Acute High Phosphate Intake Impairs Endothelial‐Dependent Vasodilation in Young Premenopausal Women

2020 ◽  
Vol 34 (S1) ◽  
pp. 1-1
Author(s):  
Brandi Stephens ◽  
Damsara Nandadeva ◽  
Jasdeep Kaur ◽  
Thales C. Barbosa ◽  
Paul J. Fadel
Keyword(s):  
Premenopausal Women ◽  
Phosphate Intake ◽  
High Phosphate

Studies in Hypophosphatasia and Response to High Phosphate Intake

1968 ◽  
Vol 225 (3) ◽  
pp. 163-170 ◽  
Author(s):  
A. M. Bongiovanni ◽  
M. M. Album ◽  
A. W. Root ◽  
J. W. Hope ◽  
J. Marino ◽  
...  
Keyword(s):  
Phosphate Intake ◽  
High Phosphate

scholarly journals Phosphate and Kidney Healthy Aging

2020 ◽  
Vol 45 (6) ◽  
pp. 802-811
Author(s):  
Isabel Rubio-Aliaga
Keyword(s):  
Healthy Aging ◽  
Kidney Injury ◽  
Serum Phosphate ◽  
Processed Food ◽  
Phosphate Intake ◽  
Risks Factors ◽  
Phosphate Source ◽  
Diabetes And Obesity ◽  
Aging Kidney ◽  
High Phosphate

<b><i>Background:</i></b> The aging population is increasing rapidly, much faster than our understanding on how to promote healthy aging free of multimorbidities. The aging kidney shows a decline in its function. Whether this decline is preventable or physiological is still debated. Main risks factors for developing CKD are aging common comorbidites, such as hypertension, diabetes, and obesity. Phosphate is vital for our organism, but it is also present in a great variety of food products as food additive and preservative. Due to the higher consumption of processed food in the last century, concern has arisen if a chronic high consumption of phosphate may be toxic impacting on healthy aging. <b><i>Summary:</i></b> Several studies show an association between higher serum phosphate levels and a higher risk of overall mortality and cardiovascular disease. Moreover, higher phosphate levels also worsen CKD progression and may contribute to renal dysfunction in healthy individuals. Acute high phosphate intake is rare but can cause acute kidney injury. Yet, the question if controlling phosphate intake may modulate serum phosphate concentrations remains unanswered, as assessment of phosphate intake is still a difficult task. Phosphate consumption estimations by dietary recalls are largely underestimated, especially in populations groups consuming high amount of processed food. <b><i>Key Message:</i></b> A healthy diet with phosphate source from food may contribute to promote healthy aging and longevity.

scholarly journals High-calcium vs high-phosphate intake and small artery tone in advanced experimental renal insufficiency

2006 ◽  
Vol 21 (10) ◽  
pp. 2754-2761 ◽  
Author(s):  
Peeter Kööbi ◽  
Tuija I. Vehmas ◽  
Pasi Jolma ◽  
Jarkko Kalliovalkama ◽  
Meng Fan ◽  
...  
Keyword(s):  
Renal Insufficiency ◽  
Small Artery ◽  
Phosphate Intake ◽  
High Calcium ◽  
High Phosphate

Adaptation of deep and superficial nephrons to changes in dietary phosphate intake

1983 ◽  
Vol 244 (3) ◽  
pp. F265-F269 ◽  
Author(s):  
A. Haramati ◽  
J. A. Haas ◽  
F. G. Knox
Keyword(s):  
Proximal Tubule ◽  
Distal Tubule ◽  
Proximal Tubules ◽  
Loop Of Henle ◽  
Phosphate Reabsorption ◽  
Phosphate Intake ◽  
Phosphate Excretion ◽  
Dietary Phosphate ◽  
Renal Phosphate Excretion ◽  
High Phosphate

Dietary phosphate intake is now recognized to be a primary regulator of renal phosphate excretion. However, the nephron sites involved in the adaptation to changes in dietary phosphate are unclear. We tested the hypothesis that deep and superficial nephrons respond differently to changes in dietary phosphate by comparing fractional phosphate delivery (FDP%) from proximal tubules of both nephron populations. Because phosphate reabsorption is not detectable in the ascending loop of Henle, FDP% to the superficial early distal tubule and papillary loop of Henle reflect delivery from superficial and deep nephron proximal tubules, respectively. Micropuncture experiments were performed in 17 acutely TPTX rats fed either a low (0.07%) or a high (1.8%) phosphate diet for 4 days prior to the experiment. In low phosphate diet, fractional phosphate excretion was 0.93 +/- 0.26%. FDP% was 7.5 +/- 0.5 and 9.1 +/- 2.2% from superficial and deep nephron proximal tubules, respectively (P greater than 0.05). In high phosphate diet, fractional phosphate excretion was 29.6 +/- 5.0%. FDP% was significantly greater from superficial proximal tubules, 33.9 +/- 4.6%, compared with that from deep nephron proximal tubules, 14.0 +/- 2.7% (P less than 0.05). We conclude that significant adaptation of phosphate reabsorption in response to changes in dietary phosphate intake occurs in the superficial but not in the deep nephron proximal tubule in acutely TPTX volume-expanded rats. In addition, the presence of distal phosphate reabsorption was not evident in high phosphate diet but must occur in low phosphate diet.

scholarly journals Hyperphosphatemia increases inflammation to exacerbate anemia and skeletal muscle wasting independently of FGF23-FGFR4 signaling

2021 ◽  
Author(s):  
Brian Czaya ◽  
Kylie Heitman ◽  
Isaac Campos ◽  
Christopher Yanucil ◽  
Dominik Kentrup ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Wasting ◽  
Genetic Disorders ◽  
Fibroblast Growth Factor 23 ◽  
Kidney Injury ◽  
Hepcidin Expression ◽  
Phosphate Intake ◽  
Skeletal Muscle Wasting ◽  
High Phosphate

Elevations in plasma phosphate concentrations (hyperphosphatemia) occur in chronic kidney disease (CKD), in certain genetic disorders, and following the intake of a phosphate-rich diet. Whether hyperphosphatemia and/or associated changes in metabolic regulators, including elevations of fibroblast growth factor 23 (FGF23) directly contribute to specific complications of CKD is uncertain. Here we report that similar to patients with CKD, mice with adenine-induced CKD develop inflammation, anemia and skeletal muscle wasting. These complications are also observed in mice fed high phosphate diet even without CKD. Ablation of pathologic FGF23-FGFR4 signaling did not protect mice on an increased phosphate diet or mice with adenine-induced CKD from these sequelae. However, low phosphate diet ameliorated anemia and skeletal muscle wasting in a genetic mouse model of CKD. Our mechanistic in vitro studies indicate that phosphate elevations induce inflammatory signaling and increase hepcidin expression in hepatocytes, a potential causative link between hyperphosphatemia, anemia and skeletal muscle dysfunction. Our study suggests that high phosphate intake, as caused by the consumption of processed food, may have harmful effects irrespective of pre-existing kidney injury, supporting not only the clinical utility of treating hyperphosphatemia in CKD patients but also arguing for limiting phosphate intake in healthy individuals.

High-phosphorus diet maximizes and low-dose calcitriol attenuates skeletal muscle changes in long-term uremic rats

2016 ◽  
Vol 120 (9) ◽  
pp. 1059-1069 ◽  
Author(s):  
Luz M. Acevedo ◽  
Ignacio López ◽  
Alan Peralta-Ramírez ◽  
Carmen Pineda ◽  
Verónica E. Chamizo ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Low Dose ◽  
Fiber Type ◽  
Standard Diet ◽  
Phosphate Intake ◽  
High Phosphorus ◽  
Muscle Changes ◽  
High Phosphorus Diet ◽  
High Phosphate

Although disorders of mineral metabolism and skeletal muscle are common in chronic kidney disease (CKD), their potential relationship remains unexplored. Elevations in plasma phosphate, parathyroid hormone, and fibroblastic growth factor 23 together with decreased calcitriol levels are common features of CKD. High-phosphate intake is a major contributor to progression of CKD. This study was primarily aimed to determine the influence of high-phosphate intake on muscle and to investigate whether calcitriol supplementation counteracts negative skeletal muscle changes associated with long-term uremia. Proportions and metabolic and morphological features of myosin-based muscle fiber types were assessed in the slow-twitch soleus and the fast-twitch tibialis cranialis muscles of uremic rats (5/6 nephrectomy, Nx) and compared with sham-operated (So) controls. Three groups of Nx rats received either a standard diet (0.6% phosphorus, Nx-Sd), or a high-phosphorus diet (0.9% phosphorus, Nx-Pho), or a high-phosphorus diet plus calcitriol (10 ng/kg 3 day/wk ip, Nx-Pho + Cal) for 12 wk. Two groups of So rats received either a standard diet or a high-phosphorus diet (So-Pho) over the same period. A multivariate analysis encompassing all fiber-type characteristics indicated that Nx-Pho + Cal rats displayed skeletal muscle phenotypes intermediate between Nx-Pho and So-Pho rats and that uremia-induced skeletal muscle changes were of greater magnitude in Nx-Pho than in Nx-Sd rats. In uremic rats, treatment with calcitriol preserved fiber-type composition, cross-sectional size, myonuclear domain size, oxidative capacity, and capillarity of muscle fibers. These data demonstrate that a high-phosphorus diet potentiates and low-dose calcitriol attenuates adverse skeletal muscle changes in long-term uremic rats.

scholarly journals A chronic high phosphate intake in mice is detrimental for bone health without major renal alterations

2021 ◽  
Author(s):  
Marko Ugrica ◽  
Carla Bettoni ◽  
Soline Bourgeois ◽  
Arezoo Daryadel ◽  
Eva-Maria Pastor-Arroyo ◽  
...  
Keyword(s):  
Bone Mineral Density ◽  
Bone Resorption ◽  
Bone Mineral ◽  
Bone Health ◽  
Ammonium Excretion ◽  
Mineral Density ◽  
Mature Adult ◽  
Phosphate Intake ◽  
The Impact ◽  
High Phosphate

Abstract Background Phosphate intake has increased in the last decades due to a higher consumption of processed foods. This higher intake is detrimental for patients with chronic kidney disease, increasing mortality and cardiovascular disease risk and accelerating kidney dysfunction. Whether a chronic high phosphate diet is also detrimental for the healthy population is still under debate. Methods We fed healthy mature adult mice over a period of one year with either a high (1.2% w/w) or a standard (0.6% w/w) phosphate diet, and investigated the impact of a high phosphate diet on mineral homeostasis, kidney function and bone health. Results The high phosphate diet increased plasma phosphate, parathyroid hormone (PTH) and calcitriol levels, with no change in fibroblast growth factor 23 levels. Urinary phosphate, calcium and ammonium excretion were increased. Measured glomerular filtration rate was apparently unaffected, while blood urea was lower and urea clearance was higher in animals fed the high phosphate diet. No change was observed in plasma creatinine levels. Blood and urinary pH were more acidic paralleled by higher bone resorption observed in animals fed a high phosphate diet. Total and cortical bone mineral density was lower in animals fed a high phosphate diet and this effect is independent of the higher PTH levels observed. Conclusions A chronic high phosphate intake did not cause major renal alterations, but affected negatively bone health, increasing bone resorption and decreasing bone mineral density.

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