Tertiary ‘Hyperphosphatoninism’ Accentuates Hypophosphatemia and Suppresses Calcitriol Levels in Renal Transplant Recipients

Evenepoel, Pieter; Naesens, Maarten; Claes, Kathleen; Kuypers, Dirk; Vanrenterghem, Yves

doi:10.1111/j.1600-6143.2007.01753.x

Cited by 145 publications

(160 citation statements)

References 41 publications

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“…This observation strengthens the notion of inappropriate hyperphosphatoninism in the early posttransplant period as put forward in previous reports (3,4). After M3, however, FGF-23 levels showed a further decline to reach concentrations at M12 that were similar to those of CKD counterparts.…”

Section: Discussionsupporting

confidence: 73%

See 1 more Smart Citation

Recovery of Hyperphosphatoninism and Renal Phosphorus Wasting One Year after Successful Renal Transplantation

Evenepoel¹,

Meijers²,

Jonge³

et al. 2008

Clinical Journal of the American Society of Nephrology

135

113

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Section: Discussionsupporting

confidence: 73%

“…Persistence of inappropriately high serum levels of fibroblast growth factor-23 (FGF-23), a recently discovered phosphaturic hormone, plays an important role in the pathogenesis of this complication (3,4).…”

mentioning

confidence: 99%

Recovery of Hyperphosphatoninism and Renal Phosphorus Wasting One Year after Successful Renal Transplantation

Evenepoel¹,

Meijers²,

Jonge³

et al. 2008

Clinical Journal of the American Society of Nephrology

135

113

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“…It promotes renal phosphate wasting through internalization of the sodium phosphate cotransporter IIa and IIc from the proximal tubular apical membrane. By month 3 after successful renal transplantation, FGF-23 levels were shown to remain elevated in the majority of patients, despite a 95% decrease from pretransplant levels (6). Moreover, increased FGF-23 levels, but not PTH levels, were independently associated with the serum phosphate nadir and increased phosphate wasting (6).…”

Section: Discussionmentioning

confidence: 99%

“…It is recognized that both hypophosphatemia and renal phosphate wasting may have a detrimental impact on bone mineralization (3,4). We and others recently reported that renal phosphate wasting in the post-transplant period is caused, at least partly, by the persistence of inappropriately high levels of fibroblast growth factor 23 (FGF-23) (5,6). This condition is often referred to as "tertiary hyperphosphatoninism."…”

mentioning

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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“…Après transplantation rénale, il n'est pas rare d'observer une hypophosphatémie en l'absence d'hyperparathyroïdie. Ces anomalies pourraient être liées à une hypersécrétion de FGF23 persistant de façon autonome au-delà de la dialyse [38], et définissant un tableau d'hyperphosphatémie autonomisé. Il n'existe pas de données chez l'homme suggérant que la surexpression de Klotho puisse protéger contre la dégradation de la fonction rénale, mais dans un modèle murin de glomérulonéphrite, Klotho diminue la sévérité des lésions rénales et l'altération du débit de filtration glomérulaire [39].…”

Section: Implication Du Fgf23 Et De Klotho Dans Des Pathologies Humaiunclassified

Le facteur de croissance des fibroblastes 23 et son récepteur Klotho

Prié

Torres²,

Friedlander

2009

Med Sci (Paris)

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Tertiary ‘Hyperphosphatoninism’ Accentuates Hypophosphatemia and Suppresses Calcitriol Levels in Renal Transplant Recipients

Cited by 145 publications

References 41 publications

Recovery of Hyperphosphatoninism and Renal Phosphorus Wasting One Year after Successful Renal Transplantation

Recovery of Hyperphosphatoninism and Renal Phosphorus Wasting One Year after Successful Renal Transplantation

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

Le facteur de croissance des fibroblastes 23 et son récepteur Klotho

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