Abe H, Shibuya T, Odashima S, Arichi S, Nagase S
Research Institute of Oriental Medicine, Kinki University, Osaka, Japan.
Nephron. 1988;50(4):351-5. doi: 10.1159/000185201.
Whether obliteration of glomerular epithelial foot processes and increases in urinary N-acetyl-beta-D-glucosaminidase (NAG) activity are the consequence or the cause of proteinuria after administrations of the aminonucleoside of puromycin was examined using Nagase analbuminemic rats. The administration of puromycin aminonucleoside to Nagase analbuminemic rats did not induce proteinuria. However, the increase in urinary NAG activity and the degree of abnormality of foot processes in the glomerular cells were similar to those in control Sprague-Dawley rats. These findings suggest that NAG excretion and the morphological alterations of epithelial cells in nephrosis are not the consequence of massive proteinuria.
使用长谷部无白蛋白血症大鼠研究了给予嘌呤霉素氨基核苷后,肾小球上皮足突的消失及尿N-乙酰-β-D-氨基葡萄糖苷酶(NAG)活性增加是蛋白尿的结果还是原因。向长谷部无白蛋白血症大鼠给予嘌呤霉素氨基核苷未诱导蛋白尿。然而,尿NAG活性的增加及肾小球细胞足突异常程度与对照的斯普拉格-道利大鼠相似。这些发现提示,肾病中NAG排泄及上皮细胞的形态学改变并非大量蛋白尿的结果。