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

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 United States, 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 700mg/day, is excreted by the kidneys. To effect this rate of excretion with a normal glomerular filtration rate (GFR), 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 will vary 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 (PTH). Most studies indicate that the modulation of tubular reabsorption of phosphate takes place in the proximal tubule [1–3], although some investigators have presented evidence suggesting distal participation in phosphate reabsorption [4, 5].