Our own studies and those of others have shown that the incidence of c
alcium oxalate stones and plaques is markedly increased by nephrotoxin
s. The possible role of oxalate as a nephrotoxin has not been fully ap
preciated. However, recent studies in experimental animals and in cult
ured cells support this possibility. The results of these studies led
us to hypothesize that hyperoxaluria promotes stone formation in sever
al ways: by providing a substrate for the formation of the most common
form of renal stones, calcium oxalate stones, and by inducing damage
to renal epithelial cells. Damaged cells in rum would produce an envir
onment favorable for crystal retention and provide membranous debris t
hat promotes crystal nucleation, aggregation and adherence. The presen
t report summarizes evidence for oxalate nephrotoxicity and discusses
the potential importance of oxalate toxicity in the pathogenesis of st
one disease.