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Tubular basement membrane

Hansen ES, Tauris P. Methicillin-induced nephropathy. A case with linear deposition of IgG and C3 on the tubular-basement-membrane. Acta Pathol Microbiol Scand [A] 1976 84(5) 440-2. [Pg.2768]

Ortiz A, Plaza JJ, Egido J. Ciprofloxacin-associated tubulointerstitial nephritis with linear tubular basement membrane deposits. Nephron. 1992 60(2) 248. [Pg.380]

Ueda S, Wakashin M, Wakashin Y, Yoshida H, Azemoto R, lesato K, Mori T, Mori Y, Ogawa M, Okuda K. Autoimmune interstitial nephritis in inbred mice. Analysis of mouse tubular basement membrane antigen and genetic control of immune response to it. Am J Pathol 1988 132 304-318. [Pg.474]

Renal 1.9 M (marked thickening of glomerular and tubular basement membranes degeneration and atrophy of tubule epithelium) ... [Pg.103]

This MRL was based on a NOAEL of 0.23 mg Hg/kg/day for renal effects in rats administered mercuric chloride 5 days a week for 6 months (Dieter et al. 1992 NTP 1993). This dose was duration-adjusted for a 5 day/week exposure and divided by an uncertainty factor of 100 (10 for extrapolation from animals to humans and 10 for human variability). Increased absolute and relative kidney weights were observed in rats exposed to 0.46 mg Hg/kg/day, the next higher treatment level. At higher doses, an increased incidence of nephropathy (described as foci of tubular regeneration, thickened tubular basement membrane, and scattered dilated tubules containing hyaline casts) was observed. Renal toxicity is a... [Pg.260]

Other secretory products of the nephron are not weU understood. For example, a significant proportion of normal urinary protein is formed by Tamm Horsfall glycoprotein (THG). This protein is secreted by the distal tubule and is thought to play a role in inhibiting kidney stone formation, but this has not been confirmed conclusively. The tubular epithelial cells also synthesize a vast range of growth factors and cytokines in response to a variety of stimuli that can have both autocrine and paracrine effects. All cells also secrete a range of cell adhesion molecules that are essential to cellular attachment to the tubular basement membrane. [Pg.1679]

Kidney Anti-TBM (tubular basement membrane) nephritis ND... [Pg.48]

When tested, the amyloid is of the secondary type, amyloid A protein. Serum amyloid A, an acute phase reactant produced by hepatocy tes, circulates complexes to high density lipoprotein and is cleaved into smaller fragments which subsequently polymerize into the P pleated sheet configuration of amyloid [23, 35]. In heroin related amyloidosis, the amyloid is heavily distributed in the tubular basement membranes, vessel walls, and interstitium as well as the glomeruli. There is greater tubular basement membrane and interstitial amyloid deposition in drug related renal amyloid than in secondary renal amyloid unrelated to heroin abuse... [Pg.388]

Figure 4. Glomerular (A) and tubular (B-D) lesions in PPD intoxication. H E staining. A. Glomerular swelling and hypercellularity. B. Inflammatory cells are present around eosinophilic intraluminal material (arrow). Some tubular epithelial cytoplasm is attenuated. C. Tubular basement membrane is distinct in some areas. D. Intraluminal inflammatory cells are seen with a small proteinaceous casts. The tubular basement membrane is indistinct. Figure 4. Glomerular (A) and tubular (B-D) lesions in PPD intoxication. H E staining. A. Glomerular swelling and hypercellularity. B. Inflammatory cells are present around eosinophilic intraluminal material (arrow). Some tubular epithelial cytoplasm is attenuated. C. Tubular basement membrane is distinct in some areas. D. Intraluminal inflammatory cells are seen with a small proteinaceous casts. The tubular basement membrane is indistinct.
Fig. 13.1. The transport of amino acids across the intestinal and tubular cells involves several steps, which are demonstrated schematically for a proximal tubular cell AAy amino acid BLMy basolateral membrane BBMy brush border membrane TBMy tubular basement membrane ly specific transporter at the luminal membrane 2, passive efflux from cytosol into tubular lumen 3, transport system at the basolateral membrane 4, transport from peritubular site into cytosol 5, energy production for electrolyte transport 5, passive efflux via paracellular gaps. (Taken from Foreman, JW and Segal, S (1987) Fanconi syndrome. In Pediatric Nephrology (eds. Holliday MA, Barratt TM and Vernier RC), pp 547-565, Williams and Wilkins, Baltimore, with permission to and modified by Brodehl J)... Fig. 13.1. The transport of amino acids across the intestinal and tubular cells involves several steps, which are demonstrated schematically for a proximal tubular cell AAy amino acid BLMy basolateral membrane BBMy brush border membrane TBMy tubular basement membrane ly specific transporter at the luminal membrane 2, passive efflux from cytosol into tubular lumen 3, transport system at the basolateral membrane 4, transport from peritubular site into cytosol 5, energy production for electrolyte transport 5, passive efflux via paracellular gaps. (Taken from Foreman, JW and Segal, S (1987) Fanconi syndrome. In Pediatric Nephrology (eds. Holliday MA, Barratt TM and Vernier RC), pp 547-565, Williams and Wilkins, Baltimore, with permission to and modified by Brodehl J)...
Direct tubular damage and glomerular degeneration by an urdcnown mechanism, in addition to calcification of tubular basement membranes... [Pg.109]


See other pages where Tubular basement membrane is mentioned: [Pg.286]    [Pg.95]    [Pg.566]    [Pg.567]    [Pg.145]    [Pg.2171]    [Pg.461]    [Pg.462]    [Pg.463]    [Pg.470]    [Pg.572]    [Pg.600]    [Pg.636]    [Pg.950]    [Pg.252]    [Pg.1405]    [Pg.136]    [Pg.136]    [Pg.299]    [Pg.675]    [Pg.884]    [Pg.246]    [Pg.358]    [Pg.54]    [Pg.309]    [Pg.310]    [Pg.310]    [Pg.317]    [Pg.421]    [Pg.684]    [Pg.117]    [Pg.120]    [Pg.115]    [Pg.486]    [Pg.280]   


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