The role of phosphorus restriction in the prevention of secondary hyperparathyroidism in chronic renal disease

Abstract

In normal man, the serum phosphate concentration is maintained within a narrow range, despite random and spontaneous variations in phosphorus ingestion. On an average diet in the U.S.A., the intake of elemental phosphorus approximates one gram per day. Of this amount, about 30% is excreted through the gastrointestinal tract and 70%, or about 700 mg/day, is excreted by the kidneys. To effect this rate of excretion with a normal glomerular filtration rate, some 15% of the filtered load of phosphate must be excreted; the tubular reabsorption of phosphate (TRP) thus is equal to about 85% of the filtered load. The absolute value for TRP varies depending upon the amount of phosphate requiring excretion, and the primary effector element in the control system which governs phosphate homeostasis appears to be parathyroid hormone. Most studies indicate that the modulation of tubular reabsorption of phosphate takes place in the proximal tubule, although some investigators have presented evidence suggesting distal participation in phosphate reabsorption. It is believed that a basis now exists for a prospective approach to the prevention of secondary hyperparathyroidism, and probably other forms of metabolic bone disease, in advancing chronic renal disease. To date, controlled studies have been performed only on dogs with experimental renal disease; however, preliminary results in patients are encouraging and long term clinical studies must now be undertaken.