In:
Journal of the American Society of Nephrology, Ovid Technologies (Wolters Kluwer Health), Vol. 30, No. 2 ( 2019-2), p. 355-365
Kurzfassung:
How bisphosphonates affect bone quality in kidney transplant recipients is unclear. This study of 34 patients with kidney transplants randomized to receive zoledronate or no treatment for 12 months found that zoledronate did not induce adynamic bone disease; decreased bone turnover experienced by both groups was unaffected by zoledronate. Total hip and lumbar spine bone mineral density increased for both groups, especially at the lumbar spine and femoral neck in the zoledronate group. However, bone biopsies from both groups showed impaired trabecular connectivity, and high-resolution imaging detected trabecular bone loss at peripheral skeleton sites, which zoledronate partially attenuated. Because fractures in patients with transplants are most commonly peripheral fractures, bisphosphonates may be considered for patients with high fracture risk and evidence of bone loss in the peripheral skeleton at the time of transplant. Background Bone and mineral disorders commonly affect kidney transplant (KTx) recipients and have been associated with a high risk of fracture. Bisphosphonates may prevent or treat bone loss in such patients, but there is concern that these drugs might induce adynamic bone disease (ABD). Methods In an open label, randomized trial to assess the safety and efficacy of zoledronate for preventing bone loss in the first year after kidney transplant, we randomized 34 patients before transplant to receive zoledronate or no treatment. We used dual-energy x-ray absorptiometry (DXA), high-resolution peripheral quantitative computed tomography (HR-pQCT), and bone biopsies to evaluate changes in bone in the 32 evaluable participants between the time of KTx and 12 months post-transplant. Results Both groups of patients experienced decreased bone turnover after KTx, but zoledronate itself did not affect this outcome. Unlike previous studies, DXA showed no post-transplant bone loss in either group; we instead observed an increase of bone mineral density in both lumbar spine and total hip sites, with a significant positive effect of zoledronate. However, bone biopsies showed post-transplant impairment of trabecular connectivity (and no benefit from zoledronate); HR-pQCT detected trabecular bone loss at the peripheral skeleton, which zoledronate partially attenuated. Conclusions Current immunosuppressive regimens do not contribute to post-transplant central skeleton trabecular bone loss, and zoledronate does not induce ABD. Because fractures in transplant recipients are most commonly peripheral fractures, clinicians should consider bisphosphonate use in patients at high fracture risk who have evidence of significantly low bone mass at these sites at the time of KTx.
Materialart:
Online-Ressource
ISSN:
1046-6673
,
1533-3450
DOI:
10.1681/ASN.2018060656
Sprache:
Englisch
Verlag:
Ovid Technologies (Wolters Kluwer Health)
Publikationsdatum:
2019
ZDB Id:
2029124-3
