scholarly journals ELECTRON MICROSCOPY OF SERUM SICKNESS NEPHRITIS

1958 ◽  
Vol 108 (6) ◽  
pp. 957-962 ◽  
Author(s):  
Joseph D. Feldman

The renal lesions of serum sickness were studied with the electron microscope. The most prominent change was a marked swelling and proliferation of glomernlar endothelial cells causing obliteration of the capillary lumen. The basement membrane also showed focal thickenings and excrescences. Deposits of electron-dense material blended into the basement membrane. On the extracapillary side epithelial foot processes were reduced in number and replaced by broad sheets of cytoplasm which were closely applied to the basement membrane. From a comparison of electron and fluorescent microscopic studies of the glomerulus in serum sickness, it would seem that antigen-antibody complexes initiated injury in endothelial cells, although the possibility of the primary reaction occurring on basement membrane cannot be excluded.

Blood ◽  
1973 ◽  
Vol 41 (3) ◽  
pp. 359-367 ◽  
Author(s):  
Arcot D. Suresh ◽  
Michael B. Stemerman ◽  
Theodore H. Spaet

Abstract Electron microscopic studies were performed on rabbit heart valves, and all four valves were found to be lined with a continuous basement membrane (BM). The valvular BM was liable to digestion by either trypsin or collagenase, but brief exposure to trypsin was suitable for desquamating endothelial cells, while leaving BM exposed and intact. Such preparations were used to determine their platelet reactivity with heparinized and citrated whole blood or with platelet-rich plasma. Although various conditions of exposure were used, including shaking and centrifugation, little or no platelet adhesion to the BM was observed. With similar conditions of exposure, preparations of collagen showed massive platelet adhesion accompanied by aggregation. This vascular BM was similarly nonreactive to platelets when endothelial cell removal was accomplished by mechanical methods. Rabbit valvular BM appears to be a poorly thrombogenic surface.


1955 ◽  
Vol 102 (5) ◽  
pp. 573-580 ◽  
Author(s):  
Carolyn F. Piel ◽  
Luther Dong ◽  
F.W.S. Modern ◽  
Joseph R. Goodman ◽  
Roger Moore

Nephrotoxic serum disease in rats has been studied by light and electron microscopy from 1 hour to 10 weeks after production of the disease. By light microscopy leucocytic infiltration of the glomerular capillary was observed between the 3rd and 6th hour. At 6 hours an increase in colloidal iron-positive material was observed coating the extraluminal surface of the capillaries. Also at this time swelling of the endothelial cells becomes prominent. By 72 hours, thickening of the basement membrane was observed. Glomerular capillary thrombi were observed in approximately half the tissue examined in the first 2 weeks of disease. 50 per cent of the animals showed severe chronic lesions, exudation into the capsular space, crescent formation, and obliteration of glomeruli. At 1 hour electron microscopic pictures showed that osmophilic material may line the foot processes of the epithelial cells and obliterate all but narrow channels of the space between the feet. By 6 hours thickening of the basement membrane was prominent. This change persisted throughout 10 weeks of observation. The tissue from animals which had severe chronic alterations by light microscopy revealed changes which could not be interpreted at this time.


1979 ◽  
Vol 150 (3) ◽  
pp. 413-425 ◽  
Author(s):  
L G Hunsicker ◽  
T P Shearer ◽  
S B Plattner ◽  
D Weisenburger

We have investigated the pathogenesis of glomerular hypercellularity seen in acute serum sickness nephritis induced in rabbits with bovine serum albumin (BSA). The increase in cellularity began with the first stages of immune clearance of BSA, with a peak cellularity occuring at the time of onset of proteinuria. Although there was a significant increase in the fraction of glomerular cells incorporating [3H]thymidine, first seen at the onset of proteinuria, this increase occurred too late and was too small to explain the observed rate of increase in glomerular cellularity. On the other hand, a striking monocytic infiltration of the glomeruli was documented by electron microscopy and by staining for nonspecific esterase. This monocytic infiltration paralleled the observed course of glomerular hypercellularity and was quantitatively sufficient to explain the total increase seen. It appears, therefore, that glomerular hypercellularity seen in this model is principally a result of monocyte infiltration.


1953 ◽  
Vol 98 (1) ◽  
pp. 1-12 ◽  
Author(s):  
Frederick G. Germuth

Cortisone markedly suppressed the cardiovascular and renal lesions of serum sickness type hypersensitivity which ordinarily develop following the intravenous injection of bovine albumin. The inhibitory effect of cortisone on the allergic granulomatous lesions of the spleen was less striking; the lesions were less extensive, but the percentage of animals affected was unchanged. Cortisone in the dosage employed had no effect on the elimination of antigen following its intravenous administration or on the appearance of circulating antibody. These findings indicate that inhibition of the lesions of serum sickness by cortisone does not depend on the suppression of antibody production. Therefore, it is inferred that cortisone somehow protects the animal from the damaging effects of antigen-antibody union.


2019 ◽  
Vol 2019 ◽  
pp. 1-4 ◽  
Author(s):  
F. Touzani ◽  
C. Geers ◽  
A. Pozdzik

Introduction. Antiangiogenic agents that inhibit vascular endothelial growth factor have emerged as important tools in cancer therapy and ocular diseases. Their systemic use can induce renal limited microangiopathy. Local use of anti-VEGF agent is supposed to be safe. We report here a unique case of early endothelial cells injury induced by intravitreal injection of bevacizumab. Case Presentation. A 72-year-old man was addressed for acute kidney injury with proteinuria. He was under treatment with intravitreal injections of bevacizumab for glaucoma. Kidney biopsy was performed and electron microscopy showed signs of early stages of glomerular microangiopathy. Bevacizumab was discontinued resulting in the improvement of renal function and albuminuria. Discussion. Bevacizumab, a humanized monoclonal antibody to VEGF is an approved therapy for metastatic cancer. Systemic adverse events including thrombotic microangiopathy have been mainly reported after its systemic injection. Podocytes produce VEGF that interacts with endothelial cells VEGF receptor-2 maintaining glomerular basement membrane integrity. Bevacizumab induce the detachment of endothelial cells from glomerular basement membrane leading to the proteinuria and renal function decline. Intravitreal bevacizumab is generally supposed to be safe. However, glomerular injury with microangiopathy features, even after intravitreal injection is possible. Conclusion. We report the electron microscopy evidence that intravitreal injection of anti-VEGF induces glomerular endothelial cells injury. Nephrologists and ophthalmologists should be aware of this complication.


1977 ◽  
Vol 14 (5) ◽  
pp. 482-489 ◽  
Author(s):  
J. R. Easley ◽  
W. H. Halliwell

Fifteen rabbits were injected with one dose of 250 milligrams per kilogram of bovine serum albumin intravenously to induce acute serum sickness. The kidneys were removed from groups of five rabbits each at 10, 12 and 14 days after injection and examined by light, electron and immunofluorescent microscopy for evidence of immune complex glomerulonephritis. Urine was examined for protein when rabbits died. Glomerulonephritis was found in eight rabbits by light microscopy and in 10 rabbits by electron microscopy. Only one rabbit had positive immunofluorescence for immunologic components and only two rabbits had proteinuria. Hypercellularity was the primary change seen by light microscopy. Ultrastructural changes were numerous and various, and the major changes recognized were irregularity of the glomerular basement membrane, increased mesangial matrix, hypercellularity, endothelial hypertrophy, mesangial deposits, epithelial foot process fusion and mesangial circumferential interposition. Subepithelial humps were seen in only four rabbits; none of these rabbits had proteinuria. We concluded that increased permeability followed the deposition of immune complexes and development of ultrastructural lesions.


1962 ◽  
Vol 115 (5) ◽  
pp. 929-936 ◽  
Author(s):  
Giuseppe A. Andres ◽  
Councilman Morgan ◽  
Konrad C. Hsu ◽  
Richard A. Rifkind ◽  
Beatrice C. Seegal

Ferritin-conjugated antibody has been used to identify by electron microscopy the sites at which nephrotoxic globulins localize in rat kidney during acute experimental glomerulonephritis. Antibody was concentrated in the glomerular basement membrane and in basement membrane-like material contained in distended cisternae of the endoplasmic reticulum. These data confirm and amplify, at the ultrastructural level, the results of studies obtained with the fluorescent antibody technique, and are consistent with the hypothesis that the cisternae and capillary basement membrane possess common proteins.


1963 ◽  
Vol 117 (4) ◽  
pp. 691-704 ◽  
Author(s):  
Giuseppe A. Andres ◽  
Beatrice C. Seegal ◽  
Konrad C. Hsu ◽  
Mildred S. Rothenberg ◽  
Madeleine L. Chapeau

Acute, subacute, and chronic glomerulonephritis, similar in certain features to human glomerulonephritis, has been produced in rabbits by repeated injections of bovine serum albumin. The ratio of antigen to antibody was the factor determining the development and type of glomerulonephritis. This is in confirmation of the observations of Dixon, Feldman, and Vazquez. With the aid of the ferritin antibody technique it was shown that antigen aggregates (probably antigen-antibody complexes) are present in the blood, cross the endothelium and the basement membrane, and accumulate as dense deposits between the basement membrane and the epithelial cytoplasm. In the deposits electron-dense aggregates formed by antigen or by antigen-antibody complexes and material which might be other endogenous proteins may be identified. In rabbits dead of anaphylactic shock following injection of bovine serum albumin, dense material was found within glomerular capillaries, presumably formed by the embolic deposition of antigen-antibody complexes, since the immunofluorescein and immunoferritin techniques demonstrated the presence of both BSA and rabbit globulin.


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