phosphorus absorption is virtually constant across a broad range of intakes suggests that the bulk of phosphorus absorption occurs by passive, concentration-dependent processes. Also, even in the face of dangerous hyperphosphatemia, phosphorus continues to be absorbed from the diet at an efficiency only slightly lower than normal (Brickman et al., 1974).
Phosphorus absorption is reduced by ingestion of aluminum-containing antacids and by pharmacologic doses of calcium carbonate. There is, however, no significant interference with phosphorus absorption by calcium at intakes within the typical adult range.
Excretion of endogenous phosphorus is mainly through the kidneys. Inorganic serum phosphate is filtered at the glomerulus and reabsorbed in the proximal tubule. The transport capacity of the proximal tubule for phosphorus is limited; it cannot exceed a certain number of mmol per unit time. This limit is called the tubular maximum for phosphate (TmP). TmP varies inversely with parathyroid hormone (PTH) concentration; PTH thereby adjusts renal clearance of Pi. At filtered loads less than the TmP (for example, at low plasma Pi values), most or all of the filtered load is reabsorbed, and thus plasma phosphate levels can be at least partially maintained. By contrast, at filtered loads above the TmP, urinary phosphorus is a linear function of plasma phosphate (Bijvoet, 1969; Lemann, 1996; Nordin, 1989). In the healthy adult, urine phosphorus is essentially equal to absorbed diet phosphorus, less small amounts of phosphorus lost in shed cells of skin and intestinal mucosa.
This regulation of phosphorus excretion is apparent from early infancy. In infants, as in adults, the major site of regulation of phosphorus retention is at the kidney. In studies of infants receiving different calcium intakes (DeVizia et al., 1985; Moya et al., 1992; Williams et al., 1970; Ziegler and Fomon, 1983), phosphorus retention did not differ even with high amounts of dietary calcium (calcium:phosphorus [Ca:P] molar ratios of 0:6, 1:1, or 1.4:1). Any reduction in absorption of phosphorus due to high amounts of dietary calcium were compensated for by parallel reductions in renal phosphorus excretion (DeVizia et al., 1985; Fomon and Nelson, 1993; Moya et al., 1992). The least renal excretory work to maintain normal phosphorus homeostasis would be achieved with human milk as the major source of minerals during the first year of life.
Pi levels are only loosely regulated. Normal Pi levels decline with age from infancy to maturity (Table 5-1). The most likely reason for the