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Biomedical subjects

F G Germuth

Publications and source records attributed to F G Germuth.

At least 19 recordsLinked to original sources
PubMed1984

Effect of human IgM rheumatoid factor on the glomerular site of localization of passively administered immune complexes in mice.

Injections of highly concentrated preparations of human RF into mice temporarily alter the major immediate (24 hr) site of predominant localization of passively administered soluble immune complexes from the glomerular mesangium to the glomerular capillary lumens, probably by increasing the size of the injected immune complexes. It is possible that larger amounts of RF may lead to a state whereby the complexes are more permanently deflected from the loops and mesangium, and continue to protect the glomerulus from the pathological effects of the complexes.

Animals↗
PubMed1982

Glomerular charge and urinary protein excretion: effects of systemic and intrarenal polycation infusion in the rat.

To study the role of the fixed anionic sites of the glomerular capillary wall in protein filtration, the negative charges were neutralized in vivo. With systemic infusion of the polycation protamine sulfate, glomerular staining for polyanion was reduced and protein excretion increased by 154%. To avoid systemic side effects in subsequent studies, small doses of a polycation were infused directly into one renal artery. The contralateral kidney was infused with the vehicle solution. Albumin excretion from the experimental kidneys in the first 1-hr collection after infusing 0.5 mg protamine sulfate was 24.3 +/- 6.3 micrograms/min/kidney (N = 13; P less than 0.01). Albuminuria declined during the subsequent 3 hr with a second infusion inducing a second proteinuric response. The degree and longevity of the albuminuric response was correlated directly to the dose of protamine sulfate. The polycations hexadimethrine and poly-l-lysine also induced proteinuria. The increased protein excretion consisted of albumin; the excretion of nonalbumin protein was identical in the experimental and control kidneys. Hemodynamic factors did not explain the increase in proteinuria. Morphologically, the polycation-treated kidneys showed scanty foot process fusion and a decrease in free negative sites in the lamina rarae of the glomerular basement membrane. The results strongly support an important role for glomerular charge in preventing filtration of circulating plasma albumin.

Albuminuria↗
PubMed1979

Passive immune complex glomerulonephritis in mice: models for various lesions found in human disease. I. High avidity complexes and mesangiopathic glomerulonephritis.

Intravenous injection of mice with soluble complexes of highly avid rabbit antibody to egg albumin, prepared by dissolution of equivalence precipitates in large quantities of antigen, resulted in a purely mesangial localization of the complexes. When animals received three injections of complexes per day for 1 day it was noted that precipitates dissolved in 80 times the equivalence amount of antigen produced slight mesangial changes. When such complexes were injected for 2 or 3 days, outright mesangiopathic glomerulonephritis was observed in an increasing proportion of the animals. Equivalent amounts of antigen alone did not produce lesions.

Animals↗
PubMed1979

Passive immune complex glomerulonephritis in mice: models for various lesions found in human disease. II. Low avidity complexes and diffuse proliferative glomerulonephritis with subepithelial deposits.

Intravenous injections of mice three times a day for 3 days with soluble complexes of 3 mg. of moderately avid rabbit antibody to chicken egg albumin prepared by dissolution of equivalence precipitates in 80 times the equivalence amount of antigen resulted in a combined mesangial and loop localization of immune complexes. With complexes formed from antibody of low avidity, injected four times a day for 3 days, a predominately subepithelial loop deposition of complexes was observed. Complexes formed from moderately avid antibody gave rise to a mainly mesangiopathic glomerulonephritis, whereas low avidity complexes were associated with a diffuse glomerulonephritis. These results, in combination with those of the previous paper, successfully reproduce the basic form of the lesions seen in active immune complex disease by passive means and suggest that antibody avidity is a major determinant of the site of localization of immune complexes and therefore of the morphologic form of the resulting glomerulonephritis. The importance of these observations for our understanding of the pathogenesis of human immune complex disease is considered.

Animals↗
PubMed1978

Immune complex disease. VII. Experimental mesangiopathic glomerulonephritis produced by chronic immunization with thyroglobulin.

Immunohistologic and electron microscipic studies were performed on the kidneys of rabbits given daily intravenous injections of porcine thyroglobulin in amounts adjusted to the immune response of the individual rabbits. Glomerular lesions were restricted to the mesangium, were characterized by varying degrees of proliferation of mesangial cells and increase of mesangial matrix, and were accompanied by accumulations of rabbit immunoglobulins, C3, and porcine thyroglobulin. Electron-dense deposits were localized to the mesangium and the adjacent subendothelial space. Less than 10 per cent of the animals with mesangila lesions developed obvious impairment of glomerular function. Thyroglobulin-containing immune complexes were found to be rapidly removed from the mesangium, so that overloading of the mesangium and consequent accumulation of complexes in the adjacent capillary loops could not occur. Thus, the results provide further evidence that when immune complex deposition is restricted to the mesangium, relatively little interference with glomerular function results. This situation is paralleled in man by the lesions of subclinical lupus nephritis, chance proteinuria and hematuria, and the early lesions of Berger's disease.

Animals↗
PubMed1978

Antibasement membrane disease. II. Mechanism of glomerular injury in an accelerated model of Masugi nephritis.

Rabbits were given injections of preformed complexes of purified goat antirabbit glomerular basement membrane antibody and rabbit antigoat immunoglobulin. When the animals were killed 24 hours later, examination of their kidneys revealed diffuse glomerulonephritis with widespread areas of localized loop necrosis, associated with extensive accumulations of polymorphonuclear leukocytes. By electron microscopy, accumulations of polymorphonuclear leukocytes in various degrees of disintegration were associated with areas of the basement membrane that appeared to be losing their structural integrity, suggesting that the damage to the membrane was brought about by the action of lysosomal enzymes. Reduction of the number of circulating polymorphonuclear leukocytes by pretreatment of the animals with nitrogen mustard completely prevented the lesions. Reduction of circulating complement levels by pretreatment of the animals with cobra venom factor prevented the occurrence of localized necrosis but allowed the development of the diffuse lesion.

Animals↗
PubMed1978

Effect of cortisone upon vascular permeability to antibody.

In rabbits actively sensitized to bovine serum albumin, intracorneal injection of 1 mg. of fluorescein-labeled bovine serum albumin evokes a circular band of fluorescence secondary to precipitation of the diffusing antigen with antibody migrating from the limbal blood vessels. Cortisone treatment prevented or markedly decreased this phenomenon indicating that cortisone exerts a definite inhibitory effect upon vascular permeability to antibody molecules.

Animals↗
PubMed1977

Immune complex disease. VI. Some determinants of the varieties of glomerular lesions in the chronic bovine serum albumin-rabbit system.

Glomerular lesions were evaluated by light, electron, and immunofluorescence microscopy in rabbits given daily injections, for prolonged periods of time, of either 12.5 mg. of bovine serum albumin (BSA) (group I) or increasing doses of BSA, paralleling the immune response (group II). In animals clearing 12.5 mg. or more of BSA per day (excluding those dying of anaphylaxis or unknown causes), marked differences were noted in the incidence of membranous glomerulonephritis (GLN) (50 per cent in group I versus 15.4 per cent in group II), of crescentic GLN (none in group I versus 26.9 per cent in group II), and of mesangiopathic GLN (11.1 per cent in group I versus 30.8 per cent in group II). On the basis of these variations and immunofluorescence microscopy findinds, it is concluded that the occurrence of membranous GLN is favored by the presence in the circulation of small concentrations of soluble immune complexes, whereas crescentic GLN results from the presence of high concentrations of such complexes. When BSA injections were discontinued in group I animals having membranous GLN, the immune deposits were sequestered by membranous transformation so that they were not readily solubilized by injections of large amounts of BSA; one such animal developed crescentic GLN. The observation that BSA was difficult to detect in the lesions of mesangiopathic GLN suggests that this lesion results from the deposition of complexes formed at equivalence or in antibody excess.

Animals↗
PubMed1975

Heparin therapy in anti-basement membrane nephritis.

The effect of heparin on the development and progression of a form of antiglomerular basement membrane nephritis was examined in the rat. Animals which received heparin before and throughout the period of immunological insult developed lesions which were as severe, and perhaps more severe, than rats which did not receive heparin. Inulin clearances were lower in heparin-treated animals than in untreated rats. Animals in both groups exhibited renal fibrin-fibrinogen deposition and had increased rates of urinary fibrin-fibrinogen related antigen excretion. These results indicate that heparin per se has no beneficial effect on the development of this form of glomerulonephritis in this species.

Animals↗
PubMed1975

Fatal immune complex glomerulonephritis without deposits.

Repeated intravenous injections of egg albumin in rabbits produced small antigen-excess complexes and severe glomerulonephritis. Immunoglobulins and complement in the glomeruli were not clearly demonstrated by immunofluorescence; deposits were found to be sparse by electron microscopy. This study demonstrates that soluble immune complexes are responsible for the glomerular reaction. The apparent absence of deposits is thus not sufficient to exclude an immune complex pathogenesis.

Animals↗