Preventing Bone Loss in Renal Transplant Recipients with Vitamin D

El‐Agroudy, Amgad E.; El-Husseini, Amr; El‐Sayed, Moharam; Ghoneim, Mohamed A.

doi:10.1097/01.asn.0000093255.56474.b4

Cited by 69 publications

(29 citation statements)

References 28 publications

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“…Consistently with these findings, our group have found that in patients randomized immediately after cardiac transplantation to 32000 IU/week of oral calcidiol for 18 months, lumbar spine BMD increased 5%, whereas those who received cyclical etidronate or nasal calcitonin, showed decreases in spine BMD (Garcia-Delgado et al, 1997). Also, alfacalcidol therapy has been associated with an increase in BMD or prevention of additional bone loss in renal (El-Agroudy et al, 2003) and cardiac recipients ( Van Cleemput et al, 1996).…”

Section: Calcidiol (25-hydroxivitamin D) and Alfacalcidol (1-hydroxisupporting

confidence: 66%

Post-Transplantation Bone Disease

Hawkins¹,

Guadalix²,

Sanchez³

et al. 2012

Osteoporosis

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Section: Calcidiol (25-hydroxivitamin D) and Alfacalcidol (1-hydroxisupporting

confidence: 66%

Post-Transplantation Bone Disease

Hawkins¹,

Guadalix²,

Sanchez³

et al. 2012

Osteoporosis

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“…De Sevaux et al (65) reported a 6-mo randomized study of 113 patients with ␣-calcidiol plus calcium that showed, as in the previous study, decreased bone loss at lumbar spine and femoral neck when compared with untreated control subjects. El-Agroudy et al (66), in another study with 40 male patients who were randomly assigned to ␣-calcidiol plus calcium or placebo, demonstrated that the bone loss that occurred during the first year after renal transplantation could be prevented by ␣-calcidiol. This same group in a recent report randomly assigned 60 adult male patients to placebo, ␣-calcidiol, oral alendronate, or intranasal salmon calcitonin and showed that all treatment groups demonstrated improvement in BMD at all sites, with decreased BMD in the control group (67).…”

Section: Use Of Vitamin D Metabolitesmentioning

confidence: 99%

Bone Disease after Renal Transplantation

Weisinger¹,

Carlini²,

Rojas³

et al. 2006

Clinical Journal of the American Society of Nephrology

125

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It has been well established that a rapid decrease in bone mineral density (BMD) occurs in the first 6 to 12 mo after a successful renal transplantation and persists, albeit at a lower rate, for many years. This rapid BMD loss significantly increases the fracture risk of these patients to levels that are even higher than those of patients who have chronic kidney disease stage 5 and are on dialysis. The presence of low BMD in renal transplant patients as a predictor of risk fracture is controversial. Indeed, as has been suggested also for patients with postmenopausal osteoporosis, there is not a compelling correlation between the decline in BMD and skeletal fractures. However, bone disease after renal transplantation probably represents a unique bone disorder that must encompass underlying renal osteodystrophy. In fact, this syndrome results from multiple factors that include pretransplantation bone status, use of glucocorticoids and other immunosuppressive drugs, hypophosphatemia, and alterations of the calcium-vitamin D axis. Recent studies have demonstrated decreased osteoblast number, reduced bone formation rate, delayed mineralization, and increased osteoblast and osteocyte apoptosis. Bisphosphonates and vitamin D metabolites may be valuable in preventing or diminishing early bone loss. However, clinicians should be careful with the use of bisphosphonates and oversuppression of bone, especially in patients with low bone turnover. New prospective, controlled trials are required to confirm the real efficacy of these drugs, particularly in long-term renal transplant patients.Clin J Am Soc Nephrol 1: 1300 -1313, 2006. doi: 10.2215/CJN.01510506 K idney, heart, lung, and liver transplantation have become fairly common and successful. As the number of transplants has grown, new challenges have arisen in the management of long-term complications of transplantation. Posttransplantation bone disease represents one such important complication, because it is observed in a substantial proportion of patients. As a consequence, bone mass loss and bone fractures are common in these patients and cause substantial morbidity.In patients with chronic kidney disease (CKD), renal osteodystrophy that begins during the early stages of the disease usually worsens during dialysis and may persist after transplantation, although in many patients, improvement in these bone lesions are observed. In addition to preexisting bone lesions, not only factors that hamper recovery but also new factors could affect bone structure after transplantation. These include the potential deleterious effects on bone of the different immunosuppressive agents, the impaired renal function that frequently is observed in renal transplant patients, and several others factors that are particular to each patient, such as postmenopausal status, presence of diabetes, gender, and time after transplantation. Changes in Bone Mineral DensityBone mineral density (BMD) as assessed by dual x-ray absorptiometry has been used as a noninvasive method to assess bone mass loss...

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“…We chose a dosage of 0.25 g twice daily on the basis of previous renal transplant studies (23,24) and studies that used calcitriol to prevent loss of BMD in other solid-organ transplants (25,26). Some subsequent renal transplant studies have used similar regimens (17,27).…”

Section: Discussionmentioning

confidence: 99%

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

Mainra

Elder

2010

Clinical Journal of the American Society of Nephrology

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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.

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Preventing Bone Loss in Renal Transplant Recipients with Vitamin D

Cited by 69 publications

References 28 publications

Post-Transplantation Bone Disease

Post-Transplantation Bone Disease

Bone Disease after Renal Transplantation

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

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