title: Bilateral noncystic renal dysplasia in a Wistar-rat.
abstract: In a young Wistar rat a bilateral renal malformation was observed microscopically. Clinical chemistry gave no evidence of impaired kidney function. The kidney weight was slightly elevated and the kidneys showed no gross pathological changes. The lesion was located in the inner cortex of both kidneys and consisted of multiple foci of abnormal renal parenchyma similar to fetal kidney. Three components could be distinguished in the foci: primitive glomerular/tubular structures, tubules resembling collecting ducts and mesenchyme. For further characterisation, histological stains (H&E, PAS, Novotny) and immunohistochemistry (vimentin, pan-cytokeratin, S 100, proliferating cell nuclear antigen, and terminal desoxyribosyl-transferase mediated dUTP nick end labelling) were applied. The glomerular and tubular structures were hyperplastic and positive for proliferating cell nuclear antigen and vimentin. The collecting duct-like tubules were positive for pan-cytokeratin and gave no evidence of proliferation. The two epithelial components of the foci were surrounded by mesenchymal cells which extended also between the normal cortical tubules so that no clear demarcation was discernible. The mesenchymal cells were uniformly spindle-shaped and associated with reticulin fibers. Immunohistochemically they were vimentin-positive and non-proliferative. With terminal desoxyribosyl-transferase mediated dUTP nick end labelling (TUNEL) and S 100 all components were nearly negative. Based on morphology and immunohistochemistry this malformation containing structures derived from the ureteric bud and from the metanephric blastema associated with oligonephronia probably represents a noncystic renal dysplasia. Transition to neoplasia was not observed. A specific cause of this unusual developmental anomaly which was not previously reported in rats could not be determined.
authors.affiliation: Department of Toxicologic Pathology, Bayer AG, Wuppertal, Germany. christine.ruehl-fehlert.cr@bayer-ag.de
authors.forename: Christine I
authors.initials: CI
authors.lastname: Ruehl-Fehlert
authors.forename: Ulrich
authors.initials: U
authors.lastname: Deschl
authors.forename: Martin
authors.initials: M
authors.lastname: Kayser
authors.forename: Elke
authors.initials: E
authors.lastname: Hartmann
mesh_terms: D000818:Animals; D004847:Epithelial Cells / Q000378:metabolism / Q000473:pathology; D007150:Immunohistochemistry; D020287:In Situ Nick-End Labeling; D007633:Keratins / Q000378:metabolism; D007672:Kidney Cortex / Q000002:abnormalities / Q000378:metabolism / Q000473:pathology*; D007674:Kidney Diseases / Q000151:congenital* / Q000378:metabolism / Q000473:pathology; D007685:Kidney Tubules, Collecting / Q000002:abnormalities / Q000378:metabolism / Q000473:pathology*; D008297:Male; D008648:Mesoderm / Q000378:metabolism / Q000473:pathology; D018809:Proliferating Cell Nuclear Antigen / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D014746:Vimentin / Q000378:metabolism
chemical_list: D018809:Proliferating Cell Nuclear Antigen; D014746:Vimentin; D007633:Keratins