Purpose-Kidney stone formation is associated with the deposition of hydroxyapatite (HA) either as sub-epithelial plaques or tubular deposits in the renal papillae. We investigated the effect of renal epithelial exposure to HA crystals in vitro to develop an insight into the pathogenesis of kidney stones.Materials and methods-NRK52E cells were exposed to 67 μg/cm 2 or 133 μg/cm 2 of HA or calcium oxalate monohydrate crystals. In some studies cells were also exposed to crystals from the basal side. After exposure of 3 or 6 hours media were analyzed for, lactate dehydrogenase (LDH), 8-isoprostane (8-IP) and hydrogen peroxide (H 2 O 2 ). Media collected after cells' exposure on the apical side was also analyzed for the production of monocyte chemoattractant-1 (MCP-1) and prostaglandin E2 (PGE2). Cells were stained with DAPI to determine apoptotic activity and examined by SEM to observe crystal-cell interaction.Results-Cell exposure to HA resulted in the production of H 2 O 2 and 8-IP as well as release of LDH. Apical exposure appeared more provocative and injurious than the basal exposure. An exposure to HA for 6 hours, resulted in increased apoptotic activity. Apical exposure also resulted in increased production of MCP-1 and PGE2.Conclusion-Cell exposure to HA crystals induces oxidative stress, lipid peroxidation, and caused upregulation of mediators of inflammation that may be responsible for the inflammation in kidneys of stone patients associated with tubular deposition of HA. They may also play a role in eruption of subepithelial Randall's plaques to the papillary surface.
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