Elsevier

Seminars in Nephrology

Volume 33, Issue 2, March 2013, Pages 180-190
Seminars in Nephrology

Management of Natural and Added Dietary Phosphorus Burden in Kidney Disease

https://doi.org/10.1016/j.semnephrol.2012.12.018Get rights and content

Summary

Phosphorus retention occurs from higher dietary phosphorus intake relative to its renal excretion or dialysis removal. In the gastrointestinal tract the naturally existing organic phosphorus is only partially (∼60%) absorbable; however, this absorption varies widely and is lower for plant-based phosphorus including phytate (<40%) and higher for foods enhanced with inorganic phosphorus-containing preservatives (>80%). The latter phosphorus often remains unrecognized by patients and health care professionals, even though it is widely used in contemporary diets, in particular, low-cost foods. In a nonenhanced mixed diet, digestible phosphorus correlates closely with total protein content, making protein-rich foods a main source of natural phosphorus. Phosphorus burden is limited more appropriately in predialysis patients who are on a low-protein diet (∼0.6 g/kg/d), whereas dialysis patients who require higher protein intake (∼1.2 g/kg/d) are subject to a higher dietary phosphorus load. An effective and patient-friendly approach to reduce phosphorus intake without depriving patients of adequate proteins is to educate patients to avoid foods with high phosphorus relative to protein such as egg yolk and those with high amounts of phosphorus-based preservatives such as certain soft drinks and enhanced cheese and meat. Phosphorus rich foods should be prepared by boiling, which reduces phosphorus as well as sodium and potassium content, or by other types of cooking-induced demineralization. The dose of phosphorus-binding therapy should be adjusted separately for the amount and absorbability of phosphorus in each meal. Dietician counseling to address the emerging aspects of dietary phosphorus management is instrumental for achieving a reduction of phosphorus load.

Section snippets

Early Phosphorus Retention in CKD

The pathogenesis of CKD-MBD is multifactorial and, in addition to hyperphosphatemia, includes changes in calcium, calcitriol, parathyroid hormone (PTH), and fibroblast growth factor-23 (FGF23).1 However, the tendency to retain phosphorus, based on an excessive dietary intake relative to residual renal function, plays a central role.6, 7, 8, 9, 10 Higher dietary phosphorus load may inhibit renal 1α-hydroxylase directly and also indirectly through the increase in FGF23; the decrease in the

Dietary Phosphorus

Phosphorus (P) is a nonmetal element with an atomic weight of 31 daltons. It is widely present in nature as phosphate (PO4). Phosphorus is also an essential constituent of all living organism because it plays a role in many fundamental biological and enzymatic reactions to maintain life as a result of its high chemical reactivity. Most of the total body phosphorus (ie, about 80%), is found in bones and teeth in the form of calcium salts, whereas about 20% is present in soft tissues and body

Circulating Level of Phosphorus

In plasma, the normal level of phosphorus is 2.5 to 4.5 mg/dL. Under normal physiologic conditions with an extracellular fluid pH of 7.4, hydrogen ion is bound to phosphate either as one (HPO42−) or dihydrogen structure (H2PO4) at a 4:1 ratio, which explains why the average phosphate valence is 1.8 in body fluids. Serum phosphorus measurement usually yields the same concentration as plasma. The serum phosphorus level remains within the normal range until the late stages of CKD; therefore, as

Phosphorus Digestibility and Intestinal Absorption

The absorption of phosphate in intestinal epithelial cells occurs via a co-transport mechanism through active sodium/phosphate (Na+/Pi) co-transporters, which involves at least three different types of Na+/Pi (ie, NPT2a, b, and c). This mechanism can be inhibited by nicotinamide, therefore the administration of niacin may be used as an effective approach to reduce the intestinal absorption of phosphorus and to decrease the circulating phosphorus level.20 Upon intake of natural (nonenhanced)

Phosphorus From Unprocessed Food

In natural foods phosphorus is present both as inorganic ions and as a constituent of phosphoproteins, but also as membrane phospholipids, adenosine triphosphate, adenosine diphosphate, DNA, and RNA. In a mixed diet, the phosphorus content usually is proportional to the amount of protein content. Indeed, protein-rich foods are historically and naturally the main source of dietary phosphorus. Several equations have been advanced to estimate the content of phosphorus based on the amount of

Changes of Phosphorus Intake by Industrial Processing: Food Preservatives

In modern society, food and beverages often are consumed a long time after their production or in places far away from the production site. Notwithstanding these facts, the dietary product must satisfy safety guidelines and taste characteristics. This is why the food industry uses progressively more food additives, also known as preservatives, (ie, substances intentionally added to food for dietetic-preservative and financial purposes) (Table 2). A food additive is a substance not normally

Changes of Phosphorus Intake by Homemade Processing: Cooking

The considerations made thus far are based on the composition of foods and refer to the phosphorus content per 100 g of uncooked food, or on the recognition of the presence of phosphorus-containing additives in food. However, many foods are consumed after cooking, and this can result in changes in the natural composition of the nutrients.46 Among the different methods of cooking, some are more favorable for health because they maintain or even improve the nutritional properties of food by

Management of Dietary Phosphorus in Clinical Practice: Need for Education

Dietary assessment of patients with CKD is possible through different methods.42 The calculation of phosphorus intake from dietary recall or interview may be inaccurate and indeed misleading. These estimates generally are based on the nutrient contents of the raw product and do not include any loss occurring via the cooking process. Moreover, they usually do not consider the phosphorus from preservatives, and they do not distinguish between the phytates and other components with differential

Conclusion

A simple and effective approach to reduce the load of dietary phosphorus without reducing protein supply consists of educating patients to mitigate consumption of foods high in absorbable phosphorus (eg, processed cheese and egg yolk), to avoid foods containing additives based on polyphosphates (such as certain types of soft drinks), and to choose vegetable-based foods that have lower phosphorus absorption, and to choose boiling versus other common methods of cooking. Table 4 provides an

References (64)

  • O. Benini et al.

    Extra-phosphate load from food additives in commonly eaten foods: a renal and insidious danger for renal patients

    J Ren Nutr

    (2011)
  • R.A. Sherman et al.

    Dietary phosphorus in dialysis patients: potential impact of processed meat, poultry, and fish products as protein sources

    Am J Kidney Dis

    (2009)
  • J.T. Daugirdas

    Proposed controlled trials of phosphate reduction in CKD: which whey should we go?

    Kidney Int

    (2010)
  • A.M. Mathewson et al.

    Dietary phosphate assessment in dialysis patients

    J Ren Nutr

    (2010)
  • W.L. Jones

    Demineralization of a wide variety of foods for the renal patient

    J Ren Nutr

    (2001)
  • A. Cupisti et al.

    Effect of boiling on dietary phosphate and nitrogen intake

    J Ren Nutr

    (2006)
  • R.D. Poduval et al.

    Hyperphosphatemia in dialysis patients: is there a role for focused counseling?

    J Ren Nutr

    (2003)
  • V. Reddy et al.

    Dietitian-led education program to improve phosphate control in a single-center hemodialysis population

    J Ren Nutr

    (2009)
  • A. Cupisti et al.

    Dietary habits and counseling focused on phosphate intake in hemodialysis patients with hyperphosphatemia

    J Ren Nutr

    (2004)
  • A. Cupisti et al.

    nutritional knowledge in hemodialysis patients and nurses: focus on phosphorus

    J Ren Nutr

    (2012)
  • J.B. Pollock et al.

    Knowledge of phosphorus compared with other nutrients in maintenance dialysis patients

    J Ren Nutr

    (2007)
  • D. Caldeira et al.

    Educational strategies to reduce serum phosphorus in hyperphosphatemic patients with chronic kidney disease: systematic review with meta-analysis

    J Ren Nutr

    (2011)
  • P. Martin et al.

    Comparison of dietary phosphate absorption after single doses of lanthanum carbonate and sevelamer carbonate in healthy volunteers: a balance study

    Am J Kidney Dis

    (2011)
  • K. Kalantar-Zadeh et al.

    Nephrology and nutrition leaders coming to Hawaii for the World Renal Nutrition Week: why is the 16th Congress in Renal Nutrition and Metabolism in Honolulu, Hawai'i, June 2012, worth attending?

    J Ren Nutr

    (2012)
  • B. Kestenbaum

    Phosphate metabolism in the setting of chronic kidney disease: significance and recommendations for treatment

    Semin Dial

    (2007)
  • M. Cozzolino et al.

    Pathophysiology of calcium and phosphate metabolism impairment in chronic kidney disease

    Blood Purif

    (2009)
  • M. Mizobuchi et al.

    Vascular calcification: the killer of patients with chronic kidney disease

    J Am Soc Nephrol

    (2009)
  • C. Zoccali et al.

    Phosphate may promote CKD progression and attenuate renoprotective effect of ACE inhibition

    J Am Soc Nephrol

    (2011)
  • P. Messa

    Impact of Ca/P disorders on risks and comorbidities

    Contrib Nephrol

    (2008)
  • F. Galetta et al.

    Left ventricular function and calcium phosphate plasma levels in uraemic patients

    J Intern Med

    (2005)
  • N. Noori et al.

    Association of dietary phosphorus intake and phosphorus to protein ratio with mortality in hemodialysis patients

    Clin J Am Soc Nephrol

    (2010)
  • O.M. Gutierrez

    Fibroblast growth factor 23 and disordered vitamin D metabolism in chronic kidney disease: updating the “trade-off” hypothesis

    Clin J Am Soc Nephrol

    (2010)
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    Financial disclosure and conflict of interest statements: AC received honoraria from Shire, Heinz-Plasmon. KKZ has received honoraria from Abbott, Amgen, DaVita, Fresenius, Genzyme, and Shire. KKZ was supported by grants from National Institute of Diabetes, Digestive and Kidney Disease of the National Institutes of Health R01 DK078106, K24 DK091419, a philanthropist grant from Mr. Harold Simmons.

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