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为了解糖尿病早期肾小管上皮细胞（ｒｅｎａｌｔｕｂｕｌａｒｅｐｉｔｈｌｉａｌｃｅｌｌｓ， 简称ＲＴＥＣｓ） 是否有损害，探讨微蛋白尿发生的机制。方法：四氧嘧啶（ａｌｌｏｘａｎ）尾静脉注射（５０ ｍｇ／ｋｇ）雄性Ｗｉｓｔａｒ 大鼠６０ 只，石蜡包埋肾切片经ＴＵＮＥＬ法和ＰＣＮＡ、ＢｒｄＵ免疫组化染色。结果：成模后２０～６０ ｄ 和９０～１４０ ｄ，ＴＵＮＥＬ法阳性ＲＴＥＣｓ 主要出现在远端小管、髓质肾小管、集合管。ＰＣＮＡ、ＢｒｄＵ 免疫组化染色阳性ＲＴＥＣｓ 主要见于注射后４０ ｄ、１３０ ～１４０ ｄ 皮质和髓质肾小管、集合管，其出现的部位、数量与凋亡基本一致。结论：本研究结果表明，高糖对ＲＴＥＣｓ 是一种亚坏死性损伤剂，导致其凋亡发生率增加，同时可能影响肾小管重吸收和分泌功能。ＲＴＥＣｓ 增殖发生略晚，但与凋亡发生率相匹配。笔者推测借此种机制糖尿病早期ＲＴＥＣｓ 的数目和肾小管的形态得以保护，造成一般组织学方法不能将ＲＴＥＣｓ 的损伤检测出来。
To investigate whether there is damage to early stage renal tubular epithelial cells (diabetes mellitus, renal tubular epithelial cells, RTECs), to explore the mechanism of microalbuminuria. METHODS: Sixty male Wistar rats were injected intravenously with alloxan (50 mg / kg). Paraffin-embedded sections were stained with TUNEL method and PCNA and BrdU immunohistochemistry. RESULTS: TUNEL-positive RTECs mainly appeared in distal tubules, medulla tubules and collecting ducts at 20-60 days and 90-140 days after injection. PCNA and BrdU positive immunohistochemical staining of RTECs were mainly found in the cortex and medulla tubules and aggregates after 40 days and 130 ~ 140 days after injection. CONCLUSIONS: The results of this study indicate that high glucose is a sub-necrotic damaging agent to RTECs, resulting in an increased incidence of apoptosis and a possible impact on renal tubular reabsorption and secretion. RTECs proliferate slightly later, but match the incidence of apoptosis. The authors hypothesize that by virtue of this mechanism, the number of early diabetic RTECs and the morphology of the renal tubules can be protected, resulting in a general histological method that can not detect RTECs lesions.