Über die allergische Gewebsreaktion der Niere

Masugi, Matazo; Sato, Yukiya

doi:10.1007/bf01961254

Cited by 87 publications

(13 citation statements)

References 23 publications

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“…The various tissue changes caused by large doses of serum or other dissolved antigens given intravenously were firsO described by Klinge and his associates (1932) (2,3), by Apitz (1933) (4), and by Masugi and his group (1934) (5)(6)(7). The cardiac lesions were well illustrated by Apitz (4), the glomerular lesions by Masugi and Sato (5), and the arterial lesions by Miura (7).…”

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confidence: 95%

Experimental Serum Disease

Ehrich

Seifter

Forman

1949

Journal of Experimental Medicine

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The intravenous injection of one large dose of serum into rabbits caused a variety of changes of considerable complexity. 1. There was an immediate proliferation of mesenchymal cells, including plasma cells, particularly in heart, lungs, and spleen. 2. The signs of serum disease developed only at the time of abundant antibody formation, before significant quantities of antibody were laid down in the vascular connective tissue. 3. Allergic arteritis, marked glomerular nephritis, myocardial necrosis, and Aschoff body-like structures were seen only after hypersensitivity had developed. It appears that most, if not all, of these pathological alterations were true Arthus phenomena. 4. There were at least two distinct varieties of allergic arteritis and glomerular nephritis, namely a proliferative one, following the first injection, and a a necrotizing one, seen only after 2 injections. It appears that the first was a subacute Arthus phenomenon, while the latter was an acute Arthus phenomenon superimposed on a subacute one. The subacute experimental glomerular nephritis resembled the intracapillary glomerulonephritis in man, while the acute variety was like human extracapillary glomerular nephritis.

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confidence: 95%

Experimental Serum Disease

Ehrich

Seifter

Forman

1949

Journal of Experimental Medicine

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“…It was apparent, furthermore, as can be judged from the illustrations (Figs. 15 to 17,19,21), that there was a preferential deposition of the fluor in the membranes of the glomerular tuft with very little, if any, staining of the arterioles of the stalk or of Bowman's capsule.…”

Section: Ilesultsmentioning

confidence: 99%

“…DISCUSSION Since it has been established in many ways that the active principle of nephrotoxic serum is antibody globulin (5-7), there appears to be no reasonable doubt that the union of this antibody with the renal antigen or antigens in situ, if not in itself an injurious event, is at least the essential initiating reaction that leads to nephrotoxic nephritis. In the pathogenetic mechanism originally formulated by Masugi (20,21), the nephritis was considered to be a degenerative and reparative process stemming wholly from a direct assault on renal antigenic structure by the injected nephrotoxic antibodies; i.e., a form of reverse anaphylaxis. While this concept might explain adequately the nephrotoxic nephritis of rats, its failure to account for the characteristic latent period of the rabbit nephritis induced by duck antisera led Kay (1, 2) to search for an alternative, indirect mechanism in the latter condition.…”

Section: Ilesultsmentioning

confidence: 99%

Analytical Pathology

Ortega

Mellors

1956

The Journal of Experimental Medicine

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Studies of the mechanism of experimental nephrotoxic nephritis (1-8) have been concerned largely with: (a) the specificity of the nephrotoxins, (b) their sites of localization, especially in the kidney, and (c) the presence and the role of immune responses in the nephritic animal. In recent years a considerable body of direct evidence relating to these problems has been furnished by the use of labelled antibody techniques, first applied to this field in the form of radioiodinated nephrotoxins by Pressman et al. (4,5,9).Among the results achieved by this group was the demonstration that nephrotoxic T-globulins are preferentially absorbed by the kidney, where they localize, at least in greater part, in the glomeruli, and that the radioactive tracer and, presumably, the intact antibody persist for up to 2 months at the sites of tissue localization. Recently, the potentialities of tracer methods have been more fully realized with the introduction by MeUors et al. (10) of fluorescein-coupled antibodies as histochemical reagents for the detection of tissue-localizing antibodies in viva. This new application of the technique developed by Coons et al. (11,12) not only makes it possible to define the sites of localization of nephrotoxic antibodies with a hitherto unattainable precision, but for the first time it permits the demonstration of deposits of autogenous antibodies as well. A highly advantageous characteristic of the technique is that it detects antigenic and, therefore, relatively intact antibodies only.In a series of papers on experimental and human nephritis studied by this method, Mellors et al. (10,13,14) have unequivocally confirmed the selective glomerular localization of nephrotoxins in the rat kidney, indicating also that it is primarily membranous, and they have demonstrated the presence of glomerular localizing autogenous antibodies in a foreign protein nephritis of rabbits and in several types of human nephritis. The present investigation is an extension of the work dealing with nephrotoxic nephritis in the rat.

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“…Thus. and similar lesions can be induced in experimental animals by foreign proteins (6)(7)(8)(9)(10)(11). and similar lesions can be induced in experimental animals by foreign proteins (6)(7)(8)(9)(10)(11).…”

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confidence: 99%