Mediation of calcium oxalate crystal growth on human kidney epithelial cells with different degrees of injury

The current study examined the role of injured human kidney tubular epithelial cell (HKC) in the mediation of formation of calcium oxalate (CaOxa) crystals by means of scanning electronic microscopy and X-ray diffraction. HKC was injured using different concentrations of H2O2. Cell injury resulted in a significant decrease in cell viability and superoxide dismutase (SOD) concentration and an increase in the level of malondialdehyde (MDA) and expression of osteopontin (OPN). Injured cells not only promote nucleation and aggregation of CaOxa crystals, but also induce the formation of calcium oxalate monohydrate (COM) crystals that strongly adhere to cells. These results imply that injured HKCs promote stone formation by providing more nucleating sites for crystals, promoting the aggregation of crystals, and inducing the formation of COM crystals.

Injured cells promote nucleation and aggregation of CaOxa crystals, induce the formation of calcium oxalate monohydrate (COM) crystals.Figure optionsDownload as PowerPoint slideHighlights
► A direct nucleation and growth of CaOxa crystals on both normal and injured cells.
► Stronger green fluorescence, i.e. OPN expression, was seen on the injury cell surface
► Injured cells promote nucleation and aggregation of CaOxa crystals.
► Injured cells induce the formation of calcium oxalate monohydrate crystals.
► H2O2 decrease cell viability in a dose-dependent manner at 0.1–1 mmol/L.