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Biomedical subjects

J Bariety

Publications and source records attributed to J Bariety.

At least 73 records · Page 4Linked to original sources
PubMed1986

Immunohistochemical demonstration of parietal epithelial cells and macrophages in human proliferative extra-capillary lesions.

The cellular composition of crescents in diffuse crescentic glomerulonephritis is still controversial. Ten renal biopsies were studied on serial sections by using antikeratin antibodies as specific markers of epithelial cells of Bowman's capsule and both anti-macrophage and anti-lymphocyte antibodies. Semiautomatic morphometry showed that cellular crescents consisted of epithelial cells of Bowman's capsule (24-61%), of macrophages (19-34%) and of unlabelled cells (12-53%). In each biopsy, parietal epithelial cells outnumbered macrophages within crescents.

Antibodies, Monoclonal↗
PubMed1986

Effect of prostaglandin E1 in brown Norway rats with mercury-induced autoimmune disease.

The effect of prostaglandin E1 on mercury-induced autoimmune disease in brown Norway rats has been investigated. Daily doses of 6 to 24 micrograms prolonged survival and significantly decreased proteinuria, deposition of immune reactants in the glomeruli, circulating anti-glomerular membrane antibody production, total serum IgE, and circulating immune complex level. A dose of 3 micrograms was also effective but to a lesser degree. These results show the efficiency of prostaglandin E1 in yet another autoimmune disease, show that the beneficial effect of prostaglandin E1 in this model is related to its immunosuppressive effects, and suggest that modification of prostaglandin-mediated suppression induced by HgCl2 might play a role in the pathogenesis of this autoimmune disease.

Alprostadil↗
PubMed1986

Selective inhibition of thromboxane synthesis partially protected while inhibition of angiotensin II formation did not protect rats against acute renal failure induced with glycerol.

Acute renal failure (ARF) was induced in 35 week-old conscious female Wistar rats, by intramuscular (IM) injection of glycerol. Intraperitoneal (IP) injection of imidazole, an inhibitor of thromboxane (TXA2) synthesis, partially protected the animals against ARF. This protection was accompanied by a significant decrease in renal TXB2 (the stable chemical metabolite of TXA2) and a significant increase in renal 6-keto-PGF1 alpha (the stable chemical metabolite of PGI2) synthesis. Intraperitoneal injection of captopril (SQ 14225) an angiotensin-converting-enzyme inhibitor, did not protect the animals against ARF. This lack of protection was accompanied by a significant increase in renal TXB2 and a significant decrease in renal 6-keto-PGF1 alpha synthesis. The results suggest that: (a) the renin-angiotensin (R-A) system does not play a role, or has only a secondary one in the development of ARF; (b) thromboxane A2 (the most potent vasoconstrictor and platelet aggregator agent known) is the preponderant agent responsible for the development of this pathological syndrome.

6-Ketoprostaglandin F1 alpha↗
PubMed1986

Immunohistochemical study of the C5b-9 complex of complement in human kidneys.

The presence and localization of the C5b-9 neoantigens of the terminal complement sequence, of antigens expressed by cleavage fragments of C3, and of Factor H antigens have been studied by immunohistochemical techniques in morphologically normal adult human kidneys and in biopsy specimens from patients with a wide range of renal diseases with and without immune deposits. In morphologically normal kidneys, C5b-9 neoantigens were observed within all connective matrices (arteriolar media, glomerular basement membrane (GBM), mesangial matrix and tubular basement membrane). The C3d and C3g antigens of the C3dg, and C3bi cleavage fragments of C3 and Factor H antigens were found in similar locations. None of the matrices stained for immunoglobulins. Immunoelectron microscopy demonstrated that C3d, C3g, H antigens and the C5b-9 neoantigens were localized on membranous and vesicular structures embedded in the connective matrices. These structures represent cell membranes shed from adjacent cells as evidenced by their ultrastructural appearance and by the fact that those which were in close vicinity to pedicles within the GBM expressed the C3b receptor antigen, a specific marker for podocyte membranes. Formation of C5b-9 complexes in the shielded environment of connective matrices may explain their persistence over long periods of time in the absence of apparent immunopathological consequences. Biopsies from pathological kidneys were classified into three groups based on the pattern of glomerular staining with anti-C5b-9 antibodies. In the first group, a sparse mesangial labeling was seen, similar to that observed in normal kidneys. In the second group, abundant clusters of C5b-9 were seen in the same location as immune deposits. Activation of the complement system to completion could be documented in the absence of detectable C3 (C3c) antigen in glomeruli. Immunoelectron microscopy demonstrated that C5b-9 neoantigens were present on cell remnants in connective matrices in all specimens that were studied. Labeled cell remnants were present in large amounts in sclerotic matrices. C5b-9 neoantigens were constantly found on old and large immune deposits, and absent or occasionally present on recent and small immune deposits. In membranous nephropathy stage I, proteinuria appeared to be independent of the presence or absence of detectable C5b-9 neoantigens on immune deposits. Thus, the presence of C5b-9 neoantigens in pathological renal tissue does not have an univocal significance, and requires analysis of the localization of the antigens and appropriate controls in order to assess the potential role of C5b-9 in tissue damage.

Adult↗
PubMed1986

Immunohistochemical analysis of C3 cleavage fragments, factor H, and the C5b-9 terminal complex of complement in de novo membranous glomerulonephritis occurring in patients with renal transplant.

Fifteen renal biopsies from 13 transplanted patients with de novo membranous nephropathy (DNMN) were investigated by immunofluorescence for the presence of C5b-9 neoantigens of the terminal sequence of complement and for antigens expressed by C3 cleavage fragments. DNMN lesions were classified as stage I, II or III upon light and electron microscopy examination. Seven biopsies were classified as stage I DNMN and 8 stage II-III. All patients were proteinuric. In six biopsies with stage I DNMN, staining for C5b-9 neoantigens was restricted to a fine granular labeling in mesangial areas which was analogous to that seen in normal kidneys in contrast with extensive parietal labeling for IgG, C3d and factor H antigens. In eight biopsies with stage II-III DNMN, the pattern of staining with anti-C5b-9 neoantigens antibodies was similar to that obtained with anti-IgG, anti-C3d and anti-factor H antibodies. These results suggest that in situ activation of the whole complement sequence throughout C5b-9 only occurs on large immune deposits (stage II-III DNMN).

Adolescent↗
PubMed1986

[Diagnosis of AL amyloidosis in the absence of detectable serum or urinary monoclonal component].

A case of massive amyloidosis without detectable monoclonal Ig component either in serum or in urines on classical electrophoresis and without obvious plasma cell proliferation is reported. Immunohistochemical study of renal and bone marrow biopsies showed that amyloid deposits were specifically stained with the anti-lambda antiserum and that 92% of the plasma cells were also lambda positive. Immunofixation following electrophoretic analysis of serum and urinary proteins exhibited a monoclonal lambda light chain at an advanced stage of the disease. Simple but not routinely used techniques are therefore of great interest to characterize apparently idiopathic amyloidosis which could have therapeutic implications.

Aged↗
PubMed1986

De novo focal glomerular sclerosis in preeclampsia.

Eleven women were selected on the presence, in postpartum renal biopsies, of focal glomerulosclerosis (FGS) superimposed to glomerular lesions of typical pregnancy-induced nephropathy. Ten out of them presented with severe preeclampsia. The renal specimens were examined by light and/or electron and/or immunofluorescence microscopy. The present study gathered clinical and morphological data suggesting that FGS might develop during preeclampsia. In these renal biopsies with FGS and lesions of pregnancy-induced nephropathy a sparse detachment of podocyte was observed at a distance from the segmental lesions by electron microscopy. The latter has also been observed in experimental models of FGS in which FGS is dependent on glomerular hemodynamic alterations. We think that the mechanism of the development of FGS in these pathological pregnancies may be analogous to these experimental models of FGS with hyperfiltration.

Adolescent↗
PubMed1985

Pharmacokinetics of pefloxacin in renal insufficiency.

The kinetics of pefloxacin has been studied after a single intravenous infusion of 8 mg X kg-1 in 15 male patients with various degrees of renal failure. No difference in distribution or elimination of the drug was observed between patients with mild or severe renal impairment. The mean volume of distribution (Vd area) and the mean plasma clearance were 2.03 l X kg-1 and 121.3 ml X min-1, respectively. The mean apparent elimination half-life was 13.5 h. These values are close to those observed in healthy subjects. No accumulation of the active N-desmethylmetabolite was observed in cases of severe failure as compared to mild impairment; its apparent elimination half-life was about twice that of the parent drug. The efficacy of a 4 haemodialysis in 6 additional anuric subjects done to remove pefloxacin from the body was poor.

Adult↗
PubMed1985

Glomerular matrix proteins in nodular glomerulosclerosis in association with light chain deposition disease and diabetes mellitus.

The diagnosis of light chain deposition nephropathy is based on the immunohistochemical demonstration of monoclonal light chain deposits within connective tissue matrix and on the presence at the ultrastructural level of electron-dense granular deposits along glomerular and tubular basement membranes. A nodular glomerulopathy characterized by amorphous periodic acid-Schiff-positive and argyrophilic widened mesangium and nodules is described in three patients with light chain deposition nephropathy. Light microscopic examination did not allow discrimination between the glomerular changes found in these specimens and the nodular glomerulosclerosis described in four patients with well-documented diabetes mellitus. Electron microscopic examination revealed microtubular fibrils 10 to 12 nm thick in mesangial areas in both groups. Such microfibrils could be glycoproteins. Immunofluorescence localization of matrix proteins, by staining with affinity-purified antibodies to types I, III, IV, and V (A, B) collagens, fibronectin, laminin, and heparan sulfate-containing proteoglycans, showed similar distributions in the two conditions. The mechanism of this abnormal accumulation of mesangial and glomerular basement membrane matrix proteins in two different conditions remains unknown.

Basement Membrane↗
PubMed1985

Association light chain deposition disease (LCDD) and amyloidosis. One case.

Up to now, light chain deposition disease (L.C.D.D.) and amyloidosis have been shown to occur in different individuals. A case of association is described in a 76 year old man with terminal renal failure and normal size kidneys. Percutaneous renal biopsy showed glomerular and peritubular fixation of labeled antikappa light chain serum. Stains for amyloidosis were positive in small vessels. Kappa free chains were found in both serum and urine and the bone marrow showed predominantly kappa-containing plasma cells. By electron microscopy both electron-dense granular deposits and amyloid like fibrils were found in the wall of arterioles and small arteries.

Aged↗
PubMed1985

Selective inhibition of renal thromboxane biosynthesis increased sodium excretion rate in normal and saline-loaded rats.

The excretion rates of renal thromboxane B2 (TXB2) and 6-ketoPGF1 alpha, the stable chemical metabolites of thromboxane A2 (TXA2) and prostaglandin I2 (PGI2) respectively, PGE2 and sodium were determined in normal and saline-loaded rats treated with the thromboxane synthetase inhibitor imidazole. In normal rats the administration of imidazole in doses which did not affect renal 6-keto-PGF1 alpha and PGE2 excretion but selectively inhibited renal TXB2 excretion, significantly increased the sodium excretion rate. Volume expansion with saline increased renal PGE2 and 6-ketoPGF1 alpha excretion but did not alter renal TXB2 excretion. The increase in renal prostaglandin excretion was accompanied by an increased sodium excretion rate. The administration of imidazole to saline-loaded animals also decreased renal TXB2 excretion but did not alter the increased excretion of renal PGE2 and 6-ketoPGF1 alpha. This reduction in renal thromboxane biosynthesis by imidazole further increased the sodium excretion rate. We suggest that TXA2 is a potent antinatriuretic factor as well as the most potent vasoconstrictor agent known.

6-Ketoprostaglandin F1 alpha↗
PubMed1985

Association of systemic light-chain deposition disease and amyloidosis: a report of three patients with renal involvement.

Three patients with renal involvement, plasma cell dyscrasia and systemic light chain deposition are reported in whom well characterized amyloid deposits were also found in the vessel walls. This association, not yet reported, is probably more frequent than believed and still brings nearer these two manifestations of monoclonal light chain deposition. Whether or not the finding of amyloid deposits during systemic light chain deposition is a separate entity and modifies the prognosis remains to be answered.

Adult↗
PubMed1984

IgG Fc membrane receptor on normal human glomerular visceral epithelial cells.

This study demonstrates that human glomerular epithelial cells are able to bind heat aggregated immunoglobulins and antigen-antibody complexes. This has been observed on kidney cryostat sections, on whole glomeruli and on cultured visceral epithelial cells. Binding depends on the presence of the Fc portion of IgG and occurs in the absence of complement, showing that the IgG Fc receptor is different from the C3b receptor. The use of heat aggregated anti-peroxidase IgG and of peroxidase anti-peroxidase complexes allowed us to demonstrate, at the ultrastructural level, that the binding of the reagents at the plasma membrane was followed by their internalization within coated pits of vesicles. These observations strongly suggest that glomerular visceral epithelial cells are capable of receptor mediated endocytosis. The role of this process in glomerular diseases remains to be established.

Antigen-Antibody Complex↗
PubMed1984

Reversible hydronephrosis in the rat: a new surgical technique assessed by radioisotopic measurements.

A new technique for experimental reversible hydronephrosis in the rat was developed. A noninvasive radioisotopic investigation, using Tc-99m dimercaptosuccinic acid, permitted sequential assessment of the separate renal function at different stages of the study. After 1 week of unilateral ureteral obstruction, reversibility was obtained by the removal of the obstructive device. Ten days after the obstruction release, the ipsilateral kidney had returned to 71 per cent of its preligation uptake value. Histological findings demonstrated the reversibility of the surgical obstruction.

Animals↗
PubMed1984

Renin storage and cell differentiation in juxtaglomerular cell tumors: an immunohistochemical and ultrastructural study of three cases.

Three renin-secreting juxtaglomerular cell tumors were studied by ultrastructural and immunocytochemical methods. Both active and inactive renins were identified in tumor extracts. By immunofluorescence and the peroxidase-antiperoxidase (PAP) method with antirenin antiserum, immunolabeling was intracytoplasmic and irregularly distributed throughout the tumor tissue. Electron microscopic examination revealed various types of secretory granules, including atypical giant crystalloid protogranules in one case, and the postembedding PAP procedure showed labeling of all types of granules. Acid phosphatase staining was observed within secretory granules and autophagic vacuoles. The process of renin storage and release is discussed. The presence in one case of a neural component and a distal tubular structure supports the view of a hamartomatous lesion.

Adult↗
PubMed1984

Immunohistochemical study of Ia antigen in the normal and diseased human kidney.

The presence and distribution of Ia antigen in normal human kidneys and biopsy specimens from patients with renal disease were investigated by immunohistochemical techniques using two monoclonal antibodies to the nonpolymorphic determinants of human HLA-DR molecules. Ia antigen was found on the endothelium of glomerular and peritubular capillaries and of veins and vasa recta. Loss of endothelial staining was found in necrotic and sclerotic glomerular and tubulointerstitial lesions. Staining or decreased staining was also not found in the severe proliferative nephritis of systemic lupus erythematosus although endothelial cells could still be identified upon light microscopic examination of the same biopsy specimen. Resting and proliferating cells in mesangial areas did not stain with anti-Ia antibody and extracapillary proliferating cells did not express Ia antigen except for occasional cells in anti-GBM crescentic glomerulonephritis, suggesting that Ia-bearing cells are not involved in mesangial and most extracapillary proliferations in human glomerulonephritis. All clustered mononuclear cells infiltrating the renal interstitium stained with anti-Ia antibody regardless of the type of nephritis where infiltrates occurred.

Antibodies, Monoclonal↗