A Long Road to Travel: Adherence to Dietary Recommendations and Adequate Dietary Phosphorus Control

Carrero, Juan Jesús; Burrowes, Jerrilynn D.; Wanner, Christoph

doi:10.1053/j.jrn.2016.03.004

Cited by 9 publications

(14 citation statements)

References 24 publications

(23 reference statements)

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“…Trends of timed serum 33 PO 4 ( Fig. 2A) were similar to those found in absolute change in serum phosphate, although 33 PO 4 exhibited higher variability. Further, the appearance of urinary 33 PO 4 was significantly higher at 120 minutes in the control group than in CKD ( Fig.…”

Section: Animal Study Resultssupporting

confidence: 67%

“…Measurement of radioactivity ( 33 PO 4 ) can be used to determine the de novo appearance of phosphate that was derived from the oral phosphate challenge in the blood, urine, and intestinal contents. At all time points for all groups, serum 33 PO 4 was higher than baseline (p < 0.07). Trends of timed serum 33 PO 4 ( Fig.…”

Section: Animal Study Resultsmentioning

confidence: 84%

“…At all time points for all groups, serum 33 PO 4 was higher than baseline (p < 0.07). Trends of timed serum 33 PO 4 ( Fig. 2A) were similar to those found in absolute change in serum phosphate, although 33 PO 4 exhibited higher variability.…”

Section: Animal Study Resultsmentioning

confidence: 84%

“…The Dietary Reference Intake for phosphate in adults, reported as phosphorus, is 580 mg/d (phosphate: 1779 mg); however, reports suggest that North Americans often consume >1500 mg/d (phosphate: 4600 mg/d) . Several recent studies have shown that additive‐containing diets substantially increased daily phosphorus intake (606 to 736 mg), with estimates suggesting that the additives make up approximately 60% of dietary phosphate . Developing an oral phosphate test, as proposed herein, can model the response that follows consumption of a meal containing primarily processed foods and provide a straightforward method for assessing acute phosphate dysregulation.…”

Section: Discussionmentioning

confidence: 99%

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Impaired Phosphate Tolerance Revealed With an Acute Oral Challenge

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Hopman

et al. 2017

Journal of Bone and Mineral Research

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Elevated serum phosphate is consistently linked with cardiovascular disease (CVD) events and mortality in the setting of normal and impaired kidney function. However, serum phosphate does not often exceed the upper limit of normal until glomerular filtration rate (GFR) falls below 30 mL/min/m 2 . It was hypothesized that the response to an oral, bioavailable phosphate load will unmask impaired phosphate tolerance, a maladaptation not revealed by baseline serum phosphate concentrations. In this study, rats with varying kidney function as well as normo-phosphatemic human subjects, with inulin-measured GFR (13.2 to 128.3mL/min), received an oral phosphate load. Hormonal and urinary responses were evaluated over 2 hours. Results revealed that the more rapid elevation of serum phosphate was associated with subjects and rats with higher levels of kidney function, greater responsiveness to acute changes in parathyroid hormone (PTH), and significantly more urinary phosphate at 2 hours. In humans, increases in urinary phosphate to creatinine ratio did not correlate with baseline serum phosphate concentrations but did correlate strongly to early increase of serum phosphate. The blunted rise in serum phosphate in rats with CKD was not the result of altered absorption. This result suggests acute tissue deposition may be altered in the setting of kidney function impairment. Early recognition of impaired phosphate tolerance could translate to important interventions, such as dietary phosphate restriction or phosphate binders, being initiated at much higher levels of kidney function than is current practice.

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Section: Animal Study Resultssupporting

confidence: 67%

Section: Animal Study Resultsmentioning

confidence: 84%

Section: Animal Study Resultsmentioning

confidence: 84%

Section: Discussionmentioning

confidence: 99%

See 2 more Smart Citations

Impaired Phosphate Tolerance Revealed With an Acute Oral Challenge

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Hopman

et al. 2017

Journal of Bone and Mineral Research

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“…It should come as no surprise that the quality of the diet of CKD patients is suboptimal. [1][2][3][4] This may be explained by a myriad of factors, including financial and social barriers often linked to CKD, an emphasis on restriction of sodium, potassium, and phosphorous at the expense of compromising overall diet quality, [5][6][7] and simply global dietary changes toward western diets, with convenience, fast, and ultra-processed foods. In the recent years, through observational studies, we are learning that dietary quality may also influence the fate of patients with CKD.…”

Section: Y Ou Are Whatyou Eat the American Nutritionistmentioning

confidence: 99%

Diet for the Management of Patients With Chronic Kidney Disease; It Is Not the Quantity, but the Quality That Matters

Campbell

Carrero

2016

Journal of Renal Nutrition

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The role of phosphate in kidney disease

Vervloet¹,

Sezer²,

Massy³

et al. 2016

Nat Rev Nephrol

181

133

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The importance of phosphate homeostasis in chronic kidney disease (CKD) has been recognized for decades, but novel insights - which are frequently relevant to everyday clinical practice - continue to emerge. Epidemiological data consistently indicate an association between hyperphosphataemia and poor clinical outcomes. Moreover, compelling evidence suggests direct toxicity of increased phosphate concentrations. Importantly, serum phosphate concentration has a circadian rhythm that must be considered when interpreting patient phosphate levels. Detailed understanding of dietary sources of phosphate, including food additives, can enable phosphate restriction without risking protein malnutrition. Dietary counselling provides an often underestimated opportunity to target the increasing exposure to dietary phosphate of both the general population and patients with CKD. In patients with secondary hyperparathyroidism, bone can be an important source of serum phosphate, and adequate appreciation of this fact should impact treatment. Dietary and pharmotherapeutic interventions are efficacious strategies to lower phosphate intake and serum concentration. However, strong evidence that targeting serum phosphate improves patient outcomes is currently lacking. Future studies are, therefore, required to investigate the effects of modern dietary and pharmacological interventions on clinically meaningful end points.

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A Long Road to Travel: Adherence to Dietary Recommendations and Adequate Dietary Phosphorus Control

Cited by 9 publications

References 24 publications

Impaired Phosphate Tolerance Revealed With an Acute Oral Challenge

Impaired Phosphate Tolerance Revealed With an Acute Oral Challenge

Diet for the Management of Patients With Chronic Kidney Disease; It Is Not the Quantity, but the Quality That Matters

The role of phosphate in kidney disease

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