Kelley V E, Cavallo T
Lab Invest. 1976 Sep;35(3):213-20.
Glomerular epithelial slit alterations and their relation to proteinuria have not been studied in detail in New Zealand Black/White (NZB/W) mice. The kidneys of proteinuric and nonproteinuric female NZB/W mice and normal Swiss albino mice were perfusion-fixed with tannic acid-glutaraldehyde and studied by light and electron microscopy. Semiquantitative studies were performed on full montages of glomeruli enlarged 10,000 times. Fine structural alterations of the epithelial slits, with emphasis on the slit diaphragm, were studied on semiserial thin sections. Proteinuric NZB/W mice with features of membraneous nephropathy exhibited: (1) wedging of electron-dense deposits below the slit diaphragm, (2) enlargement and distortion of interpedicel spaces, (3) displacement, folding, and stacking of slit diaphragms, (4) formation of occluding junctional complexes in residual slits, and (5) variable loss of foot processes. Similar alterations were not observed in controls or nonproteinuric NZB/W mice, including animals having complexes inglomerular mesangia but not in epithlialslits. These studies show that in NZB/W mice, abnormal protein excretion is associated with structural modification of the slit pore and suggest a role for such a component in the process of protein ex
在新西兰黑/白（NZB/W）小鼠中，尚未对肾小球上皮裂孔改变及其与蛋白尿的关系进行详细研究。对蛋白尿和非蛋白尿雌性NZB/W小鼠以及正常瑞士白化小鼠的肾脏用单宁酸 - 戊二醛进行灌注固定，并通过光镜和电镜进行研究。对放大10000倍的肾小球全切片进行半定量研究。在半连续薄切片上研究上皮裂孔的精细结构改变，重点是裂孔隔膜。具有膜性肾病特征的蛋白尿NZB/W小鼠表现出：（1）电子致密沉积物楔入裂孔隔膜下方；（2）足突间隙增大和变形；（3）裂孔隔膜移位、折叠和堆叠；（4）残余裂孔中形成封闭连接复合体；（5）足突可变丢失。在对照组或非蛋白尿NZB/W小鼠中未观察到类似改变，包括肾小球系膜中有复合物但上皮裂孔中没有的动物。这些研究表明，在NZB/W小鼠中，异常蛋白质排泄与裂孔孔道的结构改变有关，并提示该成分在蛋白质排泄过程中起作用。
