Polypoid and papillary epithelial hyperplasia: a potential cause of ductal obstruction in adult polycystic disease.
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.
D000818:Animals; D004195:Disease Models, Animal; D004848:Epithelium / Q000473:pathology; D006801:Humans; D006965:Hyperplasia; D007679:Kidney Medulla / Q000648:ultrastructure; D007680:Kidney Neoplasms / Q000648:ultrastructure; D007684:Kidney Tubules / Q000473:pathology*; D008297:Male; D008855:Microscopy, Electron, Scanning; D007690:Polycystic Kidney Diseases / Q000209:etiology / Q000473:pathology*; D011127:Polyps / Q000648:ultrastructure; D051381:Rats