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Biomedical subjects

P Verroust

Publications and source records attributed to P Verroust.

At least 109 records · Page 6Linked to original sources
PubMed1979

The effect of puromycin on subepithelial deposits induced by antibodies directed against tubular antigens: a quantitative study.

The mechanism of the GN induced by the intravenous injection of antibodies directed against renal tubular epithelial antigens (RTE) was studied by the use of antibody specifically purified by affinity chromatography. With this reagent RTE antigens could be demonstrated on frozen sections of glomeruli as well as on glomerular cells in culture. The antibodies were radiolabelled, and using paired label techniques glomerular binding could be measured in vivo. In normal rats, approximately 4% of the antibody injected was specifically bound in the glomeruli. Binding was not detectable on proximal tubular brush borders. In rats treated with 100 mg/kg of aminonucleoside of puromycin, a substance known to induce alterations of glomerular epithelial cells, it could be shown that glomerular binding was selectively decreased. These observations indicate that immune deposits in passive Heyman nephitis are formed mainly in situ and that local alteration of the glomerulus can markedly influence deposit formation.

Animals↗
PubMed1979

A clinical and immunopathological study of 304 cases of glomerulonephritis in Tunisia.

304 cases of glomerulonephritis were biopsied in Tunisia and studied morphologically. The incidence of glomerulonephritis with marked proliferation of endocapillary cells was 60%, a figure considerably higher than in other large series. Using a Clq binding assay, statistically significant levels of immune complexes were found in cases of acute proliferative glomerulonephritis. Amongst other types of glomerulonephritis, circulating immune complexes were frequently found in systemic lupus erythematosus but only in a low percentage of primary glomerulonephritis with or without immunoglobulin deposits.

Antigen-Antibody Complex↗
PubMed1979

Glomerular fibrinolytic activity during nephrotoxic nephritis.

The glomerular fibrinolytic activity (GFA) was measured during the development of glomerulonephritis induced by the intravenous injection of horse or rabbit antiglomerular basement membrane antibodies in rats either untreated or preimmunized with horse or rabbit Ig. A variety of nephritides was produced ranging from proteinuria with no or mild changes in glomerular architecture to severe diffuse proliferative glomerulonephritis with close to 100% crescent formation. GFA was measured on preparations of isolated glomeruli using a radioassay based on lysis of 125I fibrin adsorbed on a solid phase. In some experiments a fibrin plaque technique was also used. Both methods clearly demonstrated a marked increase in GFA with a good correlation between the two sets of results when the glomerular architecture is preserved. The increase in GFA is related both to the severity of the nephritis estimated by the percentage of glomeruli showing crescent formation and to the extent of the fibrin deposits. The results therefore indicate that the persistence of fibrin in the glomeruli and particularly in crescents is not due to a loss of GFA.

Animals↗
PubMed1978

Anti-interferon globulin inhibits the development of glomerulonephritis in mice infected at birth with lymphocytic choriomeningitis virus.

Swiss mice infected at birth with lymphocytic choriomeningitis virus develop glomerulonephritis. Injection of potent anti-mouse interferon globulin at the time of viral infection inhibited the development of these renal lesions. We conclude that the production of endogenous interferon by this virus in the first few days of life plays an important role in the pathogenesis of this glomerulonephritis.

Animals↗
PubMed1977

High affinity binding of 125I-angiotensin II to rat glomerular basement membranes.

125I-angiotensin II (AII) specifically bound to rat glomerular basement membrane (GBM). The kinetics of binding were similar to those obtained with the total glomeruli. The apparent dissociation constant was close to 50 pM with both preparations. The number of sites related to the amount of protein was two times greater with GBM than with total glomeruli. Since the amount of GBM protein extracted from a given amount of glomerular protein was about 10%, it was possible to estimate the share of the GBM binding sites for AII as representing 20% of the total number present in the entire glomerulus. Binding studies at equilibrium as a function of 125I-AII concentration and competitive binding experiments suggested either multiplicity of the binding sites or cooperativity in the binding reaction. Degradation of 125I-AII in the presence of GBM was slight and did not increase with time. The difference in the degrees of degradation of 125I-AII was too small to account for the observed difference in binding when the results obtained with GBM and isolated glomeruli preparations were compared. 125I-AII binding to GBM was increased after treatment of these membranes with collagenase, slightly diminished with neuraminidase, and almost completely abolished with trypsin suggesting the proteic nature of the receptor. 125I-AII binding to GBM was diminished after incubation of GBM with anti-GBM antibodies as a result of a decrease in the number of binding sites. 125I-AII binding was even more diminished in preparations of glomeruli isolated from rats passively immunized with anti-GBM antibodies when compared with glomeruli from control animals. This resulted from both smaller affinity for AII and decrease in the number of the binding sites. The present data provides evidence for specific binding sites for AII localized on GBM. This is noteworthy since receptors for polypeptide hormones are currently observed on the surface of cell membranes. These findings also suggest a new physiological role for AII which might involve modification of GBM permeability.

Angiotensin II↗
PubMed1971

Glomerular lesions in monoclonal gammopathies and mixed essential cryoglobulinemias IgG-IgM.

Histologic studies of renal tissue were performed in 21 cases of IgG or IgA benign monoclonal gammopathy, in 19 cases of IgM monoclonal gammopathy, and in 11 cases of mixed idiopathic IgG-IgM cryoglobulinemias. Except for myeloma, glomerular lesions were very frequent. Amyloidosis was found in one patient with myeloma, in two with benign IgG gammopathy, and in three with Waldenström macroglobulinemia. Intraglomerular deposits were found in 13 patients. In 7 of these patients (6 with Waldenström macroglobulinemia, 1 with benign IgA monoclonal gammopathy), the deposits were isolated without cellular proliferation. In the other 6 patients (one with benign IgG monoclonal gammopathy, five with IgG-IgM cryoglobulinemias) the deposits were associated with severe endocapillary proliferation. Immunohistologic study showed the presence of immunoglobulins in these deposits. The immunoglobulin(s) present in the glomerular deposits was (were) similar to the serum monoclonal immunoglobulin or immunoglobulins of the cryoglobulin. Crystals were found in the glomerular endothelial cells in one case of benign IgG gammopathy. The significance of these lesions is briefly discussed.

Acute Kidney Injury↗
PubMed1970

Drug intoxication and neurological episodes in chronic renal failure.

Of 178 episodes of neurological derangement in 103 patients with renal failure, only about 40% were due to known causes such as hypertension or electrolyte failure. One-third were due to drug intoxication and no definite aetiology was found for the remainder. Drug intoxication is due partly to the accumulation of a drug normally excreted by the kidney and partly to a greater susceptibility of the central nervous system in uraemic patients. The prognosis is favourable.

Cerebrovascular Disorders↗