scholarly journals Membranous Glomerulonephritis in Dogs Infected with Dirofilaria immitis

1975 ◽  
Vol 12 (2) ◽  
pp. 111-117 ◽  
Author(s):  
H. W. Casey ◽  
G. A. Splitter
Keyword(s):  
Basement Membrane ◽  
Immune Complex ◽  
Glomerular Basement Membrane ◽  
Dirofilaria Immitis ◽  
Complex Form ◽  
Membranous Glomerulonephritis ◽  
Capillary Wall ◽  
Immunofluorescent Study ◽  
Dense Deposits ◽  
Glomerular Lesions

Membranous glomerulonephritis was diagnosed in five dogs with patent Dirofilaria immitis infections. Electron-dense deposits were present on the epithelial side of the glomerular basement membrane. An immunofluorescent study demonstrated immunoglobulins in the capillary wall and mesangium of the glomeruli. The glomerular lesions were considered to represent an immune complex form of glomerulonephritis induced by the D. immitis infection.

scholarly journals Immunoelectron microscopic (IEM) studies on glutaraldehyde-fixed renal specimen.

1984 ◽  
Vol 32 (5) ◽  
pp. 501-509 ◽  
Author(s):  
N Shindo ◽  
E Kobayashi ◽  
M Okada
Keyword(s):  
Basement Membrane ◽  
Light Microscopy ◽  
Glomerular Basement Membrane ◽  
Membranous Nephropathy ◽  
Renal Pathology ◽  
Precise Location ◽  
Routine Diagnosis ◽  
Dense Deposits ◽  
Renal Biopsies ◽  
Glomerular Lesions

Immunofluorescent microscopy (IF) has become an essential tool in the routine diagnosis of renal pathology. It is thought that glomerular IF patterns represent different forms of immunologically mediated glomerular lesions. However, in order to preserve antigenicity IF is usually done on frozen, unfixed specimen by light microscopy and it is difficult to locate target macromolecules in tissue with precision. In order to establish the precise location of such macromolecules in glomeruli in relation to the ultrastructure, we undertook an immunoelectron microscopic (IEM) study on renal biopsies. Percutaneously biopsied tiny specimen was fixed in glutaraldehyde and processed with protease. Using peroxidase-labeled antisera, a direct IEM was done. With this technique, target macromolecules corresponded well not only to electron-dense deposits but also to IF patterns. In one case of membranous nephropathy, immunoglobulin (Ig) was found to be outside of the glomerular basement membrane (GBM), while IgA was seen to be inside the GBM. For this same case, a similar localization of immunoglobulins was not revealed by IF. In conclusion, IEM is a useful technique that can broaden our knowledge of pathogenic mechanisms in glomerular disease.

Abnormal Distribution of Anionic Sites in the Glomerular Basement Membrane in Glomerulonephritis of Dogs Infected with Dirofilaria immitis.

2000 ◽  
Vol 62 (11) ◽  
pp. 1193-1195 ◽  
Author(s):  
Junichi KAMIIE ◽  
Kinji SHIROTA ◽  
Munetaka YAMAKI ◽  
Hitoshi KITAGAWA ◽  
Masahiko WASAKI ◽  
...  
Keyword(s):  
Basement Membrane ◽  
Glomerular Basement Membrane ◽  
Dirofilaria Immitis ◽  
Anionic Sites ◽  
Abnormal Distribution

scholarly journals THE PATHOGENIC ROLE OF FIBRIN DEPOSITION IN THE GLOMERULAR LESIONS OF TOXEMIA OF PREGNANCY

1963 ◽  
Vol 118 (3) ◽  
pp. 467-478 ◽  
Author(s):  
Pierre Vassalli ◽  
Robert H. Morris ◽  
Robert T. McCluskey
Keyword(s):  
Endothelial Cells ◽  
Basement Membrane ◽  
Gamma Globulin ◽  
Fibrin Deposition ◽  
Pathogenic Role ◽  
Immunofluorescent Study ◽  
Renal Biopsies ◽  
Glomerular Lesions ◽  
Glomerular Damage

An immunofluorescent study of renal biopsies from patients with toxemia of pregnancy has been performed. It was found that the glomeruli consistently showed bright staining for fibrin within endothelial cells, as well as occasional deposits along the basement membrane. Gamma globulin was only occasionally demonstrable, generally in the form of irregular deposits along the basement membrane. ß1C was absent and albumin was not seen in glomeruli, except sometimes in the form of droplets within epithelial cells. In biopsies from pregnant patients without toxemia only equivocal staining for fibrin was seen. On the basis of these observations and other evidence discussed, it is proposed that the accumulation of fibrin in glomeruli reflects a prolonged state of intravascular clotting in toxemia and that the arrest in glomeruli of some form of circulating fibrin constitutes the basic pathogenic mechanism of the glomerular damage in this disease.

Abnormal expression of glomerular basement membrane laminins in membranous glomerulonephritis

2000 ◽  
Vol 15 (12) ◽  
pp. 1956-1964 ◽  
Author(s):  
Evelyne Fischer ◽  
Béatrice Mougenot ◽  
Patrice Callard ◽  
Pierre Ronco ◽  
Jérôme Rossert
Keyword(s):  
Basement Membrane ◽  
Glomerular Basement Membrane ◽  
Membranous Glomerulonephritis ◽  
Abnormal Expression

scholarly journals Mesangiocapillary glomerulonephritis.

1992 ◽  
Vol 2 (10) ◽  
pp. S159
Author(s):  
G D'Amico ◽  
F Ferrario
Keyword(s):  
Basement Membrane ◽  
Glomerular Basement Membrane ◽  
Inflammatory Cells ◽  
Type I ◽  
Mesangiocapillary Glomerulonephritis ◽  
Dense Deposits ◽  
Table Analysis ◽  
System Activation ◽  
Morphological Variants

The clinical and histological features of idiopathic mesangiocapillary glomerulonephritis (MCGN) have been reviewed, with a survey of the most recent literature, including the retrospective analysis of the data of the Italian Study Group of Renal Immunopathology on 368 patients. In both major types of MCGN, six morphological variants have been characterized (classical MCGN, nodular MCGN, exudative MCGN, focal segmental MCGN, MCGN with massive deposits, and crescentic MCGN) that have different etiologic, pathogenetic, or clinical outcome correlates. Actuarial renal survival 10 yr after renal biopsy has been calculated with life-table analysis to be 60 to 65% in type I MCGN, without significant differences between treated and untreated patients; none of the therapeutic regimens tested up to now for this disease have been independently demonstrated to be efficacious. As for the pathogenesis, the interrelationships between the three mechanisms that contribute to the development of the morphological features of the disease (accumulation of electron-dense deposits on the subendothelial side of the glomerular basement membrane or within the glomerular basement membrane; mesangial proliferation and peripheral interposition; and inflow of inflammatory cells, mainly monocytes) have been discussed, and the role of hypocomplementemia and circulating nephritic factors (NFa and NFt) has been analyzed. Available evidence suggests that MCGN is an immunocomplex-mediated disease, the deposition of immune deposits being the initiating phenomenon, whereas the morphologic changes and complement system activation are secondary events.

scholarly journals Localization of the membrane attack complex (MAC) in experimental immune complex glomerulonephritis.

1983 ◽  
Vol 157 (6) ◽  
pp. 1885-1905 ◽  
Author(s):  
D Koffler ◽  
G Biesecker ◽  
B Noble ◽  
G A Andres ◽  
A Martinez-Hernandez
Keyword(s):  
Basement Membrane ◽  
Immune Complex ◽  
Immune Complexes ◽  
Tissue Injury ◽  
Membrane Attack Complex ◽  
Intense Staining ◽  
Immune Complex Glomerulonephritis ◽  
Filtration Barrier ◽  
Dense Deposits ◽  
Foot Process

The role of the membrane attack complex (MAC) as a mediator of renal tissue injury was evaluated in rats affected by bovine serum albumin (BSA)-induced immune complex glomerulonephritis. Immunofluorescence studies revealed concurrent deposits of IgG, BSA, C3, and the MAC along glomerular capillary walls, although the MAC manifested a more restricted distribution than that observed for immune complexes. Immunoelectron microscopic techniques were utilized to demonstrate immune complexes, C3, and the MAC within dense deposits in the subepithelial aspect of the basement membrane. Visceral epithelial foot processes were fused in areas overlying large dense deposits and exhibited intense staining for the MAC, lesser reactivity for C3 but IgG was absent from the foot process membranes. Smaller granular deposits of immune complexes, C3, and the MAC were observed in the subendothelial region of the lamina rara interna and the lamina densa. Immune complexes may activate the classical complement pathway causing diffuse injury to the glomerular basement membrane (GBM), allowing subepithelial accumulation of complexes. These observations implicate the MAC as a mediator of GBM and juxtaposed podocyte membrane injury, thereby contributing to disruption of the glomerular filtration barrier. IgG and C3 were demonstrated within tubulointerstitial regions on the surface of collagen fibers in close proximity to the tubular basement membrane (TBM) of proximal convoluted tubules. Within the TBM, C3 localization was prominent with diminished reactivity for the MAC, but IgG was not detectable. The demonstration of C3 and scant MAC deposits in the TBM of nonimmunized control rats without evidence of interstitial IgG and C3 deposits suggests that both nonimmune and immune processes play a role in the pathogenesis of extraglomerular lesions. Evidence derived from these morphologic studies indicates that the MAC is associated with injury to the GBM, foot process membranes of visceral epithelium, and the TBM. Further experiments designed to selectively enhance or inhibit the deposition of MAC and assess consequent renal dysfunction are required to substantiate hypotheses concerning the in vivo membranolytic potential of the MAC in experimental immune complex glomerulonephritis.

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