Excretion and synthesis of basement membrane disaccharide units in Masugi nephritis (original) (raw)
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Histochemical localization of protein-polysaccharides in renal tissue
Journal of Biosciences, 1987
The purpose of this study was to investigate the distribution of proteinpolysaccharides in the glomerular and non-glomerular regions of the nephron. The techniques used include the digestion of kidney slices with specific polysaccharidases: neuraminidase, hyaluronidase, chondroitinase ABC, and collagenase followed by several cytochemical techniques to identify the glycosaminoglycans and glycoproteins at the light and electron microscope levels. Differential staining of hyaluronic acid and sulphated glycosaminoglycans was accomplished with Alcian Blue at pH 2 • 5 and pH 0 • 5, respectively. Sialoproteins were stained with Alcian Blue at pH 2 • 5. The periodic acid Schiff's reaction technique was employed for the visualization of collagen. At the electron microscope level the polysaccharides were identified with the periodic acid-chromic acid-silver methenamine reaction. Our results indicated that the major polysaccharide components of the glomerular basement membrane were sialoproteins and collagen, with smaller amounts of hyaluronic acid and various sulphated glycosaminoglycans. Hyaluronidase digestion resulted in partial detachment of epithelial processes from the glomerular basement membrane indicating the hyaluronic acid may have a role in the stability of the attachment of these processes. Tubular basement membranes also contain sialoproteins and sulphated glycosaminoglycans but in considerably lower concentrations than the glomerular basement membrane. Bowman's capsule appears to contain mostly sulphated glycosaminoglycans and has a lower concentration of sialoproteins and hyaluronic acid.
Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association, 2002
The urinary excretion of N-acetyl-beta-glucosamynidase (NAG) is increased in subjects exposed to substances toxic for renal tubular cells. In experimental and human glomerular diseases, its increased excretion is probably due to the dysfunction of tubular epithelial cells induced by increased traffic of proteins in the tubular lumen. The first aim of this study was to evaluate whether NAG excretion is correlated not only with the amount of proteinuria but also with some proteinuric components which reflect both glomerular capillary wall damage (IgG) and an impairment of tubular reabsorption of microproteins (alpha(1) microglobulin). The second aim was to assess whether NAG excretion has a predictive value on functional outcome and response to therapy. In 136 patients with primary glomerulonephritis [74 with idiopathic membranous nephropathy (IMN), 44 with primary focal segmental glomerulosclerosis (FSGS) and 18 with minimal change disease (MCD)] urinary NAG excretion was measured by...
Lack of albuminuria in the early heterologous phase of anti-GBM nephritis in beige mice
Kidney International, 1993
Lack of albusninuria in the early heterologous phase of antl-GBM nephritis in beige mice. Passive anti-glomerular basement membrane (GBM) nephritis in the mouse is accompanied by acute massive albuminuria in the early heterologous phase. As we have previously shown, this albuminuria does not occur in the beige mutant of the C57BL/6J strain which is deficient for the leukocytic neutral proteinases elastase and cathepsin G. To address the question whether an intrinsic defect in the polymorphonuclear granulocyte (PMN) or local factors in the beige kidney are responsible for the lack of albuminuria in the beige mouse strain, we conducted reciprocal bone marrow transplantations (BMT) in beige and congenic control mice. Injection of anti-GBM antibody resulted in only slight albuminuria (89 47 gIl8 hours; N = 6) in normal (that is, non-irradiated, non-reconstituted) beige mice. By contrast, in beige mice, reconstituted with bone marrow (BM) from control mice, acute albuminuria developed (3032 1408 tg/l8 hours; N = 8), to a degree comparable to that in non-irradiated control mice (4411 3405 g/l8 hours; N = 6, P < 0.01). Albuminuria in control mice, reconstituted with beige BM, was in the range of the normal beige mice (112 55 igI18 hours; N = 9). Reconstitution with syngeneic bone marrow demonstrated that BMT by itself did not influence the level of albuminuria. All mice showed similar morphological lesions, with comparable influx of PMN in the glomeruli two hours after antibody injection. Elastase activities of PMN extracts in BMT groups were not different from those in donor mice. We conclude that the absence of albuminuria in beige mice is caused by an intrinsic defect in leukocytic neutral proteinase activity.
Etiology of Increased Enzymuria in Different Morphological Forms of Glomerulonephritis
Nephron Physiology, 2004
Background: High urinary excretion of lysosomal enzymes is thought to reflect tubulointerstitial damage and is observed both in the acute and chronic phases of various morphological forms of glomerulonephritis (GN). It is related to the degree of proteinuria and secondary interstitial inflammatory process. N-acetyl-ß-D-glucosaminidase (NAG) and ß-glucuronidase (ß-GR) are the most commonly used markers of tubulointerstitial injury. NAG and ß-GR are also contained in azurophilic granulations of polymorphonuclear leukocytes (PMNs) and may be released during the activation of PMNs. Aims: The aim of this study was to elucidate the role of PMN degranulation in causing the increase of urinary excretion of lysosomal enzymes that is observed in glomerulonephritis. Material and Methods: We analyzed the urinary excretion of NAG, its B isoenzyme NAG-B, ß-GR and leukocyte elastase (EL), in 91 patients with morphologically different primary and secondary glomerulopathies, and in 12 healthy controls. Results: Excretion of NAG,
Important role for macrophages in induction of crescentic anti-GBM glomerulonephritis in WKY rats
Nephrology Dialysis Transplantation, 2004
Background. A crucial role for CD8 þ cells in induction of crescentic anti-glomerular basement membrane (GBM) glomerulonephritis (GN) in WKY rats was demonstrated in studies showing that depletion of CD8 þ cells completely suppressed glomerular accumulation of monocytes/macrophages (Mo/Mf), crescent formation and proteinuria. Because these studies did not definitively identify CD8 þ cells as the cause of tissue injury, we examined the roles of Mo/Mf in the development of anti-GBM GN. Methods. We examined correlations between the amount of urinary protein and the numbers of glomerular CD8 þ cells or Mo/Mf in rats after administrating different doses of anti-GBM antibody (5.0, 7.5, 10.0 and 25.0 ml/100 g body weight). The roles of Mo/Mf in induction of GN were examined in animals by depleting Mo/Mf in the glomerulus. To do this, rats were injected intravenously with liposome-encapsulated dichloromethylene diphosphonate (liposome-MDP) from day 3 to day 7 after anti-GBM antibody injection and they were then sacrificed at day 8. Results. Liposome-MDP treatment significantly reduced the number of ED-1 þ Mo/Mf accumulated in glomeruli from 32.1±1.2 to 1.4±0.3/glomerular cross-section (mean±SD, P<0.01), and the amount of urinary protein from 103.8±19.8 to 31.8±15.9 mg/day (P<0.01), as well as the incidence of crescentic glomeruli from 91.3±2.7 to 23.3±7.6% (P<0.01) at day 8. This treatment also reduced the number of CD8 þ cells accumulating in the glomeruli from 5.4± 0.7 to 0.5±0.1/glomerular cross-section (P<0.01). Upregulation of glomerular intercellular adhesion molecule 1 (ICAM-1) and monocyte chemoattractant protein 1 (MCP-1) mRNA expression was suppressed by Mo/Mf depletion. Conclusion. These results indicate that Mo/Mf play an important role in the induction of crescentic anti-GBM GN and glomerular injury.
Inhibition of leukotriene biosynthesis improves renal function in experimental glomerulonephritis
Journal of Lipid Mediators and Cell Signalling, 1995
The development of renal dysfunction in experimental glomerulonephritis (GN) is mediated in part by enhanced leukotriene (LT) formation. In our studies the pathophysiological role of LTs was investigated through pharmacological inhibition of LT biosynthesis in a rat model of nephrotoxic serum nephritis. MK-0591, an indirect inhibitor of Slipoxygenase activity, was co-administered to rats injected with nephrotoxic rabbit serum, followed by assessment of renal function, morphology and microsomal LTC, synthase activity on day 7. A significant improvement in glomerular function was noted (p < 0.051, together with a 50% reduction in proteinuria (p < 0.01) in animals receiving MK-0591 (60 mg kg-' day-'). In addition, the fall in renal LTC, synthase activity which occurred in nephritic rats (to 74% of control values, p < 0.01) was prevented in drug-treated animals. Based on these results, it appears that inhibition of LT biosynthesis protects against both renal impairment and alterations in LTC, synthase activity during the development of experimental GN, and may provide a useful therapeutic adjunct in the treatment of this disease. ) 428 3921. 0929-7855/95/$09.50 0 1995 Elsevier Science B.V. All rights reserved SSDZO929-7855(94)00040-9
The Journal of experimental medicine, 1989
Antiglomerular basement membrane (GBM) nephritis with massive albuminuria can be induced in mice by injection of heterologous antibodies against mouse GBM. The albuminuria and the glomerular lesions in this model are not mediated by complement, but are dependent on the presence of polymorphonuclear granulocytes (PMN) in the glomeruli. Neutral serine proteinases and reactive oxygen metabolites produced by activated PMN have been implicated as agents contributing to tissue damage. We examined the role of leukocytic neutral proteinases by comparing the glomerular damage and albuminuria after injection of rabbit anti-mouse GBM antibodies in normal control mice (C57BL/6J, +/+) and in beige mice (C57BL/6J,bg/bg) in which PMN are deficient of the neutral proteinases elastase and cathepsin G. The dose-dependent albuminuria that occurred in control mice after injection of 1.4-22 mg of anti-GBM antibodies was not observed in beige mice, despite a comparable influx of PMNs in the glomeruli. By...
Human Glomerular Basement Membrane: Chemical Composition in Glomerulonephritis and Pyelonepritis
Acta Medica Scandinavica, 2009
The chemical composition of glomerular basement membrane (GBM), isolated from 18 kidneys in advanced stage of renal disease, has been studied. On the basis of morphological changes and clinical observations 7 kidneys from -? patients were classified as showing chronic pyelonephritis, Including interstitial nephritis, 5 as chronic membranoproliferative glomerulonephritis, 2 as idiopathic membranous glomerulonephritis, and 4 as chronic glomerulonephritis of unspecified type. Ten normal kidneys were included as controls. For several consti-Acta med. scand. 194