1,25-Dihydroxyvitamin D(3) Therapy Is Protective for Renal Function and Prevents Hyperparathyroidism in Renal Allograft Recipients

Uyar, Murathan; Sezer, Sıren; Arat, Z.; Elsürer, Rengin; Özdemir, Fatma Nurhan; Haberal, Mehmet

doi:10.1016/j.transproceed.2006.06.051

Cited by 22 publications

(15 citation statements)

References 9 publications

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“…Calcitriol may be of particular benefit in kidney transplant recipients in whom calcitriol production by the transplanted kidney may be inadequate to suppress excess PTH secretion by hyperplastic parathyroid tissue [72]. Treatment with calcitriol may prevent hyperparathyroidism after both renal [73] and cardiac [62] transplantation. Calcitriol given during the first year after kidney transplantation was associated with an increase in LS, FN, and forearm BMD [74].…”

Section: Treatment Of Post-transplant Bone Loss With Vitamin D and Anmentioning

confidence: 99%

Vitamin D in organ transplantation

Stein

Shane

2011

Osteoporos Int

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Vitamin D deficiency is prevalent among patients with end-stage organ failure awaiting transplant. Low serum 25-hydroxyvitamin D (25-OHD) levels in these patients may be related to many disease-specific factors, as well as decreased sunlight exposure and limited intake of foods containing vitamin D. Low serum 25-OHD levels are also extremely common following solid organ transplantation, both during the immediate postoperative period and in long-term graft recipients. Demographic and lifestyle factors are important in determining D status in transplant recipients. Worse vitamin D status is associated with poorer general health, lower albumin, and even decreased survival among these patients. Although several studies have demonstrated that active forms of vitamin D and its analogues prevent bone loss following transplantation, the data do not show consistent benefit. These therapies may have particular utility after renal transplantation. However, given the narrow therapeutic window with respect to hypercalcemia and hypercalciuria, and the demonstrated efficacy of bisphosphonates to prevent post-transplantation bone loss, we regard these agents as adjunctive rather than primary therapy for transplantation osteoporosis. The effects of 1,25(OH)2D on the immune system, which are still being elucidated, may have potential for reducing infections and preventing allograft rejection after transplantation.

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Section: Treatment Of Post-transplant Bone Loss With Vitamin D and Anmentioning

confidence: 99%

Vitamin D in organ transplantation

Stein

Shane

2011

Osteoporos Int

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“…Evidence from animal studies suggests that administration of 1,25(OH) 2 D can prevent acute allograft rejection following liver [67,68], kidney [69], and heart [70] transplantation. While data from human studies are limited, kidney transplant recipients supplemented with calcitriol had fewer episodes of acute cellular rejection [71], reduced GC requirements [72], and decreased expression of costimulatory and HLA-DR molecules, suggesting a possible mechanism for allograft survival [73]. In one study, patients treated with calcitriol following heart transplantation had a reduction in their requirement for CsA [74].…”

Section: Role Of Vitamin D In Allograft Rejectionmentioning

confidence: 99%

“…Calcitriol levels may remain low for 18 months after transplantation [133]. Calcitriol production by the transplanted kidney may be inadequate to suppress PTH secretion by hyperplastic parathyroid tissue [136], and treatment with calcitriol may prevent hyperparathyroidism after renal transplantation [72]. Vitamin D deficiency is common and severe in patients after kidney transplantation [137,138].…”

Section: Bone Turnover and Mineral Metabolism After Kidney Transplantmentioning

confidence: 99%

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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“…Data from human studies are limited. In kidney transplant recipients, calcitriol supplementation was associated with fewer episodes of acute cellular rejection [10], reduced glucocorticoid requirements [11], and decreased expression of co-stimulatory and HLA-DR molecules, suggesting a possible mechanism for allograft survival [12]. Briffa et al found that patients treated with calcitriol following heart transplantation had a reduction in their requirement for cyclosporine [13].…”

Section: Role Of Vitamin D In Allograft Rejectionmentioning

confidence: 99%

“…In kidney transplant patients, calcitriol production by the transplanted kidney may be inadequate to suppress excess PTH secretion by hyperplastic parathyroid tissue [79]. Calcitriol treatment may be of particular benefit to these patients [11]. Treatment with calcitriol may prevent hyperparathyroidism after cardiac transplant as well [14].…”

Section: Treatment Of Post-transplant Bone Loss With Vitamin D and Anmentioning

confidence: 99%