Phosphatemic Effect of Cinacalcet in Kidney Transplant Recipients With Persistent Hyperparathyroidism

Serra, Andreas L.; Wuhrmann, Claudia; Wüthrich, Rudolf P.

doi:10.1053/j.ajkd.2008.08.012

Cited by 41 publications

(24 citation statements)

References 28 publications

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“…Consequently, hypophosphatemia is observed in up to 90% of incident renal transplant recipients in the early posttransplant period (5,12). Persistent increases in fibroblast growth factor-23 (FGF-23), a phosphaturic hormone, are also thought to contribute to the development of hypophosphatemia after renal transplantation (13,14). Although the prevalence of abnormal levels of PTH, calcium and phosphorus tend to diminish over time, disordered mineral metabolism may persist in some patients for many years after successful renal transplantation.…”

Section: Introductionmentioning

confidence: 99%

A Randomized Study Evaluating Cinacalcet to Treat Hypercalcemia in Renal Transplant Recipients With Persistent Hyperparathyroidism

Evenepoel

Cooper

Holdaas

et al. 2014

American Journal of Transplantation

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Persistent hyperparathyroidism (HPT) after kidney transplantation (KTx) is associated with hypercalcemia, hypophosphatemia and abnormally high levels of parathyroid hormone (PTH). In this randomized trial, cinacalcet was compared to placebo for the treatment of hypercalcemia in adult patients with persistent HPT after KTx. Subjects were randomized 1:1 to cinacalcet or placebo with randomization stratified by baseline corrected total serum calcium levels ( 11.2 mg/dL [2.80 mmol/L] or >11.2 mg/dL [2.80 mmol/L]). The primary end point was achievement of a mean corrected total serum calcium value <10.2 mg/dL (2.55 mmol/L) during the efficacy period. The two key secondary end points were percent change in bone mineral density (BMD) at the femoral neck and absolute change in phosphorus; 78.9% cinacalcetversus 3.5% placebo-treated subjects achieved the primary end point with a difference of 75.4% (95% confidence interval [CI]: 63.8, 87.1), p < 0.001. There was no statistical difference in the percent change in BMD at the femoral neck between cinacalcet and placebo groups, p ¼ 0.266. The difference in the change in phosphorus between the two arms was 0.45 mg/dL (95% CI: 0.26, 0.64), p < 0.001 (nominal). No new safety signals were detected. In conclusion, hypercalcemia and hypophosphatemia were effectively corrected after treatment with cinacalcet in patients with persistent HPT after KTx.

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Section: Introductionmentioning

confidence: 99%

A Randomized Study Evaluating Cinacalcet to Treat Hypercalcemia in Renal Transplant Recipients With Persistent Hyperparathyroidism

Evenepoel

Cooper

Holdaas

et al. 2014

American Journal of Transplantation

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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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“…This effect was associated with a marked decrease in PTH phosphaturic activity rather than a decrease in levels of FGF-23, which remained almost unchanged after treatment. 5 Serum phosphorus is regulated not only by renal reabsorption, but also by the interaction between renal absorption and exchange with bone. Release of phosphorus from the bone occurs as a consequence of calcium homeostasis and is accompained by movement of calcium in the same direction.Given the calcium-lowering effect of cinacalcet, the phosphatemic action of cinacalcet in KTx is less likely to depend on a substantial release of phosphorus from the bone.…”

Section: Discussionmentioning

confidence: 99%

Persistent hypophosphathemia recovered with cinacalcet in a late renal transplanted patient

2011

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Renal transplant recipients with secondary hyperparathyroidism often have hypophosphatemia that can persist for years. We report the case of a renal transplanted patient with normal allograft function showing persistent hypophosphoremia due to secondary hyperparathyroidism despite treatment with oral supplements of phosphorus and calcitriol. After initiation of treatment with cinacalcet, a normalization of serum phosphorus was rapidly achieved, and phosphorus supplementation was not necessary. Renal function remained stable. Dial. Transplant. © 2011 Wiley Periodicals, Inc.

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Phosphatemic Effect of Cinacalcet in Kidney Transplant Recipients With Persistent Hyperparathyroidism

Cited by 41 publications

References 28 publications

A Randomized Study Evaluating Cinacalcet to Treat Hypercalcemia in Renal Transplant Recipients With Persistent Hyperparathyroidism

A Randomized Study Evaluating Cinacalcet to Treat Hypercalcemia in Renal Transplant Recipients With Persistent Hyperparathyroidism

Clinical practice

Persistent hypophosphathemia recovered with cinacalcet in a late renal transplanted patient

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