The Effect of Low-Dose Cholecalciferol and Calcium Treatment on Posttransplant Bone Loss in Renal Transplant Patients: A Prospective Study

Şahin, Garip; Yaşar, Necdet Fatih; Sırmagül, Başar; Bal, Cengiz; Yalçın, Ahmet

doi:10.1080/08860220802406369

Cited by 21 publications

(13 citation statements)

References 35 publications

(51 reference statements)

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“…As far as this issue is concerned, it has been hypothesized that a full vitamin D replacement could not substantially decrease PTH levels in renal transplant allografts, given the multifactorial origin of the persistent secondary hyperparathyroidism in this setting 22. In contrast, a number of perspective studies found that cholecalciferol and calcium treatment may markedly reduce PTH levels after renal transplantation 42, 43. Even if PTH‐lowering cholecalciferol effects need further evaluation, this therapy seems to be a promising option.…”

Section: Discussionmentioning

confidence: 99%

Persistent secondary hyperparathyroidism and vertebral fractures in kidney transplantation: Role of calcium-sensing receptor polymorphisms and vitamin D deficiency

Giannini

Sella

Netto

et al. 2010

Journal of Bone and Mineral Research

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Bone morbidity remains a major problem even after successful renal transplantation. We investigated the role of calcium-sensing receptor (CaSR) polymorphisms and 25-hydroxyvitamin D levels on the persistence of secondary hyperparathyroidism (SHPT) and their relationships with vertebral fractures (VFx) in 125 renal allograft recipients transplanted 44 AE 23 months before. All patients underwent evaluation of the main biochemical parameters of calcium metabolism as well as vertebral and femoral bone density. In 87 patients, CaSR polymorphisms (A986S, R990G, and Q1011E) also were assessed. X-ray images of the lateral spine were obtained in 102 subjects to perform vertebral morphometry. High parathyroid hormone (PTH) and 25-hydroxyvitamin D lower than 80 nmol/L were found in 54% and 97% of patients, respectively, with 40% of these showing vitamin D levels lower than 30 nmol/L. VFx were detected in 57% of the subjects. After multiple adjustments, 25-hydroxyvitamin D, age, and hemodialysis duration, but not CaSR polymorphisms, were found to be significant predictors of high PTH, whereas age and time since transplant were positively related with lower 25-hydroxyvitamin D values. PTH and time since transplant were significantly associated with VFx. Patients with two or more VFx showed serum PTH levels 50% higher than patients without fractures. We therefore conclude that persistent SHPT is a very common feature after renal transplantation and that, unlike CaSR polymorphisms, low 25-hydroxyvitamin D is involved in its pathogenesis. High PTH levels, in turn, are associated with an increased VFx risk, which confirms the need for strategies aimed at lowering serum PTH in this setting as well. ß

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Section: Discussionmentioning

confidence: 99%

Persistent secondary hyperparathyroidism and vertebral fractures in kidney transplantation: Role of calcium-sensing receptor polymorphisms and vitamin D deficiency

Giannini

Sella

Netto

et al. 2010

Journal of Bone and Mineral Research

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“…Several studies have also examined the influence of vitamin D or its derivatives on vaccine responses in humans, mainly conducted in immunocompromised patients, in particular patients on haemodialysis, because vitamin D deficiency is common in this group. The administration of calcitriol at a site adjacent to influenza vaccination did not enhance humoral immunity in these subjects 153 . Vitamin D‐based therapies at earlier stages of chronic kidney disease may impact the immune status of patients who progress to require dialysis or transplantation 154 .…”

Section: Further Directions and Concluding Remarksmentioning

confidence: 98%

Vitamin D3: a helpful immuno-modulator

Rosa¹,

Malaguarnera²,

Nicoletti³

et al. 2011

Immunology

384

315

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The vitamin D3 [1,25(OH) 2 D3], is a pleiotropic hormone, which regulates calcium homeostasis of the organism, induces differentiation and inhibits proliferation of various normal and cancer cells. 1 Evidence suggests different roles of vitamin D and its active metabolites in a large number of tissues. Nearly every tissue in the body has receptors for the active form of vitamin D, 1,25 dihydroxyvitamin D3 [1,25(OH) 2 D3] or calcitriol. The immunomodulatory role for 1,25(OH) 2 D3 was proposed more than 25 years ago. This latest function was essentially based on the finding that monocytes/macrophages from patients affected by the granulomatous disease sarcoidosis constitutively synthesize the active form of vitamin D3 [1,25(OH) 2 D3] from the precursor 25-hydroxyvitamin D (25OHD), as well as on the data indicating that the receptor for vitamin D (VDR) is detectable in activated, proliferating lymphocytes. 2 Nevertheless, only recently has a clearer picture of the function of 1,25(OH) 2 D3 as a determinant of immune responsiveness been obtained. The crucial role of 1,25(OH) 2 D3 in the immune system was confirmed by other evidence. First, the intracrine induction of antimicrobial activity by 1,25(OH) 2 D3 is a pivotal function of the monocyte/macrophage response to infection. Second, sub-optimal vitamin D status is a common peculiarity of many populations throughout the world, with the possible support of monocyte/macrophage metabolism of 25OHD and subsequent synthesis and action of 1,25(OH) 2 D3. 3 These observations suggested a mechanism whereby 1,25(OH) 2 D3 produced by monocytes could act upon adjacent T cells or B cells, but the consequence of such a system on normal immune regulation is still unclear. Currently, it is know that cutaneous immunity is managed by ultraviolet (UV) irradiation, which affects keratinocytes, antigen-presenting cells, such as epidermal Langerhans cells and T lymphocytes. Peripheral regulatory T cells are responsive to environmental stimuli including UV irradiation. The T-cell effector functions depend on the activation state of Langerhans cells, which can be influenced by UV irradiation. Following their encounter with exogenous antigens the epidermal Langerhans cells migrate to the skin-draining lymph nodes where they present skin-acquired antigens to naive T cells resulting in effector T-cell differentiation. Regulatory T cells induced by UV are expanded by UV-exposed cutaneous Langerhans cells. Recently, it has been shown that epidermal expression of 1,25(OH) 2 D3 connects the environment to the immune system via expansion of CD4 + CD25 +

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“…Since nutritional vitamin D supplement can provide the subst rate (25OHD) for 1,25OH2D production, the decrease in PTH level was observed after cholecalciferol 25000 IU/mo or 400 IU/d supplementation. However, the benefit of nutritional vitamin D in preservation of bone mass was inconsistent [82,83] .…”

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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The Effect of Low-Dose Cholecalciferol and Calcium Treatment on Posttransplant Bone Loss in Renal Transplant Patients: A Prospective Study

Cited by 21 publications

References 35 publications

Persistent secondary hyperparathyroidism and vertebral fractures in kidney transplantation: Role of calcium-sensing receptor polymorphisms and vitamin D deficiency

Persistent secondary hyperparathyroidism and vertebral fractures in kidney transplantation: Role of calcium-sensing receptor polymorphisms and vitamin D deficiency

Vitamin D3: a helpful immuno-modulator

Mineral and bone disorder after kidney transplantation

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