Zimmerman S W
Am J Pathol. 1979 Feb;94(2):285-300.
Rats given N,N'-diacetyl benzidine (N,N'-DAB) by intraperitoneal injections were studied to further characterize the ensuing renal disease. Significant proteinuria and albuminuria occurred at 10 weeks and thereafter and was enhanced by prior unilateral nephrectomy. Glomerular epithelial cell vacuolization and cyst formation were marked in proteinuric rats. Focal glomerular sclerosis and synechia were present, but proliferative crescent formation was not. Glomerular fibrinogen was noted, but no immunoglobulins or C3 was detected by immunofluorescence microscopy. Glomerular epithelial cell cysts and disruption were noted ultrastructurally, but no electron-dense deposits were seen. Tubular basement membrane thickening and wrinkling were noted in N,N'-DAB rats, and maximum urine osmolarlity was decreased. None of the animals developed renal insufficiency. Parenteral N,N'-DAB-induced renal disease is different from crescentic glomerulonephritis noted in rats fed N,N'-DAB and has similarities to an experimental model of aminonucleoside induced focal sclerosis, supporting the theory of primary glomerular epithelial cell injury mediating proteinuria and focal sclerosis.
通过腹腔注射给予大鼠N,N'-二乙酰联苯胺(N,N'-DAB),以进一步明确随后发生的肾脏疾病的特征。在10周及之后出现显著的蛋白尿和白蛋白尿,并且预先进行单侧肾切除会使其加重。蛋白尿大鼠中肾小球上皮细胞空泡化和囊肿形成明显。存在局灶性肾小球硬化和粘连,但未出现增殖性新月体形成。可见肾小球纤维蛋白原,但免疫荧光显微镜检查未检测到免疫球蛋白或C3。超微结构观察到肾小球上皮细胞囊肿和破坏,但未见电子致密沉积物。在N,N'-DAB大鼠中观察到肾小管基底膜增厚和皱缩,最大尿渗透压降低。没有动物出现肾功能不全。肠外给予N,N'-DAB诱导的肾脏疾病不同于喂食N,N'-DAB的大鼠中出现的新月体性肾小球肾炎,并且与氨基核苷诱导的局灶性硬化实验模型有相似相似相似,支持原发性肾小球上皮细胞损伤介导蛋白尿和局灶性硬化的理论。