Secondary hyperparathyroidism contributes to post-transplant CKD
mineral and bone disorder.
Paricalcitol, a selective
vitamin D receptor activator, decreased serum
parathyroid hormone levels and
proteinuria in patients with
secondary hyperparathyroidism. This single-center, prospective, randomized, crossover, open-label study compared the effect of 6-month treatment with
paricalcitol (1 μg/d for 3 months and then uptitrated to 2 µg/d if tolerated) or nonparicalcitol
therapy on serum
parathyroid hormone levels (primary outcome),
mineral metabolism, and
proteinuria in 43 consenting recipients of renal transplants with
secondary hyperparathyroidism. Participants were randomized 1:1 according to a computer-generated sequence. Compared with baseline, median (interquartile range) serum
parathyroid hormone levels significantly declined on
paricalcitol from 115.6 (94.8-152.0) to 63.3 (52.0-79.7) pg/ml (P<0.001) but not on nonparicalcitol
therapy. At 6 months, levels significantly differed between treatments (P<0.001 by analysis of covariance). Serum bone-specific
alkaline phosphatase and
osteocalcin decreased on
paricalcitol therapy only and significantly differed between treatments at 6 months (P<0.001 for all comparisons). At 6 months, urinary
deoxypyridinoline-to-
creatinine ratio and 24-hour
proteinuria level decreased only on
paricalcitol (P<0.05). L3 and L4 vertebral
mineral bone density, assessed by dual-energy x-ray absorption, significantly improved with
paricalcitol at 6 months (P<0.05 for both densities).
Paricalcitol was well tolerated. Overall, 6-month
paricalcitol supplementation reduced
parathyroid hormone levels and
proteinuria, attenuated bone remodeling and
mineral loss, and reduced eGFR in renal transplant recipients with
secondary hyperparathyroidism. Long-term studies are needed to monitor directly measured GFR, ensure that the bone remodeling and
mineral effects are sustained, and determine if the reduction in
proteinuria improves renal and cardiovascular outcomes.