Phosphate homeostasis is achieved through a balance between intestinal absorption and renal excretion of phosphate, as well as an internal contribution from bone. However, compared with the kidney, much less is known about the mechanisms involved in intestinal phosphate absorption or how this process may be regulated. Yet there is growing recognition of the importance of the gut in phosphate balance, especially in chronic kidney disease with progressive renal failure, a setting in which there is disturbed phosphate balance, leading to phosphate retention, overload, and serious complications such as uncontrolled parathyroid gland over-activity (secondary hyperparathyroidism) and accelerated vascular calcification with associated high cardiovascular morbidity and mortality (20% mortality over 5 years). Classically, the type II sodium phosphate co-transporter NaPi-IIb has been considered to be the rate limiting step for intestinal phosphate absorption. However, recent studies suggest that PiT1 and PiT2 proteins, members of the SLC20 family, are also expressed at the enterocyte brush border membrane, where they may play a role in intestinal phosphate absorption, particularly during dietary phosphate restriction. The role of phosphatonins (novel phosphaturic factors such as FGF-23 and MEPE) in the regulation of phosphate balance, particularly their influence on renal phosphate handling, has been studied in some detail; although evidence is now emerging that the phosphatonins can also regulate intestinal phosphate absorption. This presentation will summarise our current understanding of intestinal phosphate transport and its regulation, its relationship to renal phosphate handling, and try to highlight the potential importance of the gut as a target in the control of hyperphosphatemia in, for example, renal failure.