Paneles de Discussión
Paneais de Discussio
Volver al Inicio cin2003
Voltar ao inicio cin2003
SOURCES OF PHOSPHORUS FOR RENAL FAILURE PATIENTS
Jaime Uribarri, MD
Division of Nephrology, Department of Medicine,
Mount Sinai School of Medicine, New York, N.Y.
Hyperphosphatemia or elevated serum phosphorus is an important preventable risk factor associated with increased cardiovascular morbidity and mortality in dialysis patients1
. Thus, maintenance of normal serum phosphorus is a critical step in the long-term management of chronic renal failure patients. In a typical dialysis patient serum phosphorus concentration reflects the balance between net intestinal absorption, net bone resorption and dialytic removal of this mineral. Removal of phosphorus using the current 3-times-a-week hemodialysis or daily peritoneal dialysis is limited and insufficient to maintain a normal serum phosphorus concentration in the presence of average intestinal absorption of this mineral from the typical American diet2,3
. Prevention of intestinal absorption of phosphorus by the current phosphorus binders is also limited. Thus, modification of the phosphorus content of the diet is of great importance in order to better control serum phosphorus in dialysis patients and ultimately reduce the risk of cardiovascular morbidity and mortality.
Phosphorus is absorbed along the small intestine by both active and passive mechanisms. The main determinants of this absorption are the phosphorus content in the diet, its bioavailability and the presence of natural and/or pharmacological phosphorus binders.
The usual daily intake of phosphorus will vary significantly depending on the way people eat. For the typical American diet, young and middle aged men consume about 1600 mg /day, while comparably aged women consume about 1000 mg /day4, 5. These estimates of dietary phosphorus intake reflect mostly the "natural" phosphorus content of foods. A true estimate of the dietary content of phosphorus, however, requires the consideration not only of the natural phosphorus contained in raw or unprocessed food, but also the amount of phosphorus added to foods during processing and the phosphorus content of dietary supplements.
In general, foods high in protein like meat, milk, dairy, eggs and cereals are also naturally high in phosphorus and contribute the largest amounts to the total dietary phosphorus intake on an average diet. Over the past few decades, however, increasing use of food processing practices, which include the addition of phosphorus, has determined a significant increase in the daily intake of this mineral6. In 1990, phosphorus containing food additives contributed an estimated 470 mg/day to the daily adult phosphorus intake in the USA, but this contribution will continue to increase as the people’s demand for convenience and fast foods escalates6. Consequently, depending on individual food choices, phosphorus intake could be increased by as much as 1.0 g/day simply increasing the percentage of processed foods in the diet7.
The bioavailability of phosphorus from various food sources is also an important consideration in the analysis of dietary phosphorus intake. In plants a large fraction of the phosphorus is in the form of phytate. Since the small intestine of humans does not secrete the enzyme phytase, which is necessary to degrade dietary phytate and release phosphorus, phytate phosphorus is not bioavailable in humans, unless the food is processed with phytase such as in the leavening of bread with phytase-containing yeast4. In contrast, phosphorus in meat is well absorbed since it is found mostly as intracellular organic compounds, which are easily hydrolyzed in the gastrointestinal tract releasing inorganic phosphorus for absorption. Phosphorus in milk is present in different fractions each one of them with different bioavailability. Phosphorus added during food processing is mostly in the form of inorganic salts and hence is almost completely absorbed and therefore, represents an even larger phosphorus burden.
The relative amount of calcium in the diet will also influence the intestinal absorption of phosphorus probably through binding and formation of insoluble calcium phosphate salts, which are not well absorbed.
As a result of the different factors mentioned above, usually only 60 % of phosphorus from a typical mixed diet is absorbed. Obviously, this percentage will change depending on the predominant food groups and the degree of processing of the foods present in selected diets. A diet with a predominance of fast food and processed meats as a protein source will provide higher fractional phosphorus absorption than a diet of similar "natural" phosphorus content but with a predominance of fresh, unprocessed foods.
The close association between phosphorus and protein content in food makes it very difficult to restrict dietary phosphorus content without simultaneously restricting dietary protein intake, especially protein of animal origin8. Thus, the minimal daily protein intake of 1.2 g/kg/day set for dialysis patients by the DOQI guidelines will almost invariably lead to hyperphosphatemia in chronic peritoneal2 and hemodialysis patients3. These guidelines for minimal protein intake are inappropriate since they prevent reaching reasonable levels of serum phosphorus and considering the lack of evidence of any benefit of this high protein intake (Table 1)2.
TABLE 1. Normophosphatemia in CAPD patients requires dietary P control
|If protein intake (DOQI guidelines) = 1.2 g/kg/day = 84 g in a 70 kg man = 1.3 g of P intake (ref 8)
Assuming P-binders reduce fractional intestinal P absorption to 50% = 0.65 g of P will be absorbed daily with above dietary intake
P concentration in the PD outflow characteristically is 75% that of serum (ref 2)
Thus, to eliminate the daily load of 0.65 g of P and maintain a stable serum P concentration one will need a CAPD prescription that assures a total PD outflow of 14.4 L/day. This is an unreasonable prescription!|
Most of the software programs available to estimate the patient's phosphorus intake and design individualized diets that are low in total phosphorus content are based on standard food composition tables, which usually do not include the phosphorus from these additives, leading to a consistent underestimation of dietary phosphorus intake.
Changes in the food labeling regulations in the USA no longer require manufacturers to list the phosphorus content in the Nutrition Facts Panel of food as they do for sodium and potassium content4. Consequently, patients have to be specifically advised to read the ingredient list on food labels to help them select food products with lower levels of phosphate additives.
Phosphate binders could theoretically prevent hyperphosphatemia even in the presence of a high intake of phosphorus if their dose is progressively increased. In clinical practice, however, increasing the dose of phosphorus binders is limited by their own set of side effects. Calcium-containing phosphate binders, the most commonly used ones, will frequently lead to hypercalcemia, particularly when patients are simultaneously exposed to either vitamin D (calcitriol, doxercalciferol) or vitamin D analog (paracalcitol) preparations, which is almost the rule at present2. Newer preparations such as sevelamer, which do not predispose to hypercalcemia, are very expensive alternatives.
Enhancing dialytic phosphorus removal should lead to normophosphatemia. In fact, experience with daily nocturnal hemodialysis has shown that ideal levels of serum phosphorus and, even hypophosphatemia, can be achieved with this form of dialysis9. However, daily hemodialysis is still not widely used and in the meantime, limiting dietary intake of phosphorus remains a cornerstone in the maintenance of a safe serum phosphorus concentration in dialysis patients.
In summary, current dialysis and phosphorus binder prescriptions are not sufficient to assure normophosphatemia in dialysis patients who are eating well. The important message is that limiting dietary intake of phosphorus requires prescription of a moderate protein intake (0.9 to 1.0 g/kg/day), increased consumption of a variety of fresh fruits and vegetables and restricted consumption of highly processed fast and convenience foods. Phosphorus added during food processing is an important source of this mineral because of its magnitude and high bioavailabilty. Because this information is often unknown to the consumer, it needs to be more extensively disseminated among health care professionals dealing with dialysis patients, a population of patients in whom a very precise determination of phosphorus intake is essential. The development of low-phosphorus containing food products would be a very useful addition for these patients
- Block GA, Hulbert-Shearon TE, Levin NW, Port FK: Association of serum phosphorus and calcium x phosphate product with mortality risk in chronic hemodialysis patients: a national study. Am J Kid Dis 31:607-617, 1998
- Uribarri J: DOQI guidelines for nutrition in long-term peritoneal dialysis patients: a dissenting view. Am J Kid Dis 37:1313-1318, 2001
- Hsu CH: Are we mismanaging calcium and phosphate metabolism in renal failure? Am J Kidney Dis 29:641-649, 1997
- Anderson JJB, Sell ML, Garner S, Calvo MS: Phosphorus. In "Present knowledge of nutrition. ILSI press, 2001
- Calvo MS, Park YK: Changing phosphorus content of the US diet: potential for adverse effects on bone. J Nutr 126:S1168-S1180,1996
- Calvo MS : Dietary considerations to prevent loss of bone and renal function. Nutrition 16: 564-566, 2000
- Bell RR, Draper HH, Tzeng DYM, Shin HK, Schmidt GR: Physiological responses of human adults to foods containing phosphate additives. J Nutr 107:42-50,1977
- Boaz M, Smetana S: Regression equation predicts dietary phosphorus intake from estimate of dietary protein intake. J Am Diet Assoc 96:1268-1270, 1996
- Pierratos A: Daily hemodialysis: an update. Curr Opin Nephrol Hypertens.