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At least 757 records · Page 42Linked to original sources
PubMed1981

Chronic interstitial nephritis. Its occurrence with oxalosis and anti-tubular basement membrane antibodies after jejunoileal bypass.

A 38-year-old woman suffered rapid onset of renal failure between 11 and 15 months after undergoing a jejunoileal bypass for morbid obesity. Microscopic examination of renal biopsy specimens revealed oxalosis and severe tubulointerstitial nephritis. Immunofluorescence microscopy disclosed linear staining of tubular basement membranes with antisera to IgG and C3, which suggests antitubular basement membrane disease, a side effect not previously recognized with jejunoileal bypass. Possible mechanisms leading to the formation of these antibodies include (1) oxalate damage to renal tubules with release of tubular basement membrane antigens, and (2) bacterial overgrowth in the bypass segment, with mucosal damage and release of intestinal mucosal antigens that share antigenetic determinants with renal proximal tubules. Anti-tubular basement membrane disease may be an additional mechanism that produces or enhances renal damage in patients with jejunoileal bypass.

Adult↗
PubMed1980

Cell-mediated immunity in interstitial nephritis. III. T lymphocyte-mediated fibroblast proliferation and collagen synthesis: an immune mechanism for renal fibrogenesis.

Fibroblast proliferation and collagen synthesis play an important role in the progression of intersititial nephritis. To evaluate the involvement of immune mechanisms in this process, we induced intersititial nephritis in guinea pigs utilizing injections of tubular antigens. Over a 3-week period, injected animals developed a nephritis characterized by mononuclear infiltrates and expanding areas of fibrotic scar formation. Involved kidneys contained increased collagen as compared to controls. To identify mediators of the observed fibrogenesis, T lymphocytes from nephritic and control animals were stimulated with soluble tubular antigens. Dialyzed supernatants from control lymphocyte cultures contained an inhibitor of both fibroblast proliferation and collagen synthesis. In contrast, supernatants from nephritic animals demonstrated absence of inhibition and a progressively increasing titer of a factor that enhanced both kidney fibroblast proliferation and collagen synthesis. As the disease progressed, however, nephritic lymphocytes also began secreting an inhibitor of proliferation that could be detected in low levels. These studies suggest, therefore, that immune mechanisms and altered lymphocyte function may play an important role in the development, progression, and regulation of renal fibrogenesis in intersititial nephritis.

Animals↗