In birds, transport processes in the lower intestine mediate absorption of ions, water and a variety of organic substrates, including significant amounts of glucose, amino acids derived from protein associated with urate spheres, and short-chain fatty acids derived from fermentation processes. These transport pathways contribute to both osmoregulation and energy homeostasis. Although birds lack a urinary bladder, evidence has shown that ureteral urine, entering the distal lower intestine, is forced into the colon, caecae and even distal portions of the small intestine. Further, substrates also enter the lower intestine from the small intestine. Thus, the lower intestine serves as an 'integrating segment' for mixing and modification of both urinary and intestinal inputs. Of particular interest is that much of the transport activity of the lower intestine is regulated by the hormone aldosterone, which in turn varies inversely with dietary salt content. Numerous studies have shown that following acclimation to low-salt diets, sodium-linked organic substrate co-transporters are largely suppressed, while electrogenic sodium channels (ENaCs) are induced. These changes can be manipulated, at least in part, by resalination of low-salt hens, or by aldosterone administration to high-salt-acclimated birds. In the coprodeum, the changes in transport are paralleled by extensive remodelling of the mucosal surface, with low-salt acclimation increasing cell numbers, microvillus density and length and the proportion of 'mitrochondrial-rich' (MR) cells. The latter may be the sites of proton secretion in the lower intestine. A cAMP-activated chloride secretion pathway is also present in both colon and coprodeum, and may be mediated by a CFTR-like Cl^- channel. There are still a number of unresolved issues, including whether other hormones contribute to the regulation of transport activity.