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

Kanaan, Nada; Claes, Kathleen; Devogelaer, Jean‐Pierre; Vanderschueren, Dirk; Depresseux, Geneviève; Goffin, Éric; Evenepoel, Pieter

doi:10.2215/cjn.00950110

Cited by 41 publications

(20 citation statements)

References 31 publications

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“…We have no bone biopsies to confirm the diagnosis, and thus, no definite conclusions can be drawn from this observation. Evenepoel et al [18] showed that low levels of iPTH and high levels of fibroblast growth factor 23 are associated with post-transplant bone mineral density loss [23] which suggests a higher risk of fractures for these patients.…”

Section: Discussionmentioning

confidence: 99%

Early Development of Secondary Hyperparathyroidism following Renal Transplantation

Isaksson

Sterner²

2012

Nephron Clin Pract

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Background: Optimal levels of intact parathyroid hormone (iPTH) in the post-transplant period are not known due to insufficient data. Therefore, we aimed to describe secondary hyperparathyroidism (SHPT) in Swedish renal transplant (RT) recipients and also report events of fractures and vascular events potentially related to levels of iPTH. Methods: Medical charts from 132 RT recipients were retrospectively reviewed. Laboratory/clinical data were obtained at regular points up to 12 months post RT. Three groups were created based on pre-RT levels of iPTH based on KDOQI recommended levels of iPTH in CKD 5. Results: One year post RT 69% had iPTH above levels recommended by KDOQI. A multiple regression analysis showed a strong relation between pre-transplant iPTH levels and iPTH levels at 12 months (β coefficient = 0.323, p < 0.001). Patients with low pre-transplant levels of iPTH had a higher rate of fractures during follow up compared to patients with higher pre-transplant levels of iPTH had a higher rate of fratures during follow-up compared to patients with higher pre-transplant levels of iPTH (p = 0.034). Conclusion: SHPT is common in Swedish RT recipients. Pre-transplant regulation of SHPT is of great importance to determine outcome post RT. Low levels of iPTH in the pre-transplant period could be associated with a high risk of fracture in the first post-transplant year.

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Section: Discussionmentioning

confidence: 99%

Early Development of Secondary Hyperparathyroidism following Renal Transplantation

Isaksson

Sterner²

2012

Nephron Clin Pract

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“…The relationships between FGF-23/ Klotho levels and bone mineral density (BMD) have been analysed in several studies, but fi ndings show either a weak relationship with BMD [23,24] or no relationship at all [25]. On the contrary, several studies have reported close relationships between FGF-23 and vascular risk, as commented later.…”

Section: Fgf-23-α Klotho Axismentioning

confidence: 99%

Alcoholism, Fibroblast Growth Factor 23 and Cardiovascular Risk

González‐Reimers¹,

Quintero-Platt²,

Martín-González³

et al. 2017

Arch Clin Hypertens

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Background: Bone metabolism is tightly regulated by several hormones that are synthesized in bone cells and that have effects not only on bone but on several distant organs. These hormones are involved in intermediate metabolism and modulate fatty acid transport, playing a role in insulin resistance, liver steatosis, atherosclerosis and cardiovascular risk. Aims:We review the association of fi broblast growth factor-23 (FGF-23) and α-Klotho with cardiovascular risk, especially in the alcoholic patient.Results: High levels of FGF-23 are associated with vascular risk, especially with vascular calcifi cations, hypertension, or left ventricular hypertrophy.Main Findings: Hyperphosphatemia constitutes a major stimulus for FGF-23 secretion, together with infl ammation and reduced iron availability, either by iron defi ciency or by iron sequestration in infl ammatory diseases. FGF-23 can be expressed by the damaged liver. Alcoholism is a proinfl ammatory condition, and in alcoholics there is an increased cardiovascular risk. Preliminary data suggest that FGF-23 is raised in alcoholics. Conclusion:Increased FGF-23 levels have been described in association with hypertension, arterial wall calcifi cation, left ventricular hypertrophy and increased cardiovascular mortality, both in patients with or without chronic kidney disease. Some data suggest that FGF-23 is also related to increased vascular risk in alcoholics.Brief Summary FGF-23 is an osteocyte derived molecule related to cardiovascular risk. Hyperphosphatemia is a major trigger mechanism for its secretion, but infl ammatory conditions are also associated with increased FGF-23 production. Some data suggest that FGF-23 may be also related with the increased vascular risk observed in chronic alcoholic patients.

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“…Kanaan and associates performed a two-center observational retrospective cohort study in 127 renal transplant recipients and found that patients with high serum FGF23 levels and/or low PTH levels at time of transplant are at risk for increased BMD loss during the first year posttransplant. 47 Fernandez and associates explored circulating FGF23 in association with fatness and insulin sensitivity, atherosclerosis, and BMD in 2 cohort studies and concluded that the associations between circulating FGF23 concentrations and glucose metabolism, BMD, and atherosclerosis are dependent on iron and obesity status-associated insulin resistance. 48 Fibroblast growth factor 23 and allograft outcomes Allograft and patient survival rates have improved steadily over the past decades as a result of advances in surgical techniques, immunosuppressive regimens, and prophylaxis against opportunistic infections.…”

Section: Bone Mineral Loss After Renal Transplantmentioning

confidence: 99%

Untitled

2016

Exp Clin Transplant

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Fibroblast growth factor 23 is likely to be the most important regulator of phosphate homeostasis, which mediates its functions through fibroblast growth factor receptors and the coreceptor Klotho. In addition to reducing expression of the sodium-phosphate cotransporters NPT2a and NPT2c in the proximal tubules, fibroblast growth factor 23 inhibits renal 1α-hydroxylase and stimulates 24-hydroxylase and appears to reduce parathyroid hormone secretion in short-term studies. Fibroblast growth factor 23 synthesis and secretion by osteocytes and osteoblasts are upregulated through 1,25-dihydroxyvitamin D3 and through an increased dietary phosphate intake. Recent studies have indicated that a low-protein diet and calcium deficiency reduce circulating fibroblast growth factor 23 levels, but magnesium deficiency increases fibroblast growth factor levels. Drugs such as phosphate binders, bisphosphonate, and estrogens have various effects on circulating fibroblast growth factor 23 levels. The high cardiovascular disease event rates and mortality associated with elevated levels of this hormone may be due to various effects on the cardiovascular system, including left ventricular hypertrophy, arterial stiffness, vascular calcifications, endothelial dysfunction, and increased levels of inflammatory markers. In addition, elevated levels of this hormone may contribute to mineral bone metabolism disorders and to patient and allograft survival after renal transplant. Here, we discuss the effects of fibroblast growth factor 23 on adverse renal, bone, and cardiovascular outcomes after kidney transplant.

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

Cited by 41 publications

References 31 publications

Early Development of Secondary Hyperparathyroidism following Renal Transplantation

Early Development of Secondary Hyperparathyroidism following Renal Transplantation

Alcoholism, Fibroblast Growth Factor 23 and Cardiovascular Risk

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