During development of the disease urinary oxalate is increased and renal epithelial cells come in contact with abnormally high levels of oxalate and calcium oxalate crystals resulting in localized inflammation. Expression of immediate early genes is induced. Production of urinary macromolecules such as osteopontin and bikunin is upregulated. Cells are injured. Some go through necrosis and others become apoptotic.
Crystal binding to renal epithelail cells is increased in response to injury.
There is evidence of oxidative stress and lipid peroxidation of cell membranes. Dead cells are sloughed off their basement membranes. Cell membrane fragments are released into the urine where they can promote further crystallization. Aggregation and retention of crystals in the renal tubules initoiate the stone formation. Last updated on August 3, 2000.