Tubulointerstitial inflammation, cast formation, and renal parenchymal damage in experimental pyelonephritis.
Some basic changes in experimental pyelonephritis were studied by transmission and scanning electron microscope. Initially, bacteria settled and multiplied in capillaries and venules. Leukocytes first marginated and then escaped from the capillaries, particularly to the wide peritubular interstitium. After opening the tubular basement membrane, the infiltrating leukocytes were immediately localized in the tubular wall between epithelial cells but were never seen between the epithelial cells and the underlying basement membrane. The inflammatory cells seemed not to be able to pass through the tight junctions of the nonnecrotic tubular epithelium. As a consequence of severe inflammatory injury, the tight junctions exhibited alterations of intermediate junction type. Where circumscribed necrosis of the tubular walls occurred, leukocytes appeared in the lumen. Thus, pus casts originated from these sites, apparently as drainage of interstitial abscesses. The secondary/regressive and regenerative/tubular changes were similar to those occurring after various tubular lesions.
D000038:Abscess / Q000473:pathology; D000818:Animals; D001424:Bacterial Infections / Q000473:pathology*; D001485:Basement Membrane / Q000648:ultrastructure; D007672:Kidney Cortex / Q000648:ultrastructure; D007684:Kidney Tubules / Q000648:ultrastructure*; D007962:Leukocytes / Q000473:pathology; D008297:Male; D008855:Microscopy, Electron, Scanning; D009395:Nephritis, Interstitial / Q000473:pathology*; D011704:Pyelonephritis / Q000473:pathology*; D051381:Rats; D011919:Rats, Inbred Strains