Association of interstitial nephritis with tubule cell injury and proliferation in NZB/NZW mice.
The relationship between renal interstitial mononuclear cell infiltration and renal tubule cell (TC) proliferation has been examined in (NZB X NZW) F1 hybrid (B/W) and control mice. TC proliferation was measured by tritiated thymidine ([3H]TdR) injection, autoradiographic examination of kidney sections and enumeration of labelled tubule cells. In B/W mice interstitial infiltration began at 5 months and reached a peak at 9 months. Proliferation of TC began at 7 months and also reached a peak at 9 months. Control mice consisting of NZB, CBA/J and C57Bl/6J mice showed no increase with age. When the percentages of labelled TC in areas adjacent to interstitial infiltrates and distant from them were compared, the TC adjacent to infiltrates showed an approximately four-fold greater amount of labelling. Ultrathin light and  electron microscopic sections demonstrated TC injury in areas in close proximity to infiltrates. These studies suggest that mononuclear cells in the interstitial infiltrate may be injurious to TC, leading to a sequence of injury and subsequent regeneration of these cells. In diseases in which interstitial nephritis is present, such as Sjögren's syndrome, the interstitial infiltrate may contribute to the observed TC dysfunction.
D000818:Animals; D005260:Female; D007684:Kidney Tubules / Q000276:immunology* / Q000648:ultrastructure; D051379:Mice; D008814:Mice, Inbred NZB / Q000276:immunology*; D008815:Mice, Inbred Strains / Q000276:immunology; D008938:Mitosis; D009000:Monocytes / Q000276:immunology; D009395:Nephritis, Interstitial / Q000276:immunology* / Q000473:pathology; D013997:Time Factors