Efficacy of low doses of pamidronate in osteopenic patients administered in the early post-renal transplant

Torregrosa, José-Vicente; Fuster, David; Monegal, Ana; Gentil, M.A.; Bravo, Juan; Guirado, Lluís; Muxí, África; Cubero, Juan José

doi:10.1007/s00198-010-1197-2

Cited by 31 publications

(37 citation statements)

References 16 publications

(21 reference statements)

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“…However, treatment is well tolerated in kidney transplant recipients with a GFR.30 ml/min per 1.73 m 2 , with no significant adverse effects compared with placebo/no treatment (30). The key RCTs using bisphosphonates in kidney transplant recipients are summarized in Table 2 (41)(42)(43)(44)(45)(46)(47)(48)(49)(50)(51)(52). Most of the studies show that bisphosphonate therapy preserves or increases BMD in the lumbar spine and femoral neck in the early post-transplantation period.…”

Section: Antiresorptive Agentsmentioning

confidence: 99%

Bone Disease after Kidney Transplantation

Bouquegneau

Salam

Delanaye

et al. 2016

CJASN

120

109

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Bone and mineral disorders occur frequently in kidney transplant recipients and are associated with a high risk of fracture, morbidity, and mortality. There is a broad spectrum of often overlapping bone diseases seen after transplantation, including osteoporosis as well as persisting high-or low-turnover bone disease. The pathophysiology underlying bone disorders after transplantation results from a complex interplay of factors, including preexisting renal osteodystrophy and bone loss related to a variety of causes, such as immunosuppression and alterations in the parathyroid hormone-vitamin D-fibroblast growth factor 23 axis as well as changes in mineral metabolism. Management is complex, because noninvasive tools, such as imaging and bone biomarkers, do not have sufficient sensitivity and specificity to detect these abnormalities in bone structure and function, whereas bone biopsy is not a widely available diagnostic tool. In this review, we focus on recent data that highlight improvements in our understanding of the prevalence, pathophysiology, and diagnostic and therapeutic strategies of mineral and bone disorders in kidney transplant recipients.

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Section: Antiresorptive Agentsmentioning

confidence: 99%

Bone Disease after Kidney Transplantation

Bouquegneau

Salam

Delanaye

et al. 2016

CJASN

120

109

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“…In previous studies, transplant recipients who were taking calcium and vitamin D achieved significantly increased BMD at the lumbar spine and femoral neck, no bone loss at the proximal femur, and decreased PTH levels compared with patients taking calcium alone or placebo [7,24]. Early bisphosphonate therapy after transplantation prevented bone loss and improved BMD, regardless of the type of bisphosphonates used, including pamidronate, alendronate, ibandronate, zoledronate, and risedronate [25][26][27][28][29]. A metaanalysis of 11 randomized controlled trials that employed bisphosphonates or active vitamin D analogues revealed that there was an increase in BMD and a significant reduction in the risk of fractures [30].…”

Section: Prevention and Treatmentmentioning

confidence: 90%

Bone disease in post-transplant patients

Jeon

Kim

Yang³

2015

Current Opinion in Endocrinology, Diabetes &Amp; Obesity

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“…In a larger, more recent study of kidney transplant recipients treated with pamidronate at months 0, 1, 4, 8, and 12, Walsh et al found that BMD improved at the LS and remained stable at the FN at 1 year in treated patients compared to controls, who had substantial losses [282]. Less frequent dosing of pamidronate (at 0 and 3 months) in renal transplant recipients reduced bone loss at the spine but not the hip in one study [283]. Aris et al, in a 2-year randomized, controlled but nonblinded trial, demonstrated that intravenous pamidronate (30 mg every 3 months) was associated with an 8% increase in both spine and hip BMD in patients who underwent lung transplantation for CF [273].…”

Section: Intravenous Pamidronatementioning

confidence: 92%

“…Intravenous pamidronate administered in repeated doses prevented bone loss at the LS and FN in kidney [271,281,283], heart [274,279], liver [284,285] and lung [273,278] transplant recipients. In a small, open but randomized clinical trial, intravenous pamidronate was administered to kidney transplant recipients at time of grafting and again 1 month later [270], completely preventing LS and FN bone loss, which fell by 6% (LS) and 9% (FN) in controls.…”

Section: Intravenous Pamidronatementioning

confidence: 97%

Osteoporosis in Organ Transplant Patients

Stein

Shane

2013

Osteoporosis

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As transplantation osteoporosis results from alterations in the bone remodeling system, a review of normal bone remodeling is helpful to understanding the pathogenesis of this disease. The bone remodeling cycle is an orderly progression of events in which old, microdamaged bone is replaced by new, mechanically stronger bone. The complete remodeling cycle at each remodeling site requires approximately 3-6 months. Bone remodeling occurs by two main processes, resorption [1] followed by formation [2], which take place on both cancellous and cortical bone surfaces. Resorption begins with activation of macrophage precursors to form osteoclasts, giant multinucleated cells that excavate a cavity on the bone surface. Osteoclasts express receptors for receptor activator of receptor activator of nuclear factor-kappaB ligand (RANKL), which is produced by osteoblasts and osteocytes, and for calcitonin, prostaglandins (PGs), calcium, and vitronectin (integrin α 1 β 3 ). Approximately 0.05 mm 3 of bone tissue is resorbed by each osteoclast, leaving small resorption pits on the bone surface called Howship's lacunae in a process that takes approximately 2-3 weeks. A brief rest period called the reversal phase follows. Next, local mesenchymal bone marrow stem cells differentiate into osteoblasts that are attracted to the empty resorption pits where they accumulate as clusters of plump cuboidal cells along the bone surface. Osteoblasts produce the collagenous and noncollagenous proteins that constitute the matrix of the newly formed bone and are responsible for mineralization of the matrix or osteoid after a period of maturation that lasts approximately 20 days. Osteoblasts express receptors for several hormones (thyroid and parathyroid hormones, estrogens, vitamin D 3 ), cell adhesion molecules (integrins), and cytokines. RANKL, receptor activator of nuclear factor-kappaB (RANK), and osteoprotegerin (OPG) are three members of the tumor necrosis factor (TNF) ligand and receptor-signaling family that are final mediators of bone resorption [3,4]. RANKL is expressed in osteoblasts, osteocytes, and bone marrow stromal cells. When sufficient concentrations of macrophage colony stimulating factor (M-CSF) are present, RANKL binds to RANK, which is expressed on the surface of osteoclast lineage cells. This binding results in rapid differentiation of osteoclast precursors in bone marrow to mature osteoclasts, increased osteoclast activity, and reduced apoptosis of mature osteoclasts. RANKL is neutralized by binding to OPG, which is secreted by cells of the osteoblast lineage. Competitive binding of RANKL to either RANK or OPG regulates bone remodeling by increasing (RANK) or decreasing (OPG) osteoclastogenesis. Immunosuppressants exert their effects on bone remodeling by interacting with the RANK/RANKL/ OPG system [5].In healthy adults, declines in bone mass as a result of remodeling imbalance occur, but are small. When bone remodeling becomes "uncoupled," such that the rate of resorption exceeds the rate of formation, bone loss will occur...

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Efficacy of low doses of pamidronate in osteopenic patients administered in the early post-renal transplant

Abstract: A low dose of pamidronate prevents bone loss in osteopenic patients when administered immediately after RT.

Cited by 31 publications

References 16 publications

Bone Disease after Kidney Transplantation

Bone Disease after Kidney Transplantation

Bone disease in post-transplant patients

Osteoporosis in Organ Transplant Patients

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