D-D patients (1.4 +/- 1.7 to 2.1 +/- 1.2, P = 0.05). In contrast, IMT-SDS (2.8 +/- 0.6 to 2.0 +/- 0.6, P < 0.005) decreased in those D-Rtx patients who had elevated values prior to transplantation. The total number of patients with elevated cIMT-SDS changed from 7 to 13 in the 24 CKD, from 8 to 11 in the 13 D-D and from 11 to 12 in the 19 D-Rtx patients. While IMT-SDS was independently correlated with blood pressure and serum phosphate in the CKD and D patients, only total dialysis vintage (r = 0.50; P < 0.05) and the IMT-SDS attained at the time of grafting (r = 0.46, P < 0.05) correlated with IMT-SDS 1 year post-Rtx. Conclusion. While vascular lesions rapidly progress in CKD and D patients, abolition of the uraemic state by Rtx leads to stabilization or partial regression of CKD-associated arteriopathy. Cumulative dialysis duration and the degree of arterial damage prevalent at the time of grafting are the main determinants of persistent arteriopathy 1 year after Rtx.

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