Dietary and Pharmacological Modification of Fibroblast Growth Factor-23 in Chronic Kidney Disease

Adema, Aaltje Y.; Borst, Martin H. de; Wee, Piet M. ter; Vervloet, Marc G.

doi:10.1053/j.jrn.2013.09.001

Cited by 19 publications

(13 citation statements)

References 108 publications

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“…Further, the use of multiple biomarkers of mineral metabolism may improve risk prediction and evaluation of pharmacologic and dietary interventions to reduce kidney disease risk. 37,38 …”

Section: Discussionmentioning

confidence: 99%

Biomarkers of Vitamin D Status and Risk of ESRD

Rebholz

Grams

Lutsey

et al. 2016

American Journal of Kidney Diseases

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Background Disordered mineral metabolism is characteristic of decreased kidney function. However, the prospective associations between circulating levels of vitamin D binding protein, vitamin D, and end-stage renal disease (ESRD) have not been extensively evaluated in epidemiologic studies. Study Design Nested case-control study Setting & Participants Middle-aged, black and white men and women from four US communities. Predictors Baseline levels of vitamin D binding protein, 25-hydroxyvitamin D (25(OH)D), and 1,25-dihydroxyvitamin D (1,25(OH)2D) were measured in blood samples collected at study visit 4 (1996–1998) of the Atherosclerosis Risk in Communities (ARIC) study. Outcome ESRD cases (n=184) were identified through hospitalization diagnostic codes from 1996–2008 and were frequency matched to controls (n=251) on categories of estimated glomerular filtration rate, albuminuria, diabetes mellitus, sex, and race. Measurements Logistic regression was used to estimate the association between mineral metabolism biomarkers (vitamin D binding protein, 25(OH)D, 1,25(OH)2D) and incident ESRD, adjusting for age, sex, race, estimated glomerular filtration rate, albuminuria, diabetes mellitus, hypertension, education, specimen type, and serum levels of calcium, phosphate, and parathyroid hormone. Results Higher vitamin D binding protein levels were associated with elevated risk of incident ESRD (OR, 1.76; 95% CI, 1.22–2.54; p=0.003). Higher free and bioavailable 25(OH)D levels were associated with reduced risk of incident ESRD (ORs of 0.65 [95% CI, 0.46–0.92; p=0.02] and 0.63 [95% CI, 0.43–0.91; p=0.02] for free and bioavailable 25(OH)D, respectively). There was no association between ESRD and overall 25(OH)D (OR, 0.83; 95% CI, 0.58–1.19; p=0.3) or 1,25(OH)2D (OR, 0.73; 95% CI, 0.48–1.13; p=0.2). Limitations Lack of direct measurement of free and bioavailable vitamin D. Conclusions In the general population, blood levels of vitamin D binding protein were positively associated and blood levels of free and bioavailable 25(OH)D were inversely associated with new-onset ESRD during follow-up.

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“…Further, the use of multiple biomarkers of mineral metabolism may improve risk prediction and evaluation of pharmacologic and dietary interventions to reduce kidney disease risk. 37,38 …”

Section: Discussionmentioning

confidence: 99%

Biomarkers of Vitamin D Status and Risk of ESRD

Rebholz

Grams

Lutsey

et al. 2016

American Journal of Kidney Diseases

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“…120 Dietary phosphate and sodium intake is strongly influenced by local socio-cultural habits, 123 and dietary interventions might reduce phosphate toxicity and FGF-23 levels in healthy individuals, 124 as well as in patients with CKD of all stages. 125 Careful education of patients to avoid food containing phosphate additives can result in partial correction of hyperphosphataemia, 126 as the dietary source of protein can influence phosphate homeostasis to varying degrees. 121 The phosphate source found in plants is in the form of phytic acid or phytate, which are not easily hydrolysed and are only absorbed to a limited extent in humans.…”

Section: Dietary Interventionsmentioning

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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“…Based on 2001-2014 NHANES data, the average adult consumes at least twice the recommended daily intake of phosphate 36 , whereby approximately 50% is estimated to be derived from high bioavailable inorganic food additives 37,38 . Inorganic sources, such as food additives, which are 90-100% absorbed, as compared to plant-or meat-derived phosphate, which is much lower (40-69%) 39 . These inorganic sources of phosphate are quickly absorbed, leading to a more rapid flux into the circulating pool.…”

Section: Discussionmentioning

confidence: 99%

Vascular calcification has a role in acute non-renal phosphate clearance

Turner

Lansing

Jeronimo

et al. 2020

Preprint

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BackgroundNon-renal extravasation of phosphate from the circulation and transient accumulation into tissues and extracellular fluid is a regulated process of acute phosphate homeostasis that is not well understood. Following oral consumption of phosphate, circulating levels normalize long before urinary excretion has been completed. This process is particularly critical in the setting of chronic kidney disease (CKD), where phosphate exposure is prolonged due to inefficient kidney excretion. Furthermore, CKD-associated dysregulation of mineral metabolism exacerbates pathological accumulation of phosphate causing vascular calcification (VC). In the present study, the objective was to determine whether the processes involved in the development and progression of VC are also normally involved in the systemic acute response to oral phosphate.MethodsAcute circulating and physiological phosphate movement and tissue deposition was assessed in two experimental rat models of VC using radio-labelled phosphate challenge. In an adenine-induced model of CKD, VC was induced with high dietary phosphate. Animals were euthanized 2 and 6 hours after oral consumption of radiolabelled phosphate. A non-CKD model of VC was induced with 0.5ug/kg calcitriol and then withdrawn, and radiolabelled phosphate was then given to assess for vascular preference for phosphate uptake with and without the presence of an active calcification stimulus. Samples of 50 different tissues were collected to assess tissue accumulation of de novo phosphate in response the challenges.ResultsAnimals with CKD and VC have a blunted elevation of circulating 33PO4 following oral phosphate administration and the discordant deposition can be traced to the calcifying vasculature. Deposition of de novo phosphate is present until at least 6 hours, which after active gut absorption. The accrual is stimulated by a phosphate challenge, and not present in the same degree during passive disposition of circulating phosphate. The extent of new transport to the calcifying vasculature correlates to the pre-existing burden of calcification, and can be substantially attenuated by removing the stimulus for calcification.ConclusionsOur data indicate that calcifying arteries alter the systemic disposition of a phosphate challenge and acutely deposit substantial phosphate. This study supports the importance of diet as it relates to acute fluctuations of circulating phosphate and the importance of bioavailability and meal-to-meal management in CKD patients as a mediator of cardiovascular risk.

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Dietary and Pharmacological Modification of Fibroblast Growth Factor-23 in Chronic Kidney Disease

Cited by 19 publications

References 108 publications

Biomarkers of Vitamin D Status and Risk of ESRD

Biomarkers of Vitamin D Status and Risk of ESRD

Phosphate and FGF-23 homeostasis after kidney transplantation

Vascular calcification has a role in acute non-renal phosphate clearance

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