Treatment With Cinacalcet in 29 Kidney Transplant Patients With Persistent Hyperparathyroidism

López, Verónica; Toledo, Rafael; Sola, E.; Gutiérrez, Cristina; Sujan, S Sri; Rodríguez, M. Arias; Cabello, Mercedes; Burgos, D.; Molina, M. González; Hernández, Domingo

doi:10.1016/j.transproceed.2009.06.055

Cited by 31 publications

(16 citation statements)

References 6 publications

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“…As shown in some post-transplant trials cinacalcet successfully corrects elevated serum calcium and PTH levels with no negative effect on renal function,114,115,120,121 and it appears to be safe in kidney transplant recipients 117,122. A favorable effect of cinacalcet on BMD in renal transplant patients was reported by several small studies (see Table 2).…”

Section: Calcimimeticsmentioning

confidence: 78%

Management of mineral and bone disorder after kidney transplantation

Kalantar-Zadeh¹,

Molnar²,

Kövesdy³

et al. 2012

Current Opinion in Nephrology and Hypertension

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Purpose of review Mineral and bone disorders (MBD), inherent complications of moderate and advanced chronic kidney disease (CKD), occur frequently in kidney transplant recipients. However, much confusion exists about clinical application of diagnostic tools and preventive or treatment strategies to correct bone loss or mineral disarrays in transplanted patients. We have reviewed the recent evidence about prevalence and consequences of MBD in kidney transplant recipients and examined diagnostic, preventive and therapeutic options to this end. Recent findings Low turnover bone disease occurs more frequently after kidney transplantation according to bone biopsy studies. The risk of fracture is high, especially in the first several months after kidney transplantation. Alterations in minerals (calcium, phosphorus and magnesium) and biomarkers of bone metabolism (PTH, alkaline phosphatase, vitamin D and FGF-23) are observed with varying impact on post-transplant outcomes. Calcineurin inhibitors are linked to osteoporosis, whereas steroid therapy may lead to both osteoporosis and varying degrees of osteonecrosis. Sirolimus and everolimus might have a bearing on osteoblasts proliferation and differentiation or decreasing osteoclast mediated bone resorption. Selected pharmacologic interventions for treatment of MBD in transplant patients include steroid withdrawal, the use of bisphosphonates, vitamin D derivatives, calcimimetics, teriparatide, calcitonin and denosumab. Summary MBD following kidney transplantation is common and characterized by loss of bone volume and mineralization abnormalities often leading to low turnover bone disease. Although there are no well-established therapeutic approaches for management of MBD in renal transplant recipients, clinicians should continue individualizing therapy as needed.

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Section: Calcimimeticsmentioning

confidence: 78%

Management of mineral and bone disorder after kidney transplantation

Kalantar-Zadeh¹,

Molnar²,

Kövesdy³

et al. 2012

Current Opinion in Nephrology and Hypertension

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“…A similar outcome was observed in adults with TIO/TIR treated with the calcimimetic, although their serum FGF23 levels remained high [37]. In hypercalcemic kidney transplant recipients, cinacalcet lowered serum calcium and raised serum phosphate levels [61,81]. By minimizing PTH-mediated phosphaturia and modestly reducing FGF23, cinacalcet might be an option in some post-renal transplant patients with hypophosphatemia, but its long-term efficacy and safety, particularly in children, has not been established.…”

Section: Treatmentmentioning

confidence: 65%

Clinical practice

Alon

2010

Eur J Pediatr

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Until a decade ago, two main hormones were recognized as directly affecting phosphate homeostasis and, with that, bone metabolism: parathyroid hormone and 1,25(OH)(2) vitamin D (calcitriol). It was only a decade ago that the third major player hormone was found, linking gut, bone, and kidney. The physiologic role of fibrinogen growth factor (FGF)23 is to maintain serum phosphate concentration within a narrow range. Secreted from osteocytes, it modulates kidney handling of phosphate reabsorption and calcitriol production. Genetic and acquired abnormalities in FGF23 structure and metabolism cause conditions of either hyper-FGF23-manifested by hypophosphatemia, low serum calcitriol, and rickets/osteomalacia-or hypo-FGF23, expressed by hyperphosphatemia, high serum calcitriol, and extra-skeletal calcifications. In patients with chronic renal failure, FGF23 levels increase as kidney functions deteriorate and are under investigation to learn if the hormone actually participates in the pathophysiology of the deranged bone and mineral metabolism typical for these patients and, if so, whether it might serve as a therapeutic target. This review addresses the physiology and pathophysiology of FGF23 and its clinical applications.

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“…However, its use in kidney transplant recipients remains off-label. Several prospective [15][16][17][18][19][20][21][22][23][24][25][26][27][28][29][30] and retrospective [31][32][33][34][35][36][37][38][39][40][41] observational cohort studies have examined the potential effects of cinacalcet in kidney transplant recipients. Most of these studies have included small cohorts with short follow-up periods, whereas only 4 studies have reported follow-up of greater than 3 years.…”

Section: Discussionmentioning

confidence: 99%

Untitled

Zavvos

Fyssa²,

Papasotiriou³

et al. 2018

Exp Clin Transplant

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Objectives: Persistent secondary hyperparathyroidism is common after successful kidney transplant, with concomitant hypercalcemia and hypophosphatemia potentially leading to reduced graft survival and increased cardiovascular risk. Cinacalcet, a calcimimetic agent that activates the calcium-sensing receptors in parathyroid glands, is a therapeutic option. In this study, we assessed the long-term treatment effects of cinacalcet for a period of up to 5 years in a cohort of kidney transplant recipients. Key words: Hypophosphatemia, Kidney function, Renal transplant IntroductionSecondary hyperparathyroidism is a frequent complication of end-stage renal disease. After successful kidney transplant, secondary hyperparathyroidism usually remits; however, it persists in 30% to 50% of patients 1 year after transplant. [1][2][3] Risk factors for the development of persistent secondary hyperparathyroidism after kidney transplant include the duration of renal replacement therapy and the severity of secondary hyperparathyroidism before transplant. 1,4 In kidney transplant recipients, persistent secondary hyperparathyroidism is characterized by elevated serum parathyroid hormone (PTH) and/or hypercalcemia and hypophosphatemia. 2,5 Parathyroid hormone increases bone resorption, inhibits fractional renal calcium excretion, and promotes calcitriol production by the kidney allograft. Calcitriol, in turn, increases calcium absorption from the intestinal tract.

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Treatment With Cinacalcet in 29 Kidney Transplant Patients With Persistent Hyperparathyroidism

Cited by 31 publications

References 6 publications

Management of mineral and bone disorder after kidney transplantation

Management of mineral and bone disorder after kidney transplantation

Clinical practice

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