Crystal/cell interaction and nephrolithiasis.

Crystals of calcium oxalate (CaOx), the major constituents of most urinary stones, are injurious to cells, create oxidative stress and evoke an inflammatory response. Renal injury results in cell damage. The damaged and dead cells are released into the urine and are capable of promoting crystal nucleation at much lower supersaturations. Damaged cell membranes also provide sites for crystal attachment and eventual retention within the kidneys. Renal epithelial damage may assist in movement of crystals from the intratubular to interstitial location and perhaps in the formation of apatitic Randall's plaques. Inflammatory response may be responsible for Randall's plaques ulceration to the renal papillary surface.