Crystal modulators play a significant role in the formation of calcium oxalate stone disease. When renal cells are subjected to oxalate stress, the loss in cell integrity leads to exposure of multiple proteins that assist and/or inhibit crystal attachment and retention. Contact between oxalate and calcium oxalate with urothelium proves fatal to cells as a result of reactive oxygen species generation and onset of oxidative stress. Hence, as a therapeutic strategy it was hypothesised that supplementation of antioxidants would suffice. On the contrary to popular belief, the detection of oxalate induced endoplasmic reticulum mediated apoptosis proved the ineffectiveness of antioxidant therapy alone. Thus, the inadequacy of antioxidant supplementation in oxalate stress invoked the presence of an alternative pathway for the induction of kidney fibrosis in hyperoxaluric rats. In addition to settling this query, the link between oxidative stress and ER stress is not well understood, especially in urolithiasis.

晶体调节剂在草酸钙结石病的形成中起重要作用。当肾细胞遭受草酸盐胁迫时，细胞完整性的丧失导致多种蛋白质的暴露，这些蛋白质有助于和/或抑制晶体的附着和保留。草酸和草酸钙与尿路上皮之间的接触被证明对细胞是致命的，这是由于活性氧的产生和氧化应激的开始。因此，作为一种治疗策略，假设补充抗氧化剂就足够了。与普遍的看法相反，草酸盐诱导的内质网介导的细胞凋亡的检测证明了单独的抗氧化剂治疗无效。从而，草酸盐应激中抗氧化剂补充的不足导致了在高草酸尿大鼠中诱导肾脏纤维化的另一种途径的存在。除了解决这个问题外，还没有很好地了解氧化应激和内质网应激之间的联系，特别是在尿石症中。