Individualized Therapy to Prevent Bone Mineral Density Loss after Kidney and Kidney-Pancreas Transplantation

Abstract

Background and objectives: Most patients who undergo kidney or kidney-pancreas transplantation have renal osteodystrophy, and immediately after transplantation bone mineral density (BMD) commonly falls. Together, these abnormalities predispose to an increased fracture incidence. Bisphosphonate or calcitriol therapy can preserve BMD after transplantation, but although bisphosphonates may be more effective, they pose potential risks for adynamic bone.Design, setting, participants, & measurements: A total of 153 kidney (61%) and kidney-pancreas (39%) transplant recipients were allocated to bisphosphonate (62%) or calcitriol (38%) therapy using an algorithm that incorporated BMD, prevalent vertebral fracture, biomarkers of bone turnover, and risk factor assessment. Patients received cholecalciferol and calcium as appropriate and were followed for 12 mo.Results: Patients who were treated with bisphosphonates had lower BMD at the lumbar spine and femoral neck and longer time on dialysis. Age and gender were similar between the groups. At 12 mo, bisphosphonate-treated patients had significant BMD increases at the lumber spine and femoral neck and a negative trend at the wrist. Patients who were allocated to calcitriol, who were assessed to have lower baseline fracture risk, had no significant change in BMD at any site. At 1 yr, mean levels of bone turnover marker and intact parathyroid hormone normalized in both groups. Incident fracture rates did not differ significantly.Conclusions: With targeted treatment, BMD levels were stable or improved and bone turnover markers normalized. This algorithm provides a guide to targeting therapy after transplantation that avoids BMD loss and may reduce suppression of bone turnover.

Outcomes of bisphosphonate therapy in kidney transplant recipients: a systematic review and meta‐analysis

“…Our analysis adds to the evidence base for the safety of bisphosphonate use in kidney transplant recipients as we did not observe higher rates of allograft dysfunction or abnormalities in serum calcium levels. Clinicians should individualize decisions when considering the use of bisphosphonates in kidney transplant recipients.…”

Vitamin D in Kidney Transplant Recipients: Mechanisms and Therapy

“…4 ) [86][87][88] , thereby becoming a well-accepted preventive therapy against bone loss in KTRs with osteopenia or osteoporosis [30,89] . A clinical investigation by Gonzalez et al [74] reported that paricalcitol induced a 30% reduction of PTH levels in 78% of 58 KTRs at 24 months of follow-up, although no data were provided on the BMD trend.…”

Phosphate and FGF-23 homeostasis after kidney transplantation

“…93 Most patients who undergo kidney or kidney-pancreas transplantation exhibit renal osteodystrophy, and consequently, bone mineral density (BMD) commonly declines immediately after transplantation. 95 Post-transplantation hypophosphataemia can have a detrimental effect on bone mineralization and might contribute to impaired osteoblastogene sis and early osteoblast apoptosis, which further contributes to post-transplantation osteoporosis. 96,97 Data from bone biopsies obtained from renal transplant recipients 22-160 days after transplantation have shown that serum phosphate levels are lower in patients with early osteoblast apoptosis, with serum phosphate levels correlating positively with osteoblast number and correlating negatively with the number of apoptotic osteoblasts.…”