IgA nephropathy in chronic liver disease.
Explore the source record for details and available documents.
Animals↗
Biomedical subjects
J Bariety
Publications and source records attributed to J Bariety.
A monoclonal antibody to brush border and passive Heymann nephritis.
An IgG2a monoclonal antibody (MoAb) reacting with the brush border of the renal proximal tubule and glomerular capillary wall was produced by fusion of NS1 myeloma cells with spleen cells from BALB/c mice immunized with renal brush border preparations from rat kidney cortex. This antibody reacts with a 90,000 mol. wt protein which can be isolated by immunoprecipitation of radiolabelled brush border or glomerular preparations and localized on these structures by immunoperoxidase electron microscopy, thus demonstrating the presence of common antigenic determinants. Survey of various organs showed that the MoAb reacted with the brush border of the gut, but also with antigens associated with the distal vascular system. In the liver antigenic determinants were located along the sinusoid walls but mainly on bile canaliculi. Specific glomerular binding could be demonstrated in vivo by immunofluorescence after an intravenous injection of 2 mg of antibody or by paired label methodology using tracer amounts. Kinetics however were dramatically different from those observed in classical passive Heymann nephritis since glomerular binding was transient during the first hours after injection. Binding was also found in tubular structures, as well as in lung, liver, spleen and heart. These results identify a well defined antigen-antibody system responsible for the formation of transient extramembranous glomerular deposits and may be relevant to some human cases of glomerulonephritis. They may also provide new models to study glomerular and tubular transfer of membrane bound antibodies.
Animals↗
[Monoclonal antibodies against surface antigens of lymphoblasts and blood cells or bone marrow recognize constituents of the human nephron].
By immunizing mice with bone marrow cells of a patient with acute lymphoblastic leukemia, monoclonal antibodies have been produced against differentiation antigens of hemopoietic cells. These antibodies also recognize cells in different parts of the normal human kidney. Two antibodies, ALB1 et ALB2, which recognize the common acute lymphoblastic leukemia antigen, (CALLA), label the podocytes and the epithelial cells of the proximal tubules of the kidney; ALB6, which recognizes the "p 24" antigen of lymphocytes, labels the distal tubules; ALB9, which recognizes lymphoblasts and granulocytes, labels the thick ascending loop of Henle and the collecting tubules; PM1, which recognizes immature granulocytic cells, labels the thick ascending loop of Henle.
Animals↗
[Changes in the renal and maternal utero-placental arteries in pregnancies complicated by hypertension].
Explore the source record for details and available documents.
Adolescent↗
Immunoelectron microscopic study of plasma protein pathways through the abnormal intestinal vasculature of HgCl2 induced immune disease in brown Norway rats.
Localization of immune deposits (ID) and the pathway of circulating serum proteins through the intestinal vasculature have been studied in 40 Brown Norway (BN) rats poisoned by mercuric chloride, using anti-peroxidase IgG as tracer. ID were found in all vessels but were initially detected along the epithelial basement membrane of villi and in pericytic venules and veins. ID were found in all the layers of the vessel walls. In pericytic or myocytic vessels, no ID were detected outside the adventitial lamina densa. ID trapped non immune IgG. Abnormal pathways were only found in venular capillaries and in pericytic venules with large gaps between endothelial junctions. ID were particularly abundant in these vessels.
Animals↗
Glomerular and vascular IgG deposits in HgCl2 nephritis: role of circulating antibodies and of immune complexes.
The respective roles of circulating anti-glomerular basement membrane antibodies and of circulating immune complexes in the appearance of glomerular linear and granular IgG deposition during HgCl2-induced glomerulonephritis in the Brown-Norway rat has been studied. Syngeneic kidney transplantations have been performed at various phases of the disease. Results show that circulating antibodies are responsible for linear IgG deposition which did not change to granular deposits during the course of the disease. Electron-dense subepithelial deposits occurred only when circulating immune complexes were detected. These experiments strongly suggest that, in the mercury model, circulating immune complexes are responsible for granular IgG deposits observed in arteries and in the subepithelial space of glomeruli.
Animals↗
Abnormalities of renin-containing cells in human glomerular and vascular renal diseases.
The distribution of renin was investigated by immunofluorescence in human kidney biopsy specimens (27 patients with lipoid nephrosis, 39 with Berger disease, 17 with membranous glomerulonephritis, 5 with thrombotic microangiopathy, and 7 with malignant nephroangiosclerosis). A semiquantitative assessment was carried out. Two ratios were found significatively increased in the study groups as compared with the control group: JGA + and JGA ++ which expressed, respectively, the number of fluorescent JGA in relation to the number of glomerular sections and the number of fluorescent JGA with more than six renin-containing cells (RCC) in relation to the number of immunoreactive JGA. Highest values were observed in patients with thrombotic microangiopathy and malignant nephroangiosclerosis (P less than 0.001). The above immunomorphological parameters were correlated with clinical and laboratory data. A positive dependency was found between JGA + and JGA ++ ratios and a low sodium diet, diuretic therapy and serum creatinine. A negative dependency was seen in the albumin and hemoglobin serum levels. No correlation was found with blood pressure values. These observations suggested that decreased plasma volume and impaired renal function could be factors leading to an increased renin production in the kidney.
Adolescent↗
Immunohistochemistry of renin in human diseased kidney.
The distribution of renin in human kidney was investigated by immunofluorescence and the peroxidase-antiperoxidase (PAP) procedure at the light and ultrastructural level. In three cases of juxtaglomerular renin-secreting tumors, renin was localized within the cytoplasm of tumor cells. In kidney biopsies, a semi-quantitative assessment was carried out, taking into account the size and the number of immunostained juxtaglomerular apparatuses. In 12 cases of ischemic kidneys and 8 cases of segmental renal hypoplasia, the increase in immunostaining for renin was striking in altered areas, while spared areas remained negative. In 2 cases of Bartter's syndrome, the pattern was similar to that found in ischemic kidneys. The study was extended to a series of 133 needle kidney biopsies from patients with various glomerular and vascular diseases; the immunomorphological parameters were correlated with serum creatinine levels but not with blood pressure values. Post-embedding immunoelectronmicroscopy using the PAP procedure performed on two of the cases of renin-secreting tumors, showed renin in all types of secretory granules.
Bartter Syndrome↗
Human antirenin antibody: a new tool for studying the renin-angiotensin system.
Explore the source record for details and available documents.
Animals↗
[Presence of the terminal complement activation complex (C5b-9) on cell remnants within connective matrices of normal human kidney].
The C5b-9 neoantigen of the terminal complex of human complement was localized on cell remnants in connective matrices of normal kidney using immunohistochemical techniques. These observations suggest that the complement system plays a role in the shedding process of plasma membranes from aging cells.
Cell Membrane↗
Accumulation of several basement membrane proteins in glomeruli of patients with preeclampsia and other hypertensive syndromes of pregnancy. Possible role of renal prostaglandins and fibronectin.
The glomerular lesions of preeclampsia consist of swelling of endothelial cells, interposition of mesangial cells and matrix between the endothelial cells and the glomerular basement membrane, and organization of subendothelial deposits of incompletely characterized material. Fibrin and immunoglobulins have previously been localized to these deposits. Laminin, a large basement membrane glycoprotein, type IV collagen, fibronectin, and a basement membrane proteoglycan were found in moderate amounts in the mesangium and prominently in the thickened glomerular capillary walls of patients with preeclampsia or other hypertensive syndromes of pregnancy. Fibrin showed the same pattern of distribution as that of fibronectin. The material deposited in the subendothelial layer of the capillary loops thus consists not only of plasma-derived proteins but also structural components of the glomerular basement membrane and of the mesangial matrix. Type I collagen deposits were demonstrated only in mesangium of pregnant patients with chronic or recurrent hypertension. Glomerular epithelial and mesangial cells synthesize in vitro the basement membrane proteins that accumulate in glomeruli of pregnant hypertensive patients. We have tested the influence of some of the pathophysiologic changes occurring during preeclampsia on the biosynthesis of collagen by rat glomerular epithelial and mesangial cells. Addition of indomethacin to the cultures transiently inhibited the synthesis of prostaglandins (PGE2) and of collagen. Addition of exogenous fibronectin to the media stimulated the production of collagen by mesangial and epithelial cells. Alterations in the metabolism of prostaglandins and the increased deposition of fibronectin observed during preeclampsia could thus play a pathogenic role in the accumulation of basement membrane proteins in glomeruli of these patients.
Basement Membrane↗
Effects of captopril on prostaglandin and natriuresis in patients with essential hypertension.
The antihypertensive, renal and hormonal effects of captopril were studied in 10 patients with essential hypertension. Captopril significantly decreased arterial blood pressure with a concomitant increase in glomerular filtration rate, natriuresis and kaliuresis and a significant selective increase in urinary (renal) prostaglandin E2; other plasma and urinary prostaglandin (F2 alpha, 6-keto-prostaglandin F1 alpha; thromboxane B2) were not significantly changed. The urinary prostaglandin E2 increase was observed even in patients with pretreatment subnormal prostaglandin E2 excretion. Increases in urinary prostaglandin E2 were significantly positively correlated with increases in urinary sodium concentration. It is concluded that the antihypertensive effect of captopril is mediated, at least partially, by prostaglandin E2 release from renal and extrarenal tissues. Captopril enhances natriuresis at a lower perfusion pressure.
Blood Pressure↗
The role of expansion, of prostaglandins and catecholamines in the development of acute renal failure.
A single injection either of isotonic or hypertonic saline solutions protected rats against acute renal failure (ARF) induced with glycerol. This protection was accompanied by increased urinary prostaglandin E (PGE) concentration. On the contrary, a single s.c. injection either of hypotonic saline or isotonic glucose solution, which did not increase urinary PGE concentration, or depletion of the endogenous catecholamines, using reserpine, did not protect the animals against acute renal failure.
Acute Kidney Injury↗
Immunoelectron microscopic study of plasma protein pathways through the different segments of the rat intestinal vasculature.
Nineteen Brown-Norway (BN) rats received intravenous injections of sheep anti-peroxidase (HRP) antibodies. Four BN rats were immunized to HRP. The anti-HRP antibodies were used to trace permeability pathways of large physiological molecules across different vessels of the small intestine. This organ was chosen because of the possibility of convenient "in situ" fixation and for the diversity of vessel types it contains. It was shown that: 1) There were no obvious transendothelial pathways in arteries with an elastic lamina. 2) The antibodies readily crossed fenestrated capillaries through the fenestrae. 3) There were two possible pathways through muscle capillaries and pericytic venules, namely transcytoplasmic vesicular "cactus-like" channels and interendothelial junctions. 4) Interendothelial permeability was a possible factor in veins with an elastic lamina. 5) Lymphatics were readily permeable through intercellular junctions and cytoplasmic vesicles.
Animals↗
Immunohistochemical study of the human glomerular C3b receptor in normal kidney and in seventy-five cases of renal diseases: loss of C3b receptor antigen in focal hyalinosis and in proliferative nephritis of systemic lupus erythematosus.
The presence and distribution of C3b receptors in normal human kidneys and in biopsies from 75 patients with renal disease were investigated by immunohistochemical techniques using monospecific rabbit antibody to the 205,000-mol wt glycoprotein that is the C3b receptor of human peripheral blood cells. Anti-C3b receptor bound exclusively to podocytes in normal renal cortex, and was homogeneously distributed on the plasma membrane of these cells. Biosynthesis of the receptor by the podocyte was suggested by the presence of antigenic activity in the Golgi apparatus. Although occupancy of receptor sites following the interaction of kidney sections with aggregated IgG preincubated with normal serum inhibited binding to glomeruli of C3b coated cells, the C3b receptor remained accessible to anti-C3b receptor antibody. No staining of podocytes was found in extra-capillary proliferating cells in rapidly progressive glomerulonephritis (GN). Segmental loss of staining was found in focal hyalinosis, nodular diabetic glomerulosclerosis, and amyloidosis while no detectable C3b receptor antigen was found in severe proliferative nephritis of systemic lupus erythematosus (SLE). Normal staining of podocytes was found in other nephropathies with endocapillary proliferation such as acute GN and mesangial GN and in renal diseases associated with immune deposits containing C3 such as mesangial proliferative and membranous SLE nephritis, idiopathic membranous GN, membranoproliferative GN types I and II, mesangial GN with IgA or C3 deposition and Henoch Schönlein's purpura. Loss of C3b receptor antigen in the diffuse proliferative nephritis of SLE distinguishes it both from nonproliferative lupus nephritis and other immunologically mediated proliferative GN.
Complement C3↗
Histochemical and ultrastructural characterization of subendothelial glycoprotein microfibrils interacting with platelets.
The interaction of human blood platelets with collagenase-treated rabbit subendothelium was studied by histochemical ultrastructural methods and by morphometric semi-quantitative analysis. Aortas were deendothelialized and incubated: 1) with a highly purified bacterial collagenase whose specificity was controlled; and 2) with the same collagenase followed by chymotrypsin. For histochemical studies, tannic acid, ruthenium red, and peroxidase-labeled Ricinus communis and concanavalin A were used. Electron microscopy showed that after digestion of fibrillar collagen by collagenase, adherent and aggregated platelets were observed on Ricinus communis-, concanavalin A-, and ruthenium red-positive glycoprotein microfibrils. After successive incubation with collagenase and chymotrypsin, the microfibrils disappeared. No platelets were observed on the remnant amorphous elastin. Morphometric analysis confirmed the interaction of platelets with collagenase-treated subendothelium. In addition, glycoproteins were extracted from collagenase-treated rabbit aortas using 5 M guanidine. Using an in vitro quantitative test, significant platelet adhesion to these glycoproteins was observed. Our results show an interaction between platelets and noncollagenic glycoprotein microfibrils.
Animals↗
Trapping of circulating proteins in immune deposits of Heymann nephritis.
The renal distribution of autologous and heterologous albumin and IgG was studied by electron microscopy using peroxidase-labeled conjugates in rats with Heymann nephritis. In addition, the renal distribution of autologous and heterologous antiperoxidase IgG and their F(ab')2 and Fab fragments was detected using peroxidase alone. All of these proteins crossed the glomerular lamina densa and passed into the urinary space by an extracellular pathway through the epithelial slits and the sites of epithelial detachment. The proteins were trapped in subepithelial immune deposits irrespective of the degree of proteinuria and regardless of the molecular weight, the autologous or heterologous origin, and the electric charges of the protein studied. The trapping was transient and easily reversed. These findings suggest that circulating proteins are able to modify the composition of immune deposits, thereby altering the course of immune complex disease.
Animals↗
Radioimmunoassay measurement of thromboxane B2 in human plasma and urine.
A radioimmunoassay method, using highly specific and sensitive rabbit antiserum, for the measurement of thromboxane (Tx)B2 in human plasma and urine, is described. Assay sensitivity was 5 pg; 50% displacement was achieved by 41 pg of cold TxB. Intra-assay variability was 10% and interassay variability 8,5%. Preliminary extraction and chromatography were necessary as direct radioimmunoassay of plasma although possible, was not reliable. The measurement of TxB2 reflects closely the synthesis of TxA2. The peripheral venous plasma TxB2 concentration in 13 young healthy volunteers (mean age 28 +/- 2 years) was 35 +/- 8 pg/ml; it was significantly higher in 14 older subjects (mean age 45 +/- 5 years) 101 +/- 14 pg/ml (p less than 0.001). Urinary TxB2 excretion was 141 +/- 15 pg/min in the younger group and 220 +/- 39 pg/min in the older group of normotensive subjects. There was a significant positive correlation between urinary TxB2 excretion and age (p less than 0.001). The increase with age of plasma and urinary TxB2 in man may have a pathophysiological importance.
Adult↗