Calcium and Calcitriol Prophylaxis Attenuates Posttransplant Bone Loss

Josephson, Michelle A.; Schumm, L. Philip; Chiu, May; Marshall, Cory F.; Thistlethwaite, J. Richard; Sprague, Stuart M.

doi:10.1097/01.tp.0000137937.44703.42

Cited by 89 publications

(39 citation statements)

References 13 publications

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“…Our results showed that both groups improved BMD during the study period (0.5% for placebo and 1.5% for ibandronate). More recent publications of prospective trials have indeed reported bone loss of only 0.1-5.7% in the lumbar spine (20)(21)(22). Number (%) of subjects experienced any such event, unless otherwise specified, with p-value for difference between groups analyzed with a chi-square test ( 1 Fishers exact test).…”

Section: Discussionmentioning

confidence: 99%

A 1-Year Randomized, Double-Blind, Placebo-Controlled Study of Intravenous Ibandronate on Bone Loss Following Renal Transplantation

Smerud

Dolgos

Olsen

et al. 2012

American Journal of Transplantation

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The clinical profile of ibandronate as add-on to calcitriol and calcium was studied in this double-blind, placebo-controlled trial of 129 renal transplant recipients with early stable renal function (≤ 28 days posttransplantation, GFR ≥ 30 mL/min). Patients were randomized to receive i.v. ibandronate 3 mg or i.v. placebo every 3 months for 12 months on top of oral calcitriol 0.25 mcg/day and calcium 500 mg b.i.d. At baseline, 10 weeks and 12 months bone mineral density (BMD) and biochemical markers of bone turnover were measured. The primary endpoint, relative change in BMD for the lumbar spine from baseline to 12 months was not different, +1.5% for ibandronate versus +0.5% for placebo (p = 0.28). Ibandronate demonstrated a significant improvement of BMD in total femur, +1.3% versus −0.5% (p = 0.01) and in the ultradistal radius, +0.6% versus −1.9% (p = 0.039). Bone formation markers were reduced by ibandronate, whereas the bone resorption marker, NTX, was reduced in both groups. Calcium and calcitriol supplementation alone showed an excellent efficacy and safety profile, virtually maintaining BMD without any loss over 12 months after renal transplantation, whereas adding ibandronate significantly improved BMD in total femur and ultradistal radius, and also suppressed biomarkers of bone turnover. Ibandronate was also well tolerated.

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Section: Discussionmentioning

confidence: 99%

A 1-Year Randomized, Double-Blind, Placebo-Controlled Study of Intravenous Ibandronate on Bone Loss Following Renal Transplantation

Smerud

Dolgos

Olsen

et al. 2012

American Journal of Transplantation

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“…Calcitriol can also prevent bone loss especially during the first year after trans plantation [76,77] . Similar to calcitriol, oral alfacalcidol can lower PTH and improve BMD in KT recipients [78,79] .…”

Section: Vitamin Dmentioning

confidence: 99%

Mineral and bone disorder after kidney transplantation

Taweesedt

Disthabanchong

2015

WJT

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After successful kidney transplantation, accumulated waste products and electrolytes are excreted and regulatory hormones return to normal levels. Despite the improvement in mineral metabolites and mineral regulating hormones after kidney transplantation, abnormal bone and mineral metabolism continues to present in most patients. During the first 3 mo, fibroblast growth factor-23 (FGF-23) and parathyroid hormone levels decrease rapidly in association with an increase in 1,25-dihydroxyvitamin D production. Renal phosphate excretion resumes and serum calcium, if elevated before, returns toward normal levels. FGF-23 excess during the first 3-12 mo results in exaggerated renal phosphate loss and hypophosphatemia occurs in some patients. After 1 year, FGF-23 and serum phosphate return to normal levels but persistent hyperparathyroidism remains in some patients. The progression of vascular calcification also attenuates. High dose corticosteroid and persistent hyperparathyroidism are the most important factors influencing abnormal bone and mineral metabolism in long-term kidney transplant (KT) recipients. Bone loss occurs at a highest rate during the first 6-12 mo after transplantation. Measurement of bone mineral density is recommended in patients with estimated glomerular filtration rate > 30 mL/min. The use of active vitamin D with or without bisphosphonate is effective in preventing early post-transplant bone loss. Steroid withdrawal regimen is also beneficial in preservation of bone mass in long-term. Calcimimetic is an alternative therapy to parathyroidectomy in KT recipients with persistent hyperparathyroidism. If parathyroidectomy is required, subtotal to near total parathyroidectomy is recommended. Performing parathyroidectomy during the waiting period prior to transplantation is also preferred in patients with severe hyperparathyroidism associated with hypercalcemia.

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“…Torres et al (68) showed that therapy with calcium supplements during 1 yr, plus intermittent calcitriol (0.5 g/d) for 3 mo, prevented bone loss at the proximal femur and decreased PTH levels more rapidly than calcium supplementation alone. Josephson et al (69) performed a prospective, randomized, double-blind study to determine whether calcium and calcitriol prevent posttransplantation bone loss. Sixty-four patients who did not have previous steroid exposure and were undergoing their first kidney or kidney-pancreas transplant were randomly assigned to calcium, calcium plus calcitriol, or placebo.…”

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

124

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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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Calcium and Calcitriol Prophylaxis Attenuates Posttransplant Bone Loss

Cited by 89 publications

References 13 publications

A 1-Year Randomized, Double-Blind, Placebo-Controlled Study of Intravenous Ibandronate on Bone Loss Following Renal Transplantation

A 1-Year Randomized, Double-Blind, Placebo-Controlled Study of Intravenous Ibandronate on Bone Loss Following Renal Transplantation

Mineral and bone disorder after kidney transplantation

Bone Disease after Renal Transplantation

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