Oxalate transport in renal tubular cells from normal and stone-forming animals.

To investigate the cellular mechanism(s) underlying kidney stone disease, we examined oxalate uptake in suspensions of renal cortical and papillary cells derived from control and stone-forming animals. In control animals, both cortical and papillary cells exhibited a time-dependent accumulation of oxalate. This uptake was mediated both by passive diffusion and by one or more transport processes sensitive to the anion transport inhibitor, DIDS. Oxalate uptake was also markedly sensitive to extracellular pH, showing increased uptake at acidic pH outside (pHo) (6.0), and reduced uptake at alkaline pHo (8.0). In renal tubular cells from stone-forming animals, oxalate uptake was markedly altered. Uptake was significantly reduced in cortical cells, whereas it was significantly stimulated in papillary cells from the same animals. Since the observed changes in oxalate handling occurred only in stone-forming animals, it is possible that alterations in renal cell oxalate transport contribute to calcium oxalate stone formation.