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Because of difficulty in obtaining cystic human kidneys for functional and morphologic study, animal models are receiving increasing attention. Most prominent among them is the renal cystic disease that is induced in rats through feeding of the antioxidant, diphenylamine, The present study examined the morphology of adult polycystic and medullary cystic kidney disease in man using scanning electron microscopy and compared them with diphenylamine-induced cystic kidney disease in rats. Diphenylamine nephropathy was induced by feeding rats 1 per cent diphenylamine for 12 to 18 months. All types of cystic disease showed changes in the renal corpuscles, including dilation of Bowman's space, podocyte fusion and degeneration, and basement membrane thickening. Cysts were noted along the entire nephron in polycystic and diphenylamine-induced cystic disease but only along the collecting ducts in medullary cystic disease. Cysts in polycystic disease were large and lined by flattened epithelium. Collecting duct cysts in diphenylamine cystic disease were lined by cells of irregular size and shape suggestive of cell hypertrophy and/or hyperplasia, whereas cysts of medullary cystic disease were lined by flattened epithelium except where the nephron entered or left the cyst. Cast material was generally found in the cysts of diphenylamine-induced and polycystic kidney disease but not medullary cystic disease. Atrophic glomeruli and tubules were found in all three diseases. Complete tubular obstruction was found in none; however, larger cysts frequently impinged on adjacent tubules and narrowed their lumina. The results of this study show that, in the terminal stages, cellular as well as gross morphologic differences exist between polycystic and medullary cystic kidney disease and that diphenylamine-induced cystic disease more closely resembles human polycystic than medullary cystic kidney disease.

The long-term pathologic effects of the antitumor drug, cis-diamminedichloroplatinum II (CP) on the structure of the rat kidney were investigated. Light microscopy and transmission and scanning electron microscopy were used to characterize the morphologic changes 2 weeks, 4 weeks, and 6 months after the intraperitoneal injection of CP to rats. At all time intervals examined, the S3 segment of the proximal tubule located in the outer stripe of the medulla showed the most consistent pattern of injury. Two weeks after CP, the proximal tubules located in the outer stripe region as well as in the medullary rays were widely dilated and lined by low-lying epithelial cells, many of which contained large atypical nuclei. Many tubules still showed evidence of necrosis, whereas other tubules appeared to be undergoing atrophic changes. After 4 weeks, proximal tubular dilation continued resulting in the formation of numerous microcysts in the region of the outer stripe. These changes appeared to progress, and after 6 months large cysts (mean diameter 2152 +/- 1241 micrometer) were identified which involved the entire outer stripe, with many of these cysts extending to the subcapsular cortex. The kidneys at this time period showed a pattern of chronic renal injury in the outer stripe, and this damage was now also observed in the cortex. In several animals, small foci of abnormal foam cells surrounded by a basal lamina could be identified. We conclude that CP has a pronounced long-term effect and causes cyst formation in the rat kidney.