Pennell J P, Yanagawa N, Hwang K H, Millard M M, Bourgoignie J J
Diabetologia. 1981 Mar;20(3):223-7. doi: 10.1007/BF00252632.
Rats with streptozotocin-induced chronic diabetes mellitus develop a glomerulopathy functionally manifested by proteinuria. The ability of the glomerular capillary wall to retard filtration of macromolecules was examined in 5 chronically diabetic Munich-Wistar rats exhibiting excessive proteinuria (39 +/- 7 mg/24 h, mean +/- SEM) and 5 age-matched normal Munich-Wistar rats without increased proteinuria (4.7 +/- 0.2 mg/24 h). Urinary albumin excretion was not increased in the diabetic rats (2.0 +/- 0.6 mg/24 h vs 1.6 +/- 0.3 mg/24 h) suggesting that the normal net electronegative charge of the glomerular capillary wall was not altered. Fractional clearances of macromolecular neutral dextrans were similar in diabetic and normal rats throughout a wide range of molecular size (18-42 A). Glomerular filtration rate was the same in the two groups of rats (2.77 +/- 0.16 ml/min in diabetics and 2.72 +/- 0.11 ml/min in normals) suggesting that renal haemodynamic factors did not influence fractional clearances of neutral dextrans in diabetic rats. We conclude that the proteinuria exhibited by these chronically diabetic rats is not attributable to alterations of size-selective properties of the glomerular capillary wall, such as increases in the size or the number of pores.
链脲佐菌素诱导的慢性糖尿病大鼠会出现以蛋白尿为功能表现的肾小球病变。在5只表现出蛋白尿过多(39±7毫克/24小时,平均值±标准误)的慢性糖尿病慕尼黑-维斯塔大鼠和5只年龄匹配、无蛋白尿增加(4.7±0.2毫克/24小时)的正常慕尼黑-维斯塔大鼠中,检测了肾小球毛细血管壁阻止大分子滤过的能力。糖尿病大鼠的尿白蛋白排泄未增加(2.0±0.6毫克/24小时对1.6±0.3毫克/24小时),这表明肾小球毛细血管壁正常的净负电荷未改变。在广泛的分子大小范围(18 - 42埃)内,糖尿病大鼠和正常大鼠中大分子中性葡聚糖的分数清除率相似。两组大鼠的肾小球滤过率相同(糖尿病大鼠为2.77±0.16毫升/分钟,正常大鼠为2.72±0.11毫升/分钟),这表明肾血流动力学因素不影响糖尿病大鼠中性葡聚糖的分数清除率。我们得出结论,这些慢性糖尿病大鼠出现的蛋白尿并非归因于肾小球毛细血管壁大小选择性特性的改变,如孔径大小或数量的增加。