Polypoid and papillary epithelial hyperplasia: a potential cause of ductal obstruction in adult polycystic disease.
Polypoid and papillary epithelial hyperplasia: a potential cause of ductal obstruction in adult polycystic disease.
复制标题
息肉样和乳头状上皮增生：成人多囊病导管阻塞的潜在原因。
作者：
A. Evan;K. Gardner;J. Bernstein
在囊性肾病的实验模型中，功能研究确定了表明对扩张或囊性肾单位流出的阻力增加的条件。形态学上，模型显示细胞增生灶和沿外髓集合管沿着形成的微息肉。在时间上，细胞增殖先于囊肿形成。模型中的这些发现导致了一种假设，即息肉样增生通过增加对肾小管尿液流出的阻力参与易感肾脏中的囊肿形成。本研究旨在确定成人多囊肾病中细胞增生的存在、程度和分布。肾脏从四个无关的个人进行了研究，通过光，透射和扫描电子显微镜。沿着肾单位的增生灶与模型中观察到的相似。这些发现描绘了迄今为止未得到赞赏的模型和人类疾病之间的形态学相似性，并进一步支持的假设，即部分小红斑梗阻参与肾囊肿疾病的发病机制，无论是遗传性或获得性，在动物和人。
In experimental models of cystic renal disease, functional studies define conditions that suggest increased resistance to outflow from dilated or cystic nephrons. Morphologically, models exhibit foci of cellular hyperplasia and micropolyp formation along outer medullary collecting tubules. Temporally, cellular proliferation precedes cyst formation. These findings in models have led to a hypothesis that polypoid hyperplasia participates in cyst formation in susceptible kidneys by increasing resistance to the outflow of tubular urine. The present study was undertaken to establish the presence, extent, and distribution of cellular hyperplasia in human adult polycystic kidney disease. Kidneys from four unrelated individuals were studied by light and by transmission and scanning electron microscopy. Foci of hocation of hyperplasia along the nephron were similar to those seen in the models. These findings delineate a heretofore unappreciated morphologic similarity between the models and human disease and add further support to the hypothesis that partial rubular obstruction participates in the pathogenesis of renal cystic disease, whether it be heritable or acquired, in animals and in man.