Urate and p-aminohippurate transport in isolated kidney tubules of normal and hyperuricemic chickens.

Urate and p-aminohippurate accumulations of kidney tubule fragments were studied in 5- to 6-week-old normal (LUA) and hyperuricemic (HUA) chickens. Tubules from LUA chicks consistently accumulated two to three-fold as much urate and p-aminohippurate as tubules from HUA chicks and thus confirmed the tubular origin of the urate transport defect in HUA chickens. A sodium gradient was required for optimal urate and p-aminohippurate accumulations and ouabain inhibited the accumulations of both compounds. Similar responses of urate and p-aminohippurate to treatments and reciprocal inhibitions between these compounds suggest that urate and p-aminohippurate are accumulated through a shared transport system.