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以离体肾小管上皮细胞为研究对象，重金属镉为损伤因素，观察了镉致肾小管上皮细胞损伤时细胞内钙稳态的变化及其与肾小管上皮细胞损伤之间关系。结果表明，用重金属镉处理后，肾小管上皮细胞内胞浆游离钙水平明显升高，且同时伴有一系列超微结构的损害；钙通道阻滞剂异丙嗪表现出明显的阻断、保护作用，本实验提示在重金属镉致肾损伤过程中钙超载机制起着很重要的作用。
In vitro renal tubular epithelial cells as the research object, heavy metal cadmium as the injury factor, observe the changes of intracellular calcium homeostasis during renal tubular epithelial cell injury and its relationship with renal tubular epithelial cell injury. The results showed that after treatment with heavy metal cadmium, the level of intracellular free calcium in renal tubular epithelial cells was significantly increased, accompanied by a series of ultrastructural damage; Promethazine, a calcium channel blocker, showed obvious blocking and protection Role, this experiment suggests that calcium overload mechanism plays a very important role in the process of kidney injury caused by heavy metal cadmium.