**5. Conclusion**

The goals of therapy have been to reduce phosphorus intake with low protein diet and phosphate binders. Since low protein diet is thought to be induce malnutrition, it is thought that strict adherence to a low protein diet is not practical. A diet rich in proteins is usually also rich in phosphorus. However, proteins with very different phosphorus contents can provide equivalent nutritional value, as can be seen from the difference in phosphorus content between meat, cheese, and eggs. Egg white is an excellent example of food with a high level of protein but low phosphorus content. Moe et al. demonstrates the importance of

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the protein source of phosphate in overall mineral metabolism after only 7 days of controlled diets. Despite equivalent protein and phosphorus concentrations in the diets, subjects had lower serum phosphorus levels, a trend toward decreased urine 24-hour phosphorus excretion, and significantly decreased FGF23 levels in the vegetarian diet compared with the meat-based diet (Moe et al., 2011).

Lafage et al. (Lafage et al., 1992) used a very low protein diet (0.3 g/kg/d) supplemented with amino acids and ketoanalogues and with only 1 g of calcium carbonate and 1,000 IU of vitamin D2 in 17 patients with advanced renal failure. They have shown not only a beneficial effect related to the control of hyperphosphatemia on the biologic and histologic parameters of hyperparathyroidism but also a correction of acidosis, which resulted in the disappearance of the osteomalacic component. Thus, dietary control often considered to be of minor importance, is actually one of the major keys to success in the management of hyperphosphataemia.
