NIV Congres

Objective Supplementation of activated vitamin D analogues has been postulated in paediatric renal transplant recipients, but there is no evidence that 1,25(OH)2D deficiency contributes to hyperparathyroidism in children with GFR >50ml/min/1.73m². The aim of the study was to investigate the prevalence of 25OHD and 1,25(OH)2D deficiency in stable paediatric kidney transplant patients as compared with pre-transplant children and search for the evidence of interaction with calcineurin inhibitors. 

Patients and methods We included 62 renal transplant recipients and compared them with 32 pre-transplant children in this retrospective cross-sectional study. Vitamin D supplementation (either alfacalcidol or cholecalciferol) and CKD stages 4 and 5 were exclusion criteria. The participants’ median age was 12 years and they were 2- 133 (median 16.5) months post transplant at baseline. The median eGFR in the transplant group was 67 ml/min/1.73m². Sixty children were on calcineurin inhibitors.

Results In the transplant groupat baseline 56% children had 25OHD deficiency or insufficiency and 45% hyperparathyroidism defined as PTH > 7.4 pmol/l. The 1,25(OH)2D levels were higher than 150 pmol/l in 50% children. PTH inversely correlated with 25OHD levels (r=-0.29, P=0.04), but not with 1,25(OH)2D. Renal transplant recipients had higher 1,25(OH)2D levels than pre-transplant children with CKD 1-3 (P=0.02) and the daily dose of tacrolimus and cyclosporine correlated with 1,25(OH)2D levels (r 0.39, P=0.038 and r 0.6 and P= 0.039, respectively).

Conclusions In contrast with 25OHD, 1,25(OH)2 levels in post-transplant children were normal to high. 25OHD deficiency was widely prevalent among paediatric renal transplant recipients and correlated with hyperparathyroidism. This implicates the use of ergo-or cholecalciferol as first-line therapy of secondary hyperparathyroidism. The high 1,25(OH)2D levels in post transplant children can result from the interaction with calcineurin inhibitors.