Early Bone Mineral Density Loss after Renal Transplantation and Pre-Transplant PTH: A Prospective Study

Bubenícek, P; Sotorník, I; Vı́tko, Štefan; Teplan, Vladimı́r

doi:10.1159/000137287

Cited by 10 publications

(6 citation statements)

References 46 publications

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“…Another important complication for patients with tertiary HPT is bone disease. The rate of osteoporosis is high in patients with a renal transplant, and tertiary HPT is associated with an increased risk of osteoporosis, and a major risk for fractures. Small trials have suggested that parathyroidectomy increases bone mineral density, in contrast to cinacalcet.…”

Section: Discussionmentioning

confidence: 99%

Systematic review of surgical and medical treatment for tertiary hyperparathyroidism

Dulfer

Franssen

Hesselink

et al. 2017

British Journal of Surgery

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Section: Discussionmentioning

confidence: 99%

Systematic review of surgical and medical treatment for tertiary hyperparathyroidism

Dulfer

Franssen

Hesselink

et al. 2017

British Journal of Surgery

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“…Previous studies have yielded conflicting data on the significance of pretransplant PTH levels as a predictor of posttransplant BMD loss: both high (20,(27)(28)(29) and low (15) pretransplant PTH levels have been correlated with BMD loss. Similar to FGF-23, pretransplant PTH levels are directly associated with post-transplant levels (7).…”

Section: Discussionmentioning

confidence: 99%

Fibroblast Growth Factor-23 and Parathyroid Hormone Are Associated with Post-Transplant Bone Mineral Density Loss

Kanaan¹,

Claes²,

Devogelaer

et al. 2010

Clinical Journal of the American Society of Nephrology

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Background and objectives: Among the multiple factors contributing to bone mineral density (BMD) loss after renal transplantation, hypophosphatemia is increasingly recognized to play an important role. Hypophosphatemia occurs in up to 90% of the renal transplant recipients in the early post-transplant period and is caused by renal phosphate wasting. We hypothesized that a high pretransplant level of the recently described phosphaturic hormone fibroblast growth factor 23 (FGF-23) is a risk factor for accelerated BMD loss occurring within the first post-transplant year.Design, setting, participants, & measurements: We performed a two-center observational retrospective cohort study in 127 incident renal transplant recipients. Serum full-length FGF-23, parathyroid hormone (PTH), and parameters of mineral metabolism were determined at the time of transplantation. BMD was assessed by osteodensitometry at the time of transplantation and 1 year later.Results: A moderate decrease of BMD was observed during the first post-transplant year. High FGF-23 levels were associated with BMD loss at the lumbar spine and total hip region, whereas low PTH levels were associated with BMD loss at all three regions. Cumulative doses of prednisone and post-transplant serum phosphate level were not correlated with BMD changes.Conclusion: Our data indicate that patients with a high serum FGF-23 level and/or a low PTH level at the time of transplantation are at risk for increased BMD loss during the first post-transplant year.

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“…99 The disturbed bone mineralization observed in renal transplant recipients might be in part the result of post-transplantation hypophosphataemia and/or dysregulated FGF-23, independent of serum phosphate. Sustained or re-developed hyperparathyroidism after kidney transplantation might also be associated with bone alterations, although data are conflicting as to whether high pre-transplantation PTH levels can 103,104 or can not 105 predict the loss of BMD, and as previously discussed, low levels of PTH following transplantation are associated with a lower BMD. 98 Persistent hyperparathyroidism after kidney transplantation is associated with hypercalcaemia and hypophosphataemia, which may be effectively corrected with cinacalcet-a calcimimetic.…”

Section: Kidney Transplantationmentioning

confidence: 99%

Phosphate and FGF-23 homeostasis after kidney transplantation

Baia

Heilberg²,

Navis

et al. 2015

Nat Rev Nephrol

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Dysregulated phosphate metabolism is a common consequence of chronic kidney disease, and is characterized by a high circulating level of fibroblast growth factor (FGF)-23, hyperparathyroidism, and hyperphosphataemia. Kidney transplantation can elicit specific alterations to phosphate metabolism that evolve over time, ranging from severe hypophosphataemia (<0.5 mmol/l) to hyperphosphataemia (>1.50 mmol/l) and high FGF-23 levels. The majority of renal transplant recipients develop hypophosphataemia during the first 3 months after transplantation as a consequence of relatively slow adaptation of FGF-23 and parathyroid hormone levels to restored renal function, and the influence of immunosuppressive drugs. By 3-12 months after transplantation, phosphate homeostasis is at least partially restored in the majority of recipients, which is paralleled by a substantially reduced risk of cardiovascular-associated morbidity and mortality compared with the pre-transplantation setting. Many renal transplant recipients, however, exhibit persistent abnormalities in phosphate homeostasis, which is often due to multifactorial causes, and may contribute to adverse outcomes on the cardiovascular system, kidney, and bone. Dietary and pharmacologic interventions might improve phosphate homeostasis in renal transplant recipients, but additional insight into the pathophysiology of transplantation-associated abnormalities in phosphate homeostasis is needed to further optimize disease management and improve prognosis for renal transplant recipients.

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Early Bone Mineral Density Loss after Renal Transplantation and Pre-Transplant PTH: A Prospective Study

Cited by 10 publications

References 46 publications

Systematic review of surgical and medical treatment for tertiary hyperparathyroidism

Systematic review of surgical and medical treatment for tertiary hyperparathyroidism

Fibroblast Growth Factor-23 and Parathyroid Hormone Are Associated with Post-Transplant Bone Mineral Density Loss

Phosphate and FGF-23 homeostasis after kidney transplantation

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