Sources of Phosphate in the Kidney Diet: What to Avoid Based on New Guidelines

Elevated serum phosphorus in patients with chronic kidney disease (CKD) has been connected to vascular calcification, progression of kidney disease and cardiac-related conditions. Serum phosphorus plays a role not only in parathyroid hormone regulation, but also fibroblast growth factor (FGF-23). Increases in FGF-23 have been shown to increase the risk of mortality due to decreased kidney function and cardiovascular risk. An increase in dietary phosphorus related to phosphate additives has been seen over the past 15 years and presents a challenge in the management of serum phosphorus. While the number of phosphate binders currently on the market is increasing, dietary modification is the foundation for managing serum phosphorus levels. This article will demonstrate how messages related to phosphorus in the diet are shifting from limiting single foods or food groups to a focus on general, healthful eating practices.

The National Kidney Foundation Kidney Disease Outcomes Quality Initiative™ guidelines

Kidney Disease Outcomes Quality Initiative (KDOQI) guidelines recommend maintaining blood phosphorus in patients with CKD stages 3 or 4 at ≥ 2.7 to ≤ 4.6 mg/dL and for patients with CKD stage 5 dialysis to lower increased phosphorus levels toward the reference range. Dialysis patients are usually given a goal of 3.5 to 5.5 mg/dL. The combination of a low phosphorus diet and phosphate binders is recommended to manage serum phosphorus. KDOQI guidelines also recommend limiting dietary phosphorus to 800 to 1,000 mg per day for the person with end stage renal disease (ESRD). Patients requiring a phosphate binder report a high pill burden related to the requirement of binders with every meal and with some snacks. As a result, continued focus is needed on dietary modification to reduce phosphorus intake.

Organic versus inorganic phosphate

Organic phosphorus, largely bound to proteins, is found in foods such as dairy products, meat, eggs, legumes, nuts and seeds. In the intestinal tract, organic phosphorus is hydrolyzed, then absorbed into the circulation as inorganic phosphate. Some of the organic phosphorus is bound to phytate and is not released during digestion. The animal-based sources of organic phosphate have an absorption rate of 40 to 80 percent, whereas plant-based sources of organic phosphate are absorbed at a rate of 20 to 40 percent. To compare, inorganic phosphorus (phosphate) comes from additives or preservatives included in a food product during processing. These additives are often found in foods requiring extended shelf life including packaged foods, fast foods and convenience meals. Studies suggest the absorption rate of inorganic phosphorus might be as high as 90 percent.

KDOQI guidelines suggest that the phosphates in the American diet might derive from additives and preservatives such as is found in fast foods and convenience-type meals. In some studies, intake from inorganic phosphate alone totaled up to 1,000 mg/day. As more is known about absorption rates of and difference between organic versus inorganic phosphate, dietary recommendations are including more education on limiting phosphate additives. In a review of NHANES data, the trend has been that phosphorus intake increased most from grain-type foods. This trend might be related to the increase in convenience foods and meals such as packaged cakes, cookies, crackers and microwave meals.

Nutrition education and the patient-centered approach

Phosphorus-containing foods and ways to limit intake are a source of confusion for patients with CKD or ESRD. Foods containing phosphorus and phosphate types vary widely and phosphorus content is not required on the Nutrition Facts label. Inorganic versus organic phosphorus as well as the amount in frequently consumed foods must be considered. Additionally, maintaining nutrition status of the ESRD patient is important due to increased risk of inflammation, malnutrition and inadequate calorie and protein intake. Recommendations to increase intake of high-biologic value protein from meats, and even from dairy products, contradicts suggestions to limit whole-food groups high in phosphorus.

In addition to the focus on limiting phosphate additives, education regarding cooking methods and how to prepare fresh foods may also decrease the amount of convenience foods eaten. Food-group based education with inclusion of low potassium fruits and vegetables, whole grains and meats has been shown to effectively reduce serum phosphorus levels. The inclusive rather than restrictive diet may also reduce risk of protein-calorie malnutrition and even improve survival rates.

Also, for the patient with CKD, earlier intervention with respect to phosphate additives may be beneficial even though increases in serum phosphorus are not seen until later stages of CKD. Early nutrition education, with focus on limiting phosphate additives, is important to maintaining phosphorus parameters within normal limits as kidney function declines.

As more is discovered about absorption of phosphorus and phosphorus content in foods and beverages, a shift in education to a focus on phosphate additives is required. Additionally, a thorough food recall and use of motivational interviewing techniques may allow the educator to make specific food- and patient-centered goals, ultimately reducing the amount of phosphorus consumed. In some cases, access to fresh food and education on cooking methods are beneficial. Finally, further research is needed on the effect of dietary education centered on phosphate additives.