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Calcium oxalate monohydrate (COM) is the most prevalent mineral component found in human kidney stones, accounting for approximately 70-80% of all cases (Basavaraj et al., 2007). The COM crystal surface acts as a primary interface for crystal growth, aggregation, and attachment to renal tubular epithelial cells, which are essential steps in the pathogenesis of nephrolithiasis (Khan et al., 2016). Therapeutic interventions target the crystal surface using small molecule inhibitors like citrate and hydroxycitrate that bind to specific lattice sites, thereby increasing the energy barrier for further ion addition and preventing the development of large, obstructive stones (Chung et al., 2016). Additionally, the surface properties of COM crystals determine their interaction with the renal epithelium, where adhesion can trigger inflammatory responses and cellular injury (Moe, 2006). Understanding the molecular interactions at the COM surface is crucial for developing effective antilithic agents that can modulate crystallization kinetics and reduce the risk of stone recurrence (Pearle et al., 2014).
Inhibition of crystal nucleation, growth, and aggregation through surface binding and site blocking, which increases the energy barrier for ion addition and prevents crystal-cell adhesion.
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