Elevated serum phosphorus is a strong independent risk factor for mortality in maintenance hemodialysis (MHD) patients, so controlling serum phosphorus levels is a priority (Kidney Int. 2006;70:771-780).

Clinicians attempt to control patients’ serum phosphorus by restricting their dietary phosphorus intake or by prescribing phosphate binders. One of the challenges with respect to dietary restrictions is that high-protein foods contain high levels of phosphorus.

Therefore, a low phosphorus diet means limiting animal and plant protein sources such as beef, cheese, legumes, and milk. While these foods are high in phosphorus, they are also excellent sources of protein; for example one eight-ounce glass of whole milk provides 8 g of protein, 150 kilocalories, and approximately 222 mg of phosphorus.

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This glass of milk would provide approximately 25% of patients’ phosphorus allowance and 10% of their protein requirements per day. Maximizing dietary protein intake in MHD patients is essential to preventing malnutrition and protein-energy wasting, both of which are also independent risk factors for mortality in MHD patients.

Optimal diet

Shinaberger et al (Am J Clin Nutr. 2008;88:1511-1518) suggests that the optimal diet for MHD patients is both high in protein and low in phosphorus. In this study, death risk was compared between increasing and decreasing dietary intakes of protein and phosphorus in 30,075 MHD patients over six months.

Normalized protein nitrogen appearance (nPNA) was used as a surrogate marker for dietary protein intake. Results of this analysis were that serum phosphorus does have an almost linear association with nPNA; death rates increase both with a declining nPNA and increasing serum phosphorus; patients with the lowest nPNA and highest serum phorsphorus had the highest mortality, and, conversely, those with the highest nPNA and lowest serum phosphorus had the lowest mortality. So what is a clinician to do?

Part of the answer may be found in the American food supply. Processed foods contain varying amounts of phosphorus as an additive, which may contribute significantly to our overall phosphorus intake.

Phosphorus is used to increase shelf life, improve or enhance flavor, and to prevent food products from dehydrating. The FDA does not require food manufacturers to put phosphorus content on food product labels. Therefore, it is extremely difficult for a patient to know how much phosphorus foods contain.

Fast food

In a study published in 2007 (J Ren Nutr. 2007;17:264-268), researchers found that MHD patients between 18 and 44 years of age consumed an average of 2.1 fast food meals per week. In a separate study (J Ren Nutr. 2008;18:466-470), the same researchers analyzed foods offered by fast food chains in the greater Cleveland area.

The foods were judged by criteria on sodium, potassium, naturally occurring phosphorus, and the presence of phosphate additives. Based on those criteria, only 16% of the foods were acceptable for a renal patient.

Phosphate additives

To combat the problem of phosphate additives patients can be taught to identify phosphate additives on food labels and to avoid foods containing these additives. This was done with positive results by Sullivan et al (JAMA. 2009;301:629-635).

Patients with baseline phosphorus concentrations greater than 5.5 mg/dL were enrolled and randomized to receive either standard of care or intensive phosphorus additive education and tools (such as a pocket sized magnifier for label reading) to assist in phosphorus identification.

At baseline, the serum phosphorus concentrations were similar between the intervention and control groups (7.2 vs. 7.1 mg/dL, respectively). Three months after receiving baseline intervention, the serum phosphorus of the treatment group had decreased by 1.0 mg/dL compared with 0.4 mg/dL in the control group.

The findings show that educating patients on phosphorus additives can effectively reduce serum phosphorus values over our current standard of care. This study did not analyze serum albumin at three months, so it is not possible to determine whether visceral protein status was impacted by these changes. Kalantar-Zadeh et al (Clin J Am Soc Nephrol. 2010; published online ahead of print) suggests using a dietary phosphorus-to-protein (mg/g) ratio for dietary prescriptions.

This ratio has advantages, such as better comparability between food items. A major limitation, however, is that we do not know the phosphorus content of many foods available to our patients. Thus, the ratio often cannot be accurately calculated.

Until it is possible to know precisely how much phosphorus is in processed and fast foods, clinicians need to take extra time to educate their patients on phosphate additives, their potential for harm, and on how to identify these additives on food labels. Meanwhile, consumption of high protein foods, which naturally contain greater amounts of phosphorus, needs to be carefully monitored to maintain a balance between optimal visceral protein status and serum phosphorus values.