Abstract

Tubular cells and nephron-derived crystal nuclei may play a significant role in determining renal calcification. The most common component of renal stones is calcium oxalate monohydrate, and crystals of COM were quickly bound and absorbed by kidney epithelial cells in monolayer culture (BSC-1 line). It was observed that renal cells and COM crystals interact by the use of scanning and transmission electron microscopes, kinetic investigation of crystals tagged with ['4C]. Electron microscopy revealed that adherent crystals on the apical cell surface serve as aggregation sites. The plasma membrane domains enclosing internalized crystals demonstrated increased binding of exogenous crystals for at least 24 hours after the first cell-crystal interaction. Within lysosomal inclusion bodies, crystals that had been internally ingested seemed to disintegrate during the next five to seven weeks. Many cells with crystals remained in the monolayer at this phase. Adhesion and internalisation have been proven to assist crystals remain in situ, although intracellular breakdown of crystals may represent a hitherto undiscovered protection against kidney calcification.

Description