The average dietary phosphate intake in humans, derived largely from dairy products, meat, and cereals, is 1200 to 1500 mg per day, two-fold to three-fold greater than the estimated
minimum requirement. Approximately 60% to 70% of phosphate in the diet is absorbed, so that net absorption is proportional to intake. Absorption probably occurs throughout the small intestine; transport is greatest in the jejunum, less in the duodenum, and minimal in the ileum.1 The movement of phosphorus from the intestinal lumen to the blood requires (1) transport across the luminal brush border membrane; (2) movement transcellularly; and (3) transport across the basolateral plasma membrane of the epithelium.

Phosphate transport at the luminal brush border membrane occurs by way of a saturable process against a lumen/intracellular electrochemical gradient at lumen phosphate concentrations below 2 mmol/L; above this concentration, transport predominantly proceeds by passive diffusion. The active transport of phosphate occurs by way of two independent carrier-mediated processes, a high-affinity and a low-affinity system. Both processes are dependent on sodium and potassium; however, the high-affinity transport system is enhanced by acid pH, whereas both alkaline pH and calcium stimulate the low-affinity system. The molecular basis for the sodium-dependent phosphate transport remains unknown.

Likewise, little is known about the cellular events that mediate the movement of phosphorus from the luminal to the basolateral membrane. Nevertheless, available evidence suggests a role for the microtubule system in conveying phosphorus transcellularly and in extrusion of phosphorus at the basolateral membrane.

Extrusion of phosphorus at the basolateral membrane of intestinal epithelial cells is passive, occurring via an anion-exchange mechanism, because the electrochemical gradient favors such movement. However, there have been reports of an ATP- and Na⁺-dependent transport process at this locus.

Calcitriol [1,25(OH)₂D₃] is the principal hormonal factor that influences gastrointestinal phosphate absorption.2,3 Facilitation of transport occurs by way of a calcium-dependent duodenal process and a calcium-independent jejunal system. The latter activity is modulated by calcitriol-induced transcription of messenger RNA. A major cause of defective phosphate absorption is calcitriol deficiency (secondary to a nutritional deficiency or caused by malabsorption). Alternatively, genetic and acquired disorders of vitamin D metabolism may decrease the availability of vitamin D (see Chap. 54, Chap. 63 and Chap. 70).