Glomerular hemodynamic changes vs. hypertrophy in experimental glomerular sclerosis.
Glomerular hemodynamic changes vs. hypertrophy in experimental glomerular sclerosis.
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实验性肾小球硬化中的肾小球血流动力学变化与肥大。
DOI：
10.1038/ki.1989.35
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发表时间：
1989
影响因子：
19.6
通讯作者：
Ichikawa,I
中科院分区：
文献类型：
--
作者：
Yoshida,Y;Fogo,A;Ichikawa,I
实验性肾小球硬化肾小球血流动力学改变与肥大的对比研究。在最近对慢性肾脏疾病动物的各种研究中，研究人员发现肾小球压力和血流的升高与肾小球肥大之间存在密切的相关性。为了探讨肾小球功能亢进和肥大之间的可能联系，我们研究了肾切除和单侧输尿管转流(UD)后的功能和形态后遗症(即在保留肾组织的情况下去除肾清除功能)。在所有9个实验组54只慕尼黑-Wistar大鼠中，通过结扎左肾动脉的两支或三支，将2/3的肾脏肿块从左肾切除。1B、2B、3B组行右肾切除(NPX)，1C、2C、3C组行UD。对照组、1A组、2A组和3A组右肾未受影响。分别于术后4天(1A、1B、1C组)、2周(2A、2B、2C组)或4周(3A、3B、3C组)进行组织学观察和组织学观察。在第4天和第2周，NPX组和UD组与对照组相比，左肾肾小球高血压、高灌流和高滤过程度显著且相当。UD组肾小球最大平面面积(PAmax)在术后4天和2周时与对照组相近，而NPX组的PAmax显著增加。在4周时，NPX组和UD组的左肾再次出现类似程度的肾小球高血压和高滤过。然而，在对照组(平均：0.02)和UD组(平均：0.19)中，四周后评估的肾小球硬化(0到4分)很轻微，而NPX组的硬化指数(平均：0.56)显著高于对照组。结果表明：1)肾单位的生理损失，除了其排泄功能的丧失外，还需要触发肾小球肥大和硬化。2)虽然肾小球肥大似乎是肾小球硬化之前的一个重要步骤，但仅有肾小球功能亢进对肾小球肥大和硬化的诱导作用很小。
Glomerular hemodynamic changes vs. hypertrophy in experimental glomerular sclerosis. In a variety of recent studies in animals with chronic renal diseases, investigators have found a tight correlation between the elevation in glomerular pressures and flows versus glomerular hypertrophy. To investigate a possible causal link between the glomerular hyperfunction and hypertrophy, we studied the functional and morphological sequelae of nephrectomy and those of unilateral ureteral diversion (UD) into the peritoneal cavity (that is, removal of renal clearance function while keeping the kidney tissue in situ). In all nine experimental groups of 54 Munich-Wistar rats, 2/3 of the renal mass was removed from the left kidney by ligation of two or three branches of the left renal artery. In addition, right nephrectomy (NPX) was performed in Groups 1B, 2B and 3B or UD in Groups 1C, 2C and 3C. The right kidney was left untouched in control groups, Groups 1A, 2A and 3A. Micropuncture measurements and histological studies were performed at four days (Groups 1A, 1B and 1C), two weeks (Groups 2A, 2B and 2C) or four weeks (Groups 3A, 3B and 3C). At both four days and two weeks, NPX and UD groups had marked and comparable degrees ofglomerular hypertension, hyperperfusion and hyperfiltration compared to the control group in the left kidney. Whereas the maximum planar area of glomeruli (PAmax) of the UD group assessed at four days and two weeks by serial section histological analysis remained at a level similar to that of the control group, PAmaxwas significantly increased in the NPX group. At four weeks, similar degrees of glomerular hypertension and hyperfiltration were again demonstrated in the left kidney of NPX and UD groups. However, whereas glomerular sclerosis (0 to 4 scale) assessed at four weeks was subtle in the control group (mean: 0.02) and in the UD group (mean: 0.19), a significantly and markedly higher sclerosis index (mean: 0.56) was noted in the NPX group. The results indicate that 1) physical loss of nephrons, in addition to loss of their excretory function, is required to trigger glomerular hypertrophy and sclerosis. 2) While glomerular hypertrophy appears to be an important step preceding glomerular sclerosis, glomerular hyperfunction alone does little to induce glomerular hypertrophy and sclerosis.