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目的比较慢性和急性染镉所致肾损伤的差异。方法给小鼠多次注射ＣｄＣｌ２（剂量：镉０．８～１．２ｍｇ／ｋｇ，每周６次，共６周），或一次给予大量注射镉金属硫蛋白复合物（ＣｄＭＴ，剂量：镉０．２～０．４ｍｇ／ｋｇ），然后比较其肾损伤。结果小鼠一次性大量注射ＣｄＭＴ主要产生肾脏近曲小管的坏死，虽然其肾镉含量仅为８μｇ／ｇ，但尿蛋白、尿糖、尿酶活力和血尿素氮含量均明显增高。与此相比，慢性染镉的小鼠肾镉含量高达１３５μｇ／ｇ，但仅有轻度近曲小管坏死及浊肿，上述尿、血指标仅略为增高。除近曲小管损伤外，慢性染镉还造成小鼠肾小球损伤，间质炎症，肾小管细胞凋亡、萎缩及再生。小鼠ＣｄＭＴ在慢性染镉后升高１００倍，达４５０μｇ／ｇ，但急性染镉仅略升高到２５μｇ／ｇ。结论用注射ＣｄＭＴ的急性染镉法来研究慢性染镉所致的肾损伤有一定的局限性。
Objective To compare the differences of chronic kidney injury and acute kidney injury caused by cadmium exposure. Methods Mice were injected with CdCl2 multiple times (dose: 0.8 ~ 1.2mg / kg cadmium, 6 times a week for 6 weeks), or a large amount of cadmium metallothionein complex (CdMT, .2 ~ 0.4mg / kg), and then compare their kidney damage. Results The single injection of CdMT into mice resulted in the necrosis of renal proximal tubule. Although the kidney cadmium content was only 8 μg / g, the proteinuria, urinary glucose, urinary enzyme activity and blood urea nitrogen were significantly increased. In contrast, cadmium in mice with chronic Cd exposure was as high as 135 μg / g, with only mild proximal tubule necrosis and turbidity, with only slightly elevated urine and blood indices. In addition to proximal tubule injury, chronic cadmium also caused glomerular injury in mice, interstitial inflammation, tubular apoptosis, atrophy and regeneration. Mouse CdMT increased 100-fold to 450 μg / g after chronic exposure to cadmium, but the level of cadmium in acute exposure rose only slightly to 25 μg / g. Conclusions There is a limitation on the study of chronic cadmium-induced renal injury by injecting CdMT into acute cadmium.