Hyaline Membrane Disease: A respiratory distress syndrome in newborn infants, usually premature infants with insufficient PULMONARY SURFACTANTS. The disease is characterized by the formation of a HYALINE-like membrane lining the terminal respiratory airspaces (PULMONARY ALVEOLI) and subsequent collapse of the lung (PULMONARY ATELECTASIS).Basement Membrane: A darkly stained mat-like EXTRACELLULAR MATRIX (ECM) that separates cell layers, such as EPITHELIUM from ENDOTHELIUM or a layer of CONNECTIVE TISSUE. The ECM layer that supports an overlying EPITHELIUM or ENDOTHELIUM is called basal lamina. Basement membrane (BM) can be formed by the fusion of either two adjacent basal laminae or a basal lamina with an adjacent reticular lamina of connective tissue. BM, composed mainly of TYPE IV COLLAGEN; glycoprotein LAMININ; and PROTEOGLYCAN, provides barriers as well as channels between interacting cell layers.Anti-Glomerular Basement Membrane Disease: An autoimmune disease of the KIDNEY and the LUNG. It is characterized by the presence of circulating autoantibodies targeting the epitopes in the non-collagenous domains of COLLAGEN TYPE IV in the basement membranes of kidney glomeruli (KIDNEY GLOMERULUS) and lung alveoli (PULMONARY ALVEOLI), and the subsequent destruction of these basement membranes. Clinical features include pulmonary alveolar hemorrhage and glomerulonephritis.Glomerular Basement Membrane: The layer of EXTRACELLULAR MATRIX that lies between the ENDOTHELIUM of the glomerular capillaries and the PODOCYTES of the inner or visceral layer of the BOWMAN CAPSULE. It is the product of these two cell types. It acts as a physical barrier and an ion-selective filter.Kidney Glomerulus: A cluster of convoluted capillaries beginning at each nephric tubule in the kidney and held together by connective tissue.Nephritis, Hereditary: A group of inherited conditions characterized initially by HEMATURIA and slowly progressing to RENAL INSUFFICIENCY. The most common form is the Alport syndrome (hereditary nephritis with HEARING LOSS) which is caused by mutations in genes for TYPE IV COLLAGEN and defective GLOMERULAR BASEMENT MEMBRANE.Hematuria: Presence of blood in the urine.Collagen Type IV: A non-fibrillar collagen found in the structure of BASEMENT MEMBRANE. Collagen type IV molecules assemble to form a sheet-like network which is involved in maintaining the structural integrity of basement membranes. The predominant form of the protein is comprised of two alpha1(IV) subunits and one alpha2(IV) subunit, however, at least six different alpha subunits can be incorporated into the heterotrimer.Glomerulonephritis: Inflammation of the renal glomeruli (KIDNEY GLOMERULUS) that can be classified by the type of glomerular injuries including antibody deposition, complement activation, cellular proliferation, and glomerulosclerosis. These structural and functional abnormalities usually lead to HEMATURIA; PROTEINURIA; HYPERTENSION; and RENAL INSUFFICIENCY.Nephritis, Interstitial: Inflammation of the interstitial tissue of the kidney. This term is generally used for primary inflammation of KIDNEY TUBULES and/or surrounding interstitium. For primary inflammation of glomerular interstitium, see GLOMERULONEPHRITIS. Infiltration of the inflammatory cells into the interstitial compartment results in EDEMA, increased spaces between the tubules, and tubular renal dysfunction.Autoantigens: Endogenous tissue constituents that have the ability to interact with AUTOANTIBODIES and cause an immune response.Autoantibodies: Antibodies that react with self-antigens (AUTOANTIGENS) of the organism that produced them.Proteinuria: The presence of proteins in the urine, an indicator of KIDNEY DISEASES.Podocytes: Highly differentiated epithelial cells of the visceral layer of BOWMAN CAPSULE of the KIDNEY. They are composed of a cell body with major CELL SURFACE EXTENSIONS and secondary fingerlike extensions called pedicels. They enwrap the KIDNEY GLOMERULUS capillaries with their cell surface extensions forming a filtration structure. The pedicels of neighboring podocytes interdigitate with each other leaving between them filtration slits that are bridged by an extracellular structure impermeable to large macromolecules called the slit diaphragm, and provide the last barrier to protein loss in the KIDNEY.Laminin: Large, noncollagenous glycoprotein with antigenic properties. It is localized in the basement membrane lamina lucida and functions to bind epithelial cells to the basement membrane. Evidence suggests that the protein plays a role in tumor invasion.Nephritis: Inflammation of any part of the KIDNEY.Tolazoline: A vasodilator that apparently has direct actions on blood vessels and also increases cardiac output. Tolazoline can interact to some degree with histamine, adrenergic, and cholinergic receptors, but the mechanisms of its therapeutic effects are not clear. It is used in treatment of persistent pulmonary hypertension of the newborn.Microscopy, Electron: Microscopy using an electron beam, instead of light, to visualize the sample, thereby allowing much greater magnification. The interactions of ELECTRONS with specimens are used to provide information about the fine structure of that specimen. In TRANSMISSION ELECTRON MICROSCOPY the reactions of the electrons that are transmitted through the specimen are imaged. In SCANNING ELECTRON MICROSCOPY an electron beam falls at a non-normal angle on the specimen and the image is derived from the reactions occurring above the plane of the specimen.Kidney: Body organ that filters blood for the secretion of URINE and that regulates ion concentrations.Collagen: A polypeptide substance comprising about one third of the total protein in mammalian organisms. It is the main constituent of SKIN; CONNECTIVE TISSUE; and the organic substance of bones (BONE AND BONES) and teeth (TOOTH).Heparitin Sulfate: A heteropolysaccharide that is similar in structure to HEPARIN. It accumulates in individuals with MUCOPOLYSACCHARIDOSIS.Heparan Sulfate Proteoglycans: Ubiquitous macromolecules associated with the cell surface and extracellular matrix of a wide range of cells of vertebrate and invertebrate tissues. They are essential cofactors in cell-matrix adhesion processes, in cell-cell recognition systems, and in receptor-growth factor interactions. (From Cancer Metastasis Rev 1996; 15(2): 177-86; Hepatology 1996; 24(3): 524-32)Fluorescent Antibody Technique: Test for tissue antigen using either a direct method, by conjugation of antibody with fluorescent dye (FLUORESCENT ANTIBODY TECHNIQUE, DIRECT) or an indirect method, by formation of antigen-antibody complex which is then labeled with fluorescein-conjugated anti-immunoglobulin antibody (FLUORESCENT ANTIBODY TECHNIQUE, INDIRECT). The tissue is then examined by fluorescence microscopy.Glomerulonephritis, Membranous: A type of glomerulonephritis that is characterized by the accumulation of immune deposits (COMPLEMENT MEMBRANE ATTACK COMPLEX) on the outer aspect of the GLOMERULAR BASEMENT MEMBRANE. It progresses from subepithelial dense deposits, to basement membrane reaction and eventual thickening of the basement membrane.Glomerular Filtration Barrier: A specialized barrier in the kidney, consisting of the fenestrated CAPILLARY ENDOTHELIUM; GLOMERULAR BASEMENT MEMBRANE; and glomerular epithelium (PODOCYTES). The barrier prevents the filtration of PLASMA PROTEINS.Nephrotic Syndrome: A condition characterized by severe PROTEINURIA, greater than 3.5 g/day in an average adult. The substantial loss of protein in the urine results in complications such as HYPOPROTEINEMIA; generalized EDEMA; HYPERTENSION; and HYPERLIPIDEMIAS. Diseases associated with nephrotic syndrome generally cause chronic kidney dysfunction.Nephrosis: Pathological processes of the KIDNEY without inflammatory or neoplastic components. Nephrosis may be a primary disorder or secondary complication of other diseases. It is characterized by the NEPHROTIC SYNDROME indicating the presence of PROTEINURIA and HYPOALBUMINEMIA with accompanying EDEMA.Infant, Newborn: An infant during the first month after birth.Glomerulonephritis, Membranoproliferative: Chronic glomerulonephritis characterized histologically by proliferation of MESANGIAL CELLS, increase in the MESANGIAL EXTRACELLULAR MATRIX, and a thickening of the glomerular capillary walls. This may appear as a primary disorder or secondary to other diseases including infections and autoimmune disease SYSTEMIC LUPUS ERYTHEMATOSUS. Various subtypes are classified by their abnormal ultrastructures and immune deposits. Hypocomplementemia is a characteristic feature of all types of MPGN.Diabetic Nephropathies: KIDNEY injuries associated with diabetes mellitus and affecting KIDNEY GLOMERULUS; ARTERIOLES; KIDNEY TUBULES; and the interstitium. Clinical signs include persistent PROTEINURIA, from microalbuminuria progressing to ALBUMINURIA of greater than 300 mg/24 h, leading to reduced GLOMERULAR FILTRATION RATE and END-STAGE RENAL DISEASE.Immune Complex Diseases: Group of diseases mediated by the deposition of large soluble complexes of antigen and antibody with resultant damage to tissue. Besides SERUM SICKNESS and the ARTHUS REACTION, evidence supports a pathogenic role for immune complexes in many other IMMUNE SYSTEM DISEASES including GLOMERULONEPHRITIS, systemic lupus erythematosus (LUPUS ERYTHEMATOSUS, SYSTEMIC) and POLYARTERITIS NODOSA.Antigen-Antibody Complex: The complex formed by the binding of antigen and antibody molecules. The deposition of large antigen-antibody complexes leading to tissue damage causes IMMUNE COMPLEX DISEASES.Glomerular Mesangium: The thin membranous structure supporting the adjoining glomerular capillaries. It is composed of GLOMERULAR MESANGIAL CELLS and their EXTRACELLULAR MATRIX.Infant, Premature: A human infant born before 37 weeks of GESTATION.Fetal Organ Maturity: Functional competence of specific organs or body systems of the FETUS in utero.Capillaries: The minute vessels that connect the arterioles and venules.Nephrosis, Lipoid: A kidney disease with no or minimal histological glomerular changes on light microscopy and with no immune deposits. It is characterized by lipid accumulation in the epithelial cells of KIDNEY TUBULES and in the URINE. Patients usually show NEPHROTIC SYNDROME indicating the presence of PROTEINURIA with accompanying EDEMA.Anions: Negatively charged atoms, radicals or groups of atoms which travel to the anode or positive pole during electrolysis.Negative Staining: The technique of washing tissue specimens with a concentrated solution of a heavy metal salt and letting it dry. The specimen will be covered with a very thin layer of the metal salt, being excluded in areas where an adsorbed macromolecule is present. The macromolecules allow electrons from the beam of an electron microscope to pass much more readily than the heavy metal; thus, a reversed or negative image of the molecule is created.Albuminuria: The presence of albumin in the urine, an indicator of KIDNEY DISEASES.Membranes: Thin layers of tissue which cover parts of the body, separate adjacent cavities, or connect adjacent structures.Glycosaminoglycans: Heteropolysaccharides which contain an N-acetylated hexosamine in a characteristic repeating disaccharide unit. The repeating structure of each disaccharide involves alternate 1,4- and 1,3-linkages consisting of either N-acetylglucosamine or N-acetylgalactosamine.Puromycin Aminonucleoside: PUROMYCIN derivative that lacks the methoxyphenylalanyl group on the amine of the sugar ring. It is an antibiotic with antineoplastic properties and can cause nephrosis.Glomerulosclerosis, Focal Segmental: A clinicopathological syndrome or diagnostic term for a type of glomerular injury that has multiple causes, primary or secondary. Clinical features include PROTEINURIA, reduced GLOMERULAR FILTRATION RATE, and EDEMA. Kidney biopsy initially indicates focal segmental glomerular consolidation (hyalinosis) or scarring which can progress to globally sclerotic glomeruli leading to eventual KIDNEY FAILURE.Proteoglycans: Glycoproteins which have a very high polysaccharide content.Cell Membrane: The lipid- and protein-containing, selectively permeable membrane that surrounds the cytoplasm in prokaryotic and eukaryotic cells.Immunoglobulin G: The major immunoglobulin isotype class in normal human serum. There are several isotype subclasses of IgG, for example, IgG1, IgG2A, and IgG2B.Lupus Nephritis: Glomerulonephritis associated with autoimmune disease SYSTEMIC LUPUS ERYTHEMATOSUS. Lupus nephritis is histologically classified into 6 classes: class I - normal glomeruli, class II - pure mesangial alterations, class III - focal segmental glomerulonephritis, class IV - diffuse glomerulonephritis, class V - diffuse membranous glomerulonephritis, and class VI - advanced sclerosing glomerulonephritis (The World Health Organization classification 1982).Chondroitin Sulfate Proteoglycans: Proteoglycans consisting of proteins linked to one or more CHONDROITIN SULFATE-containing oligosaccharide chains.Kidney Tubules: Long convoluted tubules in the nephrons. They collect filtrate from blood passing through the KIDNEY GLOMERULUS and process this filtrate into URINE. Each renal tubule consists of a BOWMAN CAPSULE; PROXIMAL KIDNEY TUBULE; LOOP OF HENLE; DISTAL KIDNEY TUBULE; and KIDNEY COLLECTING DUCT leading to the central cavity of the kidney (KIDNEY PELVIS) that connects to the URETER.Kidney Diseases: Pathological processes of the KIDNEY or its component tissues.Membrane Lipids: Lipids, predominantly phospholipids, cholesterol and small amounts of glycolipids found in membranes including cellular and intracellular membranes. These lipids may be arranged in bilayers in the membranes with integral proteins between the layers and peripheral proteins attached to the outside. Membrane lipids are required for active transport, several enzymatic activities and membrane formation.Antibodies: Immunoglobulin molecules having a specific amino acid sequence by virtue of which they interact only with the ANTIGEN (or a very similar shape) that induced their synthesis in cells of the lymphoid series (especially PLASMA CELLS).Respiration, Artificial: Any method of artificial breathing that employs mechanical or non-mechanical means to force the air into and out of the lungs. Artificial respiration or ventilation is used in individuals who have stopped breathing or have RESPIRATORY INSUFFICIENCY to increase their intake of oxygen (O2) and excretion of carbon dioxide (CO2).Microscopy, Immunoelectron: Microscopy in which the samples are first stained immunocytochemically and then examined using an electron microscope. Immunoelectron microscopy is used extensively in diagnostic virology as part of very sensitive immunoassays.Extracellular Matrix: A meshwork-like substance found within the extracellular space and in association with the basement membrane of the cell surface. It promotes cellular proliferation and provides a supporting structure to which cells or cell lysates in culture dishes adhere.Pulmonary Surfactants: Substances and drugs that lower the SURFACE TENSION of the mucoid layer lining the PULMONARY ALVEOLI.Microbial Collagenase: A metalloproteinase which degrades helical regions of native collagen to small fragments. Preferred cleavage is -Gly in the sequence -Pro-Xaa-Gly-Pro-. Six forms (or 2 classes) have been isolated from Clostridium histolyticum that are immunologically cross-reactive but possess different sequences and different specificities. Other variants have been isolated from Bacillus cereus, Empedobacter collagenolyticum, Pseudomonas marinoglutinosa, and species of Vibrio and Streptomyces. EC 3.4.24.3.Complement C3: A glycoprotein that is central in both the classical and the alternative pathway of COMPLEMENT ACTIVATION. C3 can be cleaved into COMPLEMENT C3A and COMPLEMENT C3B, spontaneously at low level or by C3 CONVERTASE at high level. The smaller fragment C3a is an ANAPHYLATOXIN and mediator of local inflammatory process. The larger fragment C3b binds with C3 convertase to form C5 convertase.Nail-Patella Syndrome: A syndrome of multiple abnormalities characterized by the absence or hypoplasia of the PATELLA and congenital nail dystrophy. It is a genetically determined autosomal dominant trait.Intracellular Membranes: Thin structures that encapsulate subcellular structures or ORGANELLES in EUKARYOTIC CELLS. They include a variety of membranes associated with the CELL NUCLEUS; the MITOCHONDRIA; the GOLGI APPARATUS; the ENDOPLASMIC RETICULUM; LYSOSOMES; PLASTIDS; and VACUOLES.Disease Models, Animal: Naturally occurring or experimentally induced animal diseases with pathological processes sufficiently similar to those of human diseases. They are used as study models for human diseases.Immunohistochemistry: Histochemical localization of immunoreactive substances using labeled antibodies as reagents.Epithelium: One or more layers of EPITHELIAL CELLS, supported by the basal lamina, which covers the inner or outer surfaces of the body.Infant, Premature, DiseasesFicoll: A sucrose polymer of high molecular weight.Biopsy: Removal and pathologic examination of specimens in the form of small pieces of tissue from the living body.Membrane Potentials: The voltage differences across a membrane. For cellular membranes they are computed by subtracting the voltage measured outside the membrane from the voltage measured inside the membrane. They result from differences of inside versus outside concentration of potassium, sodium, chloride, and other ions across cells' or ORGANELLES membranes. For excitable cells, the resting membrane potentials range between -30 and -100 millivolts. Physical, chemical, or electrical stimuli can make a membrane potential more negative (hyperpolarization), or less negative (depolarization).Permeability: Property of membranes and other structures to permit passage of light, heat, gases, liquids, metabolites, and mineral ions.Membranes, Artificial: Artificially produced membranes, such as semipermeable membranes used in artificial kidney dialysis (RENAL DIALYSIS), monomolecular and bimolecular membranes used as models to simulate biological CELL MEMBRANES. These membranes are also used in the process of GUIDED TISSUE REGENERATION.Gestational Age: The age of the conceptus, beginning from the time of FERTILIZATION. In clinical obstetrics, the gestational age is often estimated as the time from the last day of the last MENSTRUATION which is about 2 weeks before OVULATION and fertilization.Serum Sickness: Immune complex disease caused by the administration of foreign serum or serum proteins and characterized by fever, lymphadenopathy, arthralgia, and urticaria. When they are complexed to protein carriers, some drugs can also cause serum sickness when they act as haptens inducing antibody responses.Pupil Disorders: Conditions which affect the structure or function of the pupil of the eye, including disorders of innervation to the pupillary constrictor or dilator muscles, and disorders of pupillary reflexes.Endothelium: A layer of epithelium that lines the heart, blood vessels (ENDOTHELIUM, VASCULAR), lymph vessels (ENDOTHELIUM, LYMPHATIC), and the serous cavities of the body.Rats, Inbred Strains: Genetically identical individuals developed from brother and sister matings which have been carried out for twenty or more generations or by parent x offspring matings carried out with certain restrictions. This also includes animals with a long history of closed colony breeding.Antigens: Substances that are recognized by the immune system and induce an immune reaction.Heparinoids: Heparin derivatives. The term has also been used more loosely to include naturally occurring and synthetic highly-sulphated polysaccharides of similar structure. Heparinoid preparations have been used for a wide range of applications including as anticoagulants and anti-inflammatories and they have been claimed to have hypolipidemic properties. (From Martindale, The Extra Pharmacopoeia, 30th, p232)Microscopy, Electron, Transmission: Electron microscopy in which the ELECTRONS or their reaction products that pass down through the specimen are imaged below the plane of the specimen.Cattle: Domesticated bovine animals of the genus Bos, usually kept on a farm or ranch and used for the production of meat or dairy products or for heavy labor.Lung: Either of the pair of organs occupying the cavity of the thorax that effect the aeration of the blood.Agrin: A protein component of the synaptic basal lamina. It has been shown to induce clustering of acetylcholine receptors on the surface of muscle fibers and other synaptic molecules in both synapse regeneration and development.Dirofilaria immitis: A filarial parasite primarily of dogs but occurring also in foxes, wolves, and humans. The parasite is transmitted by mosquitoes.Membrane Glycoproteins: Glycoproteins found on the membrane or surface of cells.Respiratory Distress Syndrome, Newborn: A condition of the newborn marked by DYSPNEA with CYANOSIS, heralded by such prodromal signs as dilatation of the alae nasi, expiratory grunt, and retraction of the suprasternal notch or costal margins, mostly frequently occurring in premature infants, children of diabetic mothers, and infants delivered by cesarean section, and sometimes with no apparent predisposing cause.Infant, Low Birth Weight: An infant having a birth weight of 2500 gm. (5.5 lb.) or less but INFANT, VERY LOW BIRTH WEIGHT is available for infants having a birth weight of 1500 grams (3.3 lb.) or less.Fibronectins: Glycoproteins found on the surfaces of cells, particularly in fibrillar structures. The proteins are lost or reduced when these cells undergo viral or chemical transformation. They are highly susceptible to proteolysis and are substrates for activated blood coagulation factor VIII. The forms present in plasma are called cold-insoluble globulins.Plastic Embedding: The infiltrating of histological specimens with plastics, including acrylic resins, epoxy resins and polyethylene glycol, for support of the tissues in preparation for sectioning with a microtome.Glomerular Filtration Rate: The volume of water filtered out of plasma through glomerular capillary walls into Bowman's capsules per unit of time. It is considered to be equivalent to INULIN clearance.Dirofilariasis: Infection with nematodes of the genus DIROFILARIA, usually in animals, especially dogs, but occasionally in man.Rabbits: The species Oryctolagus cuniculus, in the family Leporidae, order LAGOMORPHA. Rabbits are born in burrows, furless, and with eyes and ears closed. In contrast with HARES, rabbits have 22 chromosome pairs.Polyethyleneimine: Strongly cationic polymer that binds to certain proteins; used as a marker in immunology, to precipitate and purify enzymes and lipids. Synonyms: aziridine polymer; Epamine; Epomine; ethylenimine polymer; Montrek; PEI; Polymin(e).Cells, Cultured: Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others.Epithelial Cells: Cells that line the inner and outer surfaces of the body by forming cellular layers (EPITHELIUM) or masses. Epithelial cells lining the SKIN; the MOUTH; the NOSE; and the ANAL CANAL derive from ectoderm; those lining the RESPIRATORY SYSTEM and the DIGESTIVE SYSTEM derive from endoderm; others (CARDIOVASCULAR SYSTEM and LYMPHATIC SYSTEM) derive from mesoderm. Epithelial cells can be classified mainly by cell shape and function into squamous, glandular and transitional epithelial cells.Serum Albumin, Bovine: Serum albumin from cows, commonly used in in vitro biological studies. (From Stedman, 25th ed)HexosaminesImmune Sera: Serum that contains antibodies. It is obtained from an animal that has been immunized either by ANTIGEN injection or infection with microorganisms containing the antigen.Neuraminic AcidsKidney Cortex: The outer zone of the KIDNEY, beneath the capsule, consisting of KIDNEY GLOMERULUS; KIDNEY TUBULES, DISTAL; and KIDNEY TUBULES, PROXIMAL.Electrophoresis, Polyacrylamide Gel: Electrophoresis in which a polyacrylamide gel is used as the diffusion medium.Antigen-Antibody Reactions: The processes triggered by interactions of ANTIBODIES with their ANTIGENS.Erythrocyte Membrane: The semi-permeable outer structure of a red blood cell. It is known as a red cell 'ghost' after HEMOLYSIS.Membrane Fluidity: The motion of phospholipid molecules within the lipid bilayer, dependent on the classes of phospholipids present, their fatty acid composition and degree of unsaturation of the acyl chains, the cholesterol concentration, and temperature.Molecular Sequence Data: Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.Amino Acids: Organic compounds that generally contain an amino (-NH2) and a carboxyl (-COOH) group. Twenty alpha-amino acids are the subunits which are polymerized to form proteins.Molecular Weight: The sum of the weight of all the atoms in a molecule.Antibodies, Monoclonal: Antibodies produced by a single clone of cells.Antibodies, Antinuclear: Autoantibodies directed against various nuclear antigens including DNA, RNA, histones, acidic nuclear proteins, or complexes of these molecular elements. Antinuclear antibodies are found in systemic autoimmune diseases including systemic lupus erythematosus, Sjogren's syndrome, scleroderma, polymyositis, and mixed connective tissue disease.Mice, Inbred C57BLDiabetes Mellitus, Experimental: Diabetes mellitus induced experimentally by administration of various diabetogenic agents or by PANCREATECTOMY.Microscopy, Fluorescence: Microscopy of specimens stained with fluorescent dye (usually fluorescein isothiocyanate) or of naturally fluorescent materials, which emit light when exposed to ultraviolet or blue light. Immunofluorescence microscopy utilizes antibodies that are labeled with fluorescent dye.Fluorescent Antibody Technique, Indirect: A form of fluorescent antibody technique commonly used to detect serum antibodies and immune complexes in tissues and microorganisms in specimens from patients with infectious diseases. The technique involves formation of an antigen-antibody complex which is labeled with fluorescein-conjugated anti-immunoglobulin antibody. (From Bennington, Saunders Dictionary & Encyclopedia of Laboratory Medicine and Technology, 1984)Cell Adhesion: Adherence of cells to surfaces or to other cells.Glomerulonephritis, IGA: A chronic form of glomerulonephritis characterized by deposits of predominantly IMMUNOGLOBULIN A in the mesangial area (GLOMERULAR MESANGIUM). Deposits of COMPLEMENT C3 and IMMUNOGLOBULIN G are also often found. Clinical features may progress from asymptomatic HEMATURIA to END-STAGE KIDNEY DISEASE.Mice, Knockout: Strains of mice in which certain GENES of their GENOMES have been disrupted, or "knocked-out". To produce knockouts, using RECOMBINANT DNA technology, the normal DNA sequence of the gene being studied is altered to prevent synthesis of a normal gene product. Cloned cells in which this DNA alteration is successful are then injected into mouse EMBRYOS to produce chimeric mice. The chimeric mice are then bred to yield a strain in which all the cells of the mouse contain the disrupted gene. Knockout mice are used as EXPERIMENTAL ANIMAL MODELS for diseases (DISEASE MODELS, ANIMAL) and to clarify the functions of the genes.Cell Membrane Permeability: A quality of cell membranes which permits the passage of solvents and solutes into and out of cells.Staining and Labeling: The marking of biological material with a dye or other reagent for the purpose of identifying and quantitating components of tissues, cells or their extracts.Glycoproteins: Conjugated protein-carbohydrate compounds including mucins, mucoid, and amyloid glycoproteins.Infant, Very Low Birth Weight: An infant whose weight at birth is less than 1500 grams (3.3 lbs), regardless of gestational age.Cerebral Hemorrhage: Bleeding into one or both CEREBRAL HEMISPHERES including the BASAL GANGLIA and the CEREBRAL CORTEX. It is often associated with HYPERTENSION and CRANIOCEREBRAL TRAUMA.Lung Diseases: Pathological processes involving any part of the LUNG.Rats, Inbred BNAutoimmune Diseases: Disorders that are characterized by the production of antibodies that react with host tissues or immune effector cells that are autoreactive to endogenous peptides.Sclerosis: A pathological process consisting of hardening or fibrosis of an anatomical structure, often a vessel or a nerve.Complement System Proteins: Serum glycoproteins participating in the host defense mechanism of COMPLEMENT ACTIVATION that creates the COMPLEMENT MEMBRANE ATTACK COMPLEX. Included are glycoproteins in the various pathways of complement activation (CLASSICAL COMPLEMENT PATHWAY; ALTERNATIVE COMPLEMENT PATHWAY; and LECTIN COMPLEMENT PATHWAY).Histocytochemistry: Study of intracellular distribution of chemicals, reaction sites, enzymes, etc., by means of staining reactions, radioactive isotope uptake, selective metal distribution in electron microscopy, or other methods.Mutation: Any detectable and heritable change in the genetic material that causes a change in the GENOTYPE and which is transmitted to daughter cells and to succeeding generations.Carbohydrates: The largest class of organic compounds, including STARCH; GLYCOGEN; CELLULOSE; POLYSACCHARIDES; and simple MONOSACCHARIDES. Carbohydrates are composed of carbon, hydrogen, and oxygen in a ratio of Cn(H2O)n.Antibody Specificity: The property of antibodies which enables them to react with some ANTIGENIC DETERMINANTS and not with others. Specificity is dependent on chemical composition, physical forces, and molecular structure at the binding site.Time Factors: Elements of limited time intervals, contributing to particular results or situations.Enzyme-Linked Immunosorbent Assay: An immunoassay utilizing an antibody labeled with an enzyme marker such as horseradish peroxidase. While either the enzyme or the antibody is bound to an immunosorbent substrate, they both retain their biologic activity; the change in enzyme activity as a result of the enzyme-antibody-antigen reaction is proportional to the concentration of the antigen and can be measured spectrophotometrically or with the naked eye. Many variations of the method have been developed.Models, Biological: Theoretical representations that simulate the behavior or activity of biological processes or diseases. For disease models in living animals, DISEASE MODELS, ANIMAL is available. Biological models include the use of mathematical equations, computers, and other electronic equipment.Polysaccharide-Lyases: A group of carbon-oxygen lyases. These enzymes catalyze the breakage of a carbon-oxygen bond in polysaccharides leading to an unsaturated product and the elimination of an alcohol. EC 4.2.2.RNA, Messenger: RNA sequences that serve as templates for protein synthesis. Bacterial mRNAs are generally primary transcripts in that they do not require post-transcriptional processing. Eukaryotic mRNA is synthesized in the nucleus and must be exported to the cytoplasm for translation. Most eukaryotic mRNAs have a sequence of polyadenylic acid at the 3' end, referred to as the poly(A) tail. The function of this tail is not known for certain, but it may play a role in the export of mature mRNA from the nucleus as well as in helping stabilize some mRNA molecules by retarding their degradation in the cytoplasm.Amino Acid Sequence: The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining PROTEIN CONFORMATION.

Goodpasture antigen: expression of the full-length alpha3(IV) chain of collagen IV and localization of epitopes exclusively to the noncollagenous domain. (1/267)

BACKGROUND: Tissue injury in Goodpasture (GP) syndrome (rapidly progressive glomerular nephritis and pulmonary hemorrhage) is mediated by antibasement membrane antibodies that are targeted to the alpha3(IV) chain of type IV collagen, one of five alpha(IV) chains that occur in the glomerular basement membrane. GP antibodies are known to bind epitopes within the carboxyl terminal noncollagenous domain (NC1) of the alpha3(IV) chain, termed the GP autoantigen. Whether epitopes also exist in the 1400-residue collagenous domain is unknown because studies to date have focused solely on the NC1 domain. A knowledge of GP epitopes is important for the understanding of the etiology and pathogenesis of the disease and for the development of therapeutic strategies. METHODS: A cDNA construct was prepared for the full-length human alpha3(IV) chain. The construct was stably transfected into human embryonic kidney 293 cells. The purified full-length r-alpha3(IV) chain was characterized by electrophoresis and electron microscopy. The capacity of this chain for binding of GP antibodies from five patients was compared with that of the human r-alpha3(IV)NC1 domain by competitive enzyme-linked immunosorbent assay. RESULTS: The r-alpha3(IV) chain was secreted from 293 cells as a single polypeptide chain that did not spontaneously undergo assembly into a triple-helical molecule. An analysis of GP-antibody binding to the full-length r-alpha3(IV) chain showed binding exclusively to the globular NC1 domain. CONCLUSION: The full-length human alpha3(IV) chain possesses the capacity to bind GP autoantibodies. The epitope(s) is found exclusively on the nontriple-helical NC1 domain of the alpha3(IV) chain, indicating the presence of specific immunogenic properties. The alpha3(IV) chain alone does not spontaneously undergo assembly into a triple-helical homotrimeric molecule, suggesting that coassembly with either the alpha4(IV) and/or the alpha5(IV) chain may be required for triple-helix formation.  (+info)

Identification of a clinically relevant immunodominant region of collagen IV in Goodpasture disease. (2/267)

BACKGROUND: The characteristic feature of Goodpasture disease is the occurrence of an autoantibody response to the noncollagenous domain of the alpha3 chain of type IV collagen [alpha3(IV)NC1] in the alveolar and glomerular basement membrane. These antibodies are associated with the development of a rapidly progressive glomerulonephritis, with or without lung hemorrhage, whereas autoantibodies specific for the other alpha chains of the heterotrimeric type IV collagen probably do not cause disease. In this study, we have investigated whether differences in fine specificity of autoimmune recognition of the alpha3(IV)NC1 correlate with clinical outcome. METHODS: For mapping of antibody binding to type IV collagen, chimeric collagen constructs were generated in which parts of the alpha3(IV)NC1 domain were replaced by the corresponding sequences of homologous nonreactive alpha1(IV). The different recombinant collagen chimeras allowed the analysis of antibody specificities in 77 sera from well-documented patients. RESULTS: One construct that harbors the aminoterminal third of the alpha3(IV)NC1 was recognized by all sera, indicating that it represents the dominant target of the B-cell response in Goodpasture disease. Seventy percent of the samples recognized other parts of the molecule as well. However, only reactivity to the N-terminus of the alpha3(IV)NC1 correlated with prognosis, that is, kidney survival after six months of follow-up. CONCLUSION: The results indicate the crucial importance of antibody recognition of this particular domain for the pathogenesis of Goodpasture disease, thereby opening new avenues for the development of better diagnostic and therapeutic procedures.  (+info)

Angiotensin II plays a pathogenic role in immune-mediated renal injury in mice. (3/267)

Several lines of evidence show the importance of angiotensin II (AII) in renal injuries, especially when hemodynamic abnormalities are involved. To elucidate the role of AII in immune-mediated renal injury, we studied anti-glomerular basement membrane (GBM) nephritis in AII type 1a receptor (AT1a)-deficient homozygous (AT1a-/-) and wild-type (AT1a+/+) mice. A transient activation of the renin-angiotensin system (RAS) was observed in both groups of mice at around day 1. A renal expression of monocyte chemoattractant protein-1 (MCP-1) was transiently induced at six hours in both groups, which was then downregulated at day 1. In the AT1a+/+ mice, after RAS activation, the glomerular expression of MCP-1 was exacerbated at days 7 and 14. Thereafter, severe proteinuria developed, and the renal expressions of transforming growth factor-beta1 (TGF-beta1) and collagen type I increased, resulting in severe glomerulosclerosis and interstitial fibrosis. In contrast, glomerular expression of MCP-1, proteinuria, and tissue damage were markedly ameliorated in the AT1a-/- mice. Because this amelioration is likely due to the lack of AT1a, we can conclude that AII action, mediated by AT1a, plays a pathogenic role in anti-GBM nephritis, in which AII may contribute to the exacerbation of glomerular MCP-1 expression. These results suggest the involvement of AII in immune-mediated renal injuries.  (+info)

P-selectin deficiency exacerbates experimental glomerulonephritis: a protective role for endothelial P-selectin in inflammation. (4/267)

P-selectin is a leukocyte adhesion receptor present in endothelial cells and platelets. We examined the role of P-selectin in the autologous phase of an accelerated model of anti-glomerular basement membrane (GBM) glomerulonephritis using P-selectin-deficient mice and chimeric mice expressing P-selectin only in platelets or endothelial cells. P-selectin-deficient mice exhibited more severe glomerular damage with increased interstitial mononuclear leukocytic infiltrates, and had significantly increased proteinuria and mortality when compared to wild-type mice. P-selectin on the endothelium was predominantly responsible for protection from the exacerbated disease, because chimeric mice with endothelial P-selectin, and not mice with platelet P-selectin, showed glomerular injury similar to that in wild-type animals. Levels of soluble circulating P-selectin were increased in nephritic wild-type mice and in chimeric mice with endothelial P-selectin, but not platelet P-selectin. Levels of soluble P-selectin, which has been shown to be anti-inflammatory in vitro, were inversely associated with the severity of disease. P-selectin was not expressed in the endothelium of the glomerulus or interstitium. Thus, the protective effect in wild-type mice may be accounted for, in part by soluble P-selectin shed by non-renal endothelial cells, although other endothelial P-selectin-dependent mechanisms cannot be ruled out.  (+info)

IL-1 up-regulates osteopontin expression in experimental crescentic glomerulonephritis in the rat. (5/267)

Osteopontin (OPN) is a macrophage chemotactic and adhesion molecule that acts to promote macrophage infiltration in rat anti-glomerular basement membrane (GBM) glomerulonephritis. The present study investigated the role of interleukin-1 (IL-1) in the up-regulation of renal OPN expression in this disease model. Accelerated anti-GBM glomerulonephritis was induced in groups of six rats. Animals were treated by a constant infusion of the IL-1 receptor antagonist or saline (control) over days -1 to 14 (induction phase) or days 7 to 21 (established disease). In normal rat kidney, OPN was expressed in a few tubules (<5%) and absent from glomeruli. During the development of rat anti-GBM disease (days 7 to 21), there was substantial up-regulation of OPN mRNA and protein expression in glomeruli (>5 cells per glomerular cross-section) and tubular epithelial cells (50-75% OPN-positive). Up-regulation of OPN expression was associated with macrophage accumulation within the kidney, severe proteinuria, loss of renal function, and severe histological damage including glomerular crescentic formation and tubulointerstitial fibrosis. In contrast, IL-1 receptor antagonist treatment of either the induction phase of disease or established disease significantly reduced OPN mRNA and protein expression in glomeruli (/75-85%, P < 0.001) and tubules (/45-60%, P < 0.001). The reduction in OPN expression was associated with significant inhibition of macrophage accumulation and progressive renal injury. In vitro, the addition of IL-1 to the normal rat tubular epithelial cell line NRK52E up-regulated OPN mRNA and protein levels, an effect that was dose-dependent and inhibited by the addition of IL-1 receptor antagonist, thus demonstrating that IL-1 can act directly to up-regulate renal OPN expression. In conclusion, this study provides in vivo and in vitro evidence that IL-1 up-regulates OPN expression in experimental kidney disease and support for the argument that inhibition of OPN expression is one mechanism by which IL-1 receptor antagonist treatment suppresses macrophage-mediated renal injury.  (+info)

Development of scarring and renal failure in a rat model of crescentic glomerulonephritis. (6/267)

BACKGROUND: The aim of this study was to develop and characterize a rat model of crescentic glomerulonephritis which progresses to glomerulosclerosis and renal failure. METHODS: Glomerulonephritis was induced in Wistar Kyoto rats by a single injection of rabbit anti-glomerular basement membrane antiserum. Albuminuria and serum creatinine were monitored. Kidneys were examined, from 2.5 h to 44 days, using light-microscopy and immunohistochemistry. To characterize the glomerular inflammatory infiltrate, glomeruli were digested to single cells and analysed by fluorescence-activated cell sorter (FACS) and by immunohistochemistry on cytospins. RESULTS: Rats developed albuminuria by 4 days and increased serum creatinine by day 18. Histology showed glomerular fibrinoid necrosis by day 4 and cellular crescents in a mean of 63% of glomeruli by day 11. By 6 weeks, rats had developed renal failure (mean creatinine >300 micromol/l) with 94% of the glomeruli showing glomerulosclerosis. The kidneys were also affected by severe interstitial nephritis and tubular loss. The glomeruli were infiltrated by monocytes/ macrophages (ED1+) and CD8+ (OX8+) cells. FACS analysis showed that CD8+ cells did not express T-cell markers (CD3, TCRalphabeta or TCRgammadelta) or the NK-cell marker (NKR-P1). FACS analysis of peripheral blood mononuclear cells demonstrated a population of monocytes reactive with OX8, and double-labelling of cytospin preparations of glomerular digests showed that a proportion of the CD8+ cells were a subset of ED1+ monocyte/macrophages. CONCLUSIONS: We have characterized a reproducible model of crescentic glomerulonephritis which rapidly progresses to chronic renal failure with glomerulosclerosis and tubulo-interstitial scarring. This model will be useful for testing new therapeutic approaches in crescentic glomerulonephritis.  (+info)

Increased susceptibility to immunologically mediated glomerulonephritis in IFN-gamma-deficient mice. (7/267)

It is postulated that IFN-gamma confers susceptibility to immunologically mediated tissue injury. To test this hypothesis, we compared the intensity of accelerated anti-glomerular basement membrane glomerulonephritis between wild-type (IFN-gamma+/+) and IFN-gamma gene knockout (IFN-gamma-/-) mice. This disease model is initiated by binding of heterologous (sheep) anti-glomerular basement membrane Abs to the glomeruli of mice preimmunized with sheep IgG. The secondary cellular and humoral immune responses to the planted Ag then lead to albuminuria and glomerular pathology. We found that IFN-gamma-/- mice or IFN-gamma+/+ mice injected with IFN-gamma-neutralizing Ab develop worse albuminuria and glomerular pathology than IFN-gamma+/+ mice. The humoral response to sheep IgG (serum mouse anti-sheep IgG titers and intraglomerular mouse IgG deposits) was comparable in the IFN-gamma+/+ and IFN-gamma-/- groups. In contrast, IFN-gamma-/- mice mounted a stronger cellular immune response (cutaneous delayed-type hypersensitivity reaction) to sheep IgG than IFN-gamma+/+ mice. These findings provide evidence that endogenous IFN-gamma has a protective role in immunologically mediated glomerulonephritis initiated by foreign Ags.  (+info)

Goodpasture disease. Characterization of a single conformational epitope as the target of pathogenic autoantibodies. (8/267)

Goodpasture disease is a prototype autoimmune disease characterized by the formation of autoantibodies against the heterotrimeric basement membrane collagen type IV, which causes a rapidly progressive glomerulonephritis. The pathogenic antibody response is directed to the non-collagenous (NC1) domain of the alpha3 chain of type IV collagen (alpha3(IV)NC1), but not to the homologous region of the alpha1(IV)NC1. To identify the conformation-dependent immunodominant epitope on the alpha3(IV)NC1, a variety of recombinant NC1 domains were constructed by replacing single residues of alpha3(IV) with the corresponding amino acids from the nonreactive alpha1(IV) chain. Replacement mutations were identified that completely destroyed the Goodpasture epitope in the alpha3(IV) chain. Based on the identification of these critical positions, the epitope was finally reconstructed within the frame of the alpha1(IV) chain. The substitution of nine discontinuous positions in the alpha1(IV)NC1 with amino acid residues from the alpha3 chain resulted in a recombinant construct that was recognized by all patients' sera (n = 20) but by none of the sera from healthy controls (n = 10). This provides, for the first time, the molecular characterization of a single immunodominant conformational epitope recognized by pathogenic autoantibodies in a human autoimmune disease, representing the basis for the development of new epitope-specific strategies in the treatment of Goodpasture disease.  (+info)

*Perlecan

Decreased perlecan in the glomerular basement membrane has a central role in the development of diabetic albuminuria. Perlecan ... It seems that there may be some overlap in diseases stemming from loss of heparan sulfate proteoglycan expression and loss of ... The theory put forward in this study is that perlecan plays an anti-proliferative role for VSMCs once a certain developmental ... which requires a pre-formed basement membrane. Collagen gels have promoted formation of a complete basement membrane by corneal ...

*Alport syndrome

Electron microscopy shows a characteristic sequence of changes from thinning of the glomerular basement membrane (GBM), ... "EdRen - Edinburgh Royal Infirmary Renal Unit - Alport anti-GBM disease". www.edren.org. Retrieved 2016-02-17. Tryggvason K, ... Basement membranes are thin, sheet-like structures that separate and support cells in many tissues. Type IV collagen '112' type ... delivering it to the podocytes in the glomerulus that normally produce the type IV collagen in the glomerular basement membrane ...

*Glomerular basement membrane

... "anti-glomerular basement membrane disease". Capillaries become inflamed as a result of damage to the basement membrane by ... "Basement Membrane" JCI - New articles published glomerular basement membrane at the US National Library of Medicine Medical ... The glomerular basement membrane (GBM) of the kidney is the basal lamina layer of the glomerulus. The glomerular endothelial ... syndrome is a change in the structure of the glomerular filtration mechanism usually in the glomerular basement membrane. Some ...

*List of MeSH codes (C12)

... anti-glomerular basement membrane disease MeSH C12.777.419.570.363.304.300 --- goodpasture syndrome MeSH C12.777.419.570. ... hartnup disease MeSH C12.777.419.815.279 --- bartter syndrome MeSH C12.777.419.815.368 --- cystinosis MeSH C12.777.419.815. ... reiter disease MeSH C12.777.809.186 --- bladder calculi MeSH C12.777.809.503 --- kidney calculi MeSH C12.777.809.851 --- ... polycystic kidney diseases MeSH C12.777.419.403.875.500 --- polycystic kidney, autosomal dominant MeSH C12.777.419.403.875.510 ...

*Anti-glomerular basement membrane antibody

Some sources consider "anti-GBM disease" and "Goodpasture disease" to be synonymous terms describing histological presentation ... glomerular basement membrane ped/117 at eMedicine antiglomerular basement membrane antibody at the US National Library of ... Anti-glomerular basement membrane antibody (anti-GBM Ab) is an antibody which is found in Goodpasture's syndrome but not found ...

*Rapidly progressive glomerulonephritis

The presence of anti-Glomerular basement membrane (GBM) antibodies suggests type I RPGN; antinuclear antibodies (ANA) may ... The majority of type I disease, however, features anti-GBM antibodies alone; these cases are considered idiopathic. RPGN caused ... type I RPGN is characterized by the presence of autoantibodies directed against the glomerular basement membrane (GBM). It is ... Thus any immune complex disease that involves the glomerulus may progress to RPGN if severe enough. These diseases include ...

*Anti-nuclear antibody

Some anti-dsDNA antibodies are cross reactive with other antigens found on the glomerular basement membrane (GBM) of the kidney ... anti-Ro and anti-La antibodies correlate with early onset, increased disease duration, parotid gland enlargement, disease ... anti-La antibodies, anti-Sm antibodies, anti-nRNP antibodies, anti-Scl-70 antibodies, anti-dsDNA antibodies, anti-histone ... anti-Sm and anti-RNP antibodies were discovered in 1966 and 1971, respectively. In the 1970s, the anti-Ro/anti-SS-A and anti-La ...

*Anakinra

Inflammatory reactions caused by anti-dsDNA complexes with extracellular DNA in the glomerular basement membrane cause ... "Anti-Interleukin-1 Agents in Adult Onset Still's Disease". Hindawi. 2012-02-07. Retrieved 2012-10-13. "New type of drug helpful ... Under continued therapy anakinra has been shown to slow progression of disease over a period of at least 12 month evidenced by ... had an absence of clinical improvement of symptoms or inadequate response in therapy with one or more disease-modifying anti- ...

*Anti-neutrophil cytoplasmic antibody

Sinclair, D; Stevens, JM (Sep 2007). "Role of antineutrophil cytoplasmic antibodies and glomerular basement membrane antibodies ... In addition, in patients with active disease, treated with Rituximab, an anti-CD20 antibody which remove circulating B-cells, ... Anti-neutrophil cytoplasmic antibodies (ANCAs) are a group of autoantibodies, mainly of the IgG type, against antigens in the ... 1990). "Anti-neutrophil cytoplasmic autoantibodies induce neutrophils to degranulate and produce oxygen radicals in vitro". ...

*Glomerulonephritis

Thin basement membrane disease is an autosomal dominant inherited disease characterized by thin glomerular basement membranes ... Anti-GBM, Complement levels, Antinuclear antibodies Biopsy of the kidney Renal ultrasonography is useful for prognostic ... MGN is characterized by a thickened glomerular basement membrane without a hyperproliferation of the glomerular cells. ... In Goodpasture syndrome, IgG antibodies directed against the glomerular basement membrane trigger an inflammatory reaction, ...

*Anti-dsDNA antibodies

... of immune complexes that arise by indirect binding to DNA or nucleosomes that are adhered to the glomerular basement membrane ( ... Higher titres of anti-dsDNA antibodies are more suggestive of SLE and lower titres can be found in people without the disease. ... The levels of circulating anti-dsDNA antibodies fluctuate with disease activity in SLE. Increases in titres of the antibodies ... A single array could consist of hundreds of autoantigens for screening of multiple autoimmune diseases simultaneously. If anti- ...

*Membranous glomerulonephritis

As the disease progresses, the deposits will eventually be cleared, leaving cavities in the basement membrane. These cavities ... The immune complexes are formed by binding of antibodies to antigens in the glomerular basement membrane. The antigens may be ... or anti-proteinuric therapies. A large part of this difficulty is due to a lack of ability to predict which people will ... On electron microscopy, subepithelial deposits that nestle against the glomerular basement membrane seems to be the cause of ...

*Systemic lupus erythematosus

This finding is due to immune complex deposition along the glomerular basement membrane, leading to a typical granular ... which also appears in systemic sclerosis and mixed connective tissue disease), SS-A (or anti-Ro) and SS-B (or anti-La; both of ... The anti-dsDNA antibody titers also tend to reflect disease activity, although not in all cases. Other ANA that may occur in ... In the presence of autoreactive T cells, a chronic autoimmune disease may be the consequence. Anti-nRNP autoantibodies to nRNP ...

*Tumstatin

Since tumstatin is cleaved by MMP from the collagen in the basement membrane, it has been found that there are much lower ... tumstatin may have implications in treating the disease. It was found that VEGF is one of the mediators of glomerular ... Wang Shu-jing; Liu Xing-han; Ji Yu-bin; Chen Ning (6-8 July 2007). "The Effect of Tumstatin Anti-tumor Peptide on Proliferation ... Type-IV collagen is present in the basement membrane within normal lungs, and this is reduced in asthmatic patients. There are ...

*Ernest William Goodpasture

... as well as glomerular-capillary, basement membranes. After leaving Harvard in 1921, Goodpasture worked at the University of the ... Valentini, Rudolph P. Pediatric Anti-GBM Disease (Goodpasture Syndrome). Accessed 8-28-2009. Harris Riley, Jr., "Ernest William ... ISBN 1-57736-251-9. Salama, A D; Levy J B; Lightstone L; Pusey C D (September 2001). "Goodpasture's disease". Lancet. 358 (9285 ... This technique made possible the development and production of a wide range of vaccines against viral diseases. Goodpasture was ...

*Margo Cohen

As a visiting scientist in England, she examined effects of diabetes on basement membranes. In Israel, Cohen discovered the ... Kennedy, Laurence; Pilar Solano, Maria; Meneghini, Luigi; Lo, Margaret; Cohen, Margo P. (2010). "Anti-glycation and anti- ... Its first FDA-approved diagnostic product was Albuwell, a test that detects diabetic kidney disease, followed by other ... October 8, 2001). "Inhibiting albumin glycation in vivo ameliorates glomerular overexpression of TGF-bold beta1". Kidney ...

*PODXL

... epithelial cells with interdigitating foot processes covering the outer aspect of the glomerular basement membrane. Other ... "Overexpression of the anti-adhesin podocalyxin is an independent predictor of breast cancer progression". Cancer Research. 64 ( ... "Expression of podocyte-associated molecules in acquired human kidney diseases". Journal of the American Society of Nephrology. ... Takeda T, McQuistan T, Orlando RA, Farquhar MG (Jul 2001). "Loss of glomerular foot processes is associated with uncoupling of ...
Anti-glomerular basement membrane disease is a rare autoimmune disorder characterized by pulmonary hemorrhage, crescentic glomerulonephritis and the presence of circulating anti-glomerular basement membrane antibodies. The simultaneous occurrence of both anti-glomerular basement membrane disease and membranous nephropathy is rare. A 59-year-old Hispanic man presented with acute onset of nausea and vomiting and was found to have renal insufficiency. Work-up included a kidney biopsy, which revealed anti-glomerular basement membrane disease with underlying membranous nephropathy. He was treated with emergent hemodialysis, intravenous corticosteroids, plasmapheresis, and cyclophosphamide without improvement in his renal function. Simultaneous anti-glomerular basement membrane disease and membranous nephropathy is very rare. There have been 16 previous case reports in the English language literature that have been associated with a high mortality and morbidity, and a very high rate of renal failure resulting
AIM Cases with anti-glomerular basement membrane (GBM) disease have been reported with linear deposit of immunoglobulin G (IgG) along GBM, but have undetectable anti-GBM antibodies in circulation by enzyme linked immunosorbent assays (ELISA). We speculated that the structure of the antigens recognized by these antibodies may contribute to the negative results of ELISA. METHODS Sera from four patients were collected, with typical linear deposit of IgG along GBM but no anti-GBM reactivity by commercial ELISA kits. Circulating anti-GBM antibodies were detected by indirect immunofluorescence. Antigen specificity and its conformational structure was investigated by western-blot analysis, using recombinant human α1-α5(IV)NC1 and chimeric proteins E(A) and E(B) as antigens. RESULTS The presence of circulating anti-GBM antibodies were confirmed by indirect immunofluorescence with linear deposit of IgG towards cryptic epitopes along GBM on normal kidney sections. These antibodies did not recognize
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PubMed comprises more than 30 million citations for biomedical literature from MEDLINE, life science journals, and online books. Citations may include links to full-text content from PubMed Central and publisher web sites.
Goodpasture syndrome (GPS) is a rare autoimmune disease in which antibodies attack the basement membrane in lungs and kidneys, leading to bleeding from the lungs and kidney failure. It is thought to attack the alpha-3 subunit of type IV collagen, which has therefore been referred to as Goodpastures antigen. Goodpasture syndrome may quickly result in permanent lung and kidney damage, often leading to death. It is treated with immunosuppressant drugs such as corticosteroids and cyclophosphamide, and with plasmapheresis, in which the antibodies are removed from the blood. The disease was first described by an American pathologist Ernest Goodpasture of Vanderbilt University in 1919 and was later named in his honor. Play media The antiglomerular basement membrane (GBM) antibodies primarily attack the kidneys and lungs, although, generalized symptoms like malaise, weight loss, fatigue, fever, and chills are also common, as are joint aches and pains. 60 to 80% of those with the condition experience ...
Goodpastures syndrome is a pulmonary-renal syndrome, which is a group of acute illnesses involving the kidneys and lungs. Goodpasture syndrome includes all of the following conditions:. Glomerulonephritis - inflammation of the glomeruli, which are tiny clusters of looping blood vessels in the kidneys that help filter wastes and extra water from the blood.. The presence of anti-glomerular basement membrane (GBM) antibodies; the GBM is part of the glomeruli and is composed of collagen and other proteins.. Bleeding in the lungs. ...
Your bodies have immune system and this system produces antibodies which are nothing other than proteins and they help to fight infections. However, when you are infected with Goodpastures Syndrome your body starts making antibodies that attack and damage your body. They mainly target the lining of your lungs and kidney and there is no particular reason why your antibodies begin to attack your own lungs and kidneys.. However there are some factors that are believed to trigger the disease. When you are exposed to viral lung infections, or you smoke or you are breathing in vapors from organic solvents, you stand a chance of being affected by the disease.. Caucasian people (mostly men) between ages 20 and 30 or above 60 suffer from this disease. If you have suffered from lupus erythematosus or Wegeners granulomatosis then your chance of contracting Goodpastures Syndrome is considerably more.. ...
Goodpastures, or anti-glomerular basement membrane (anti-GBM), disease is an uncommon, yet usually severe human autoimmune disorder characterised primarily by rapidly progressive glomerulonephritis (RPGN) and lung haemorrhage. The disease results from a sustained autoimmune response in which pathogenic autoantibodies are directed against the Goodpasture antigen [3(IV)NCI], a specific component, of certain basement membranes. Antigen presenting cells (APC) play a leading part in determining an individuals immune responsiveness by controlling how antigens will be displayed to CD4+ T-cells. APC are responsible for the internalisation, processing and presentation of extracellular antigens in association with MHC class II molecules at their surface. Further, the striking association between particular autoimmune diseases and HLA type suggests that HLA determined differences in presentation of self antigens may also influence the susceptibility to autoimmunity. The primary purpose of this project ...
... is a rare autoimmune disease that affects the lungs and kidneys. Normally, the immune system makes antibodies to fight off germs. With Goodpasture syndrome, however, the immune system mistakenly makes antibodies that attack the lungs and kidneys. This condition can quickly progress to glomerulonephritis and kidney failure.
... is a rare autoimmune disease that affects the lungs and kidneys. Normally, the immune system makes antibodies to fight off germs. With Goodpasture syndrome, however, the immune system mistakenly makes antibodies that attack the lungs and kidneys. This condition can quickly progress to glomerulonephritis and kidney failure.
Goodpasture disease is defined by the presence of autoantibodies to the alpha-3 chain of type IV collagen. It presents with rapidly progressive renal dysfunction often combined with lung hemorrhage. Simultaneous hemoptysis and renal failure (the pulmonary renal syndrome) has many causes, but wher...
Two patients with Goodpastures syndrome are reported. One showed an apparently spontaneous remission and has survived in good health for over five years since the onset of his illness; he was treated for part of this time with steroids and chlorambucil. The second patient failed to respond to steroids but appeared to improve rapidly from a moribund state on administration of azathioprine; he rema
Background: Renal injury of anti-glomerular basement membrane (GBM) disease is defined by the linear deposition of IgG along GBM and rapidly progressive glomerulonephritis. To date, the distribution of anti-GBM IgG subclasses on renal tissue is still unclear. In the current study, we investigated the deposition of the four IgG subclasses using immunohistochemistry in the renal biopsy specimens from 46 patients with anti-GBM disease.. Results: All four IgG subclasses can be detected within the GBM. Anti-GBM IgG3 was detected in all patients (100%), with 39 (84.8%) patients presenting with weak segmental staining and 7 (15.2%) patients with strong linear deposition. Anti-GBM IgG2 was detected in 22 (47.8%) patients, with 20 (90.9%) patients having weak segmental deposition and 2 (9.1%) patients presenting strong linear staining. Anti-GBM IgG1 and IgG4 were detected in 9 (19.6%) and 7 (15.2%) patients, respectively. IgG deposition along tubular basement membrane (TBM) was also detected in 31 ...
in Kidney International (1987), 31(1), 32-40. A proliferative glomerulonephritis was induced in rats pre-immunized with rabbit IgG by injecting intravenously a sub-nephrotoxic dose of rabbit anti-glomerular basement membrane (GBM) IgG (A rats). Most ... [more ▼]. A proliferative glomerulonephritis was induced in rats pre-immunized with rabbit IgG by injecting intravenously a sub-nephrotoxic dose of rabbit anti-glomerular basement membrane (GBM) IgG (A rats). Most rats (80%) developed a severe proteinuria (greater than 100 mg/24 hr) within two to five days after the injection of anti-GBM IgG. At the same time, microscopic examination of the kidneys revealed a glomerular infiltration by mononuclear phagocytes and a prominent decrease in the intensity of the colloidal iron reaction in glomeruli. A non-proliferative glomerular disease was induced in another group of rats (B rats) by intraperitoneal administration of aminonucleoside of puromycin. A marked proteinuria (greater than 100 mg/24 hr) ...
Goodpasture syndrome (also known as anti-GBM disease) is characterized by the presence of auto-antibodies to a component of lung and kidney tissue. It is an exceptionally rare disease, which impacts approximately 1 in every million people, though it is more common in white European and Asian populations. Goodpasture syndrome most typically presents as a combinations of lung and kidney problems although it can present less frequently as an isolated issue with either organ system. A patient such as ours, who presents with both coughing and urinating blood (known as hemoptysis and hematuria respectively) should at least prompt the consideration of Goodpasture syndrome in the differential diagnosis. Other symptoms of lung or kidney disease include chest pain with cough, high blood pressure, and swelling of the legs, all of which our patient had on initial presentation. Other nonspecific findings include fever, rash, fatigue, and an enlarged liver and spleen, all of which occur in much more common ...
Anti-GBM antibody disease is one of the three major forms of rapidly progressive (or crescentic) glomerulonephritis. Although some patients present with relatively mild renal insufficiency, this disorder is typically associated with severe renal inju
John W. Stirling and Alan Curry. 1.1 The Role of Transmission Electron Microscopy (TEM) in Renal Diagnostics 1. 1.2 Ultrastructural Evaluation and Interpretation 2. 1.3 The Normal Glomerulus 3. 1.4 Ultrastructural Diagnostic Features 5. 1.5 Granular and Amorphous Deposits 6. 1.6 Organised Immune-Related Fibrils and Tubules 7. 1.7 Nonspecific Fibrils 11. 1.8 General and Nonspecific Inclusions and Deposits 11. 1.9 Fibrin 12. 1.10 Tubuloreticular Bodies (Tubuloreticular Inclusions) 12. 1.11 The Glomerular Basement Membrane 13. 1.12 The Mesangial Matrix 14. 1.13 Cellular Components of the Glomerulus 14. 1.14 Mesangial Cells 16. 1.15 The Capillary Lumen 16. 1.16 The Ultrastructural Pathology of the Major Glomerular Diseases 16. 1.17 Focal Segmental Glomerulosclerosis 17. 1.18 Pauci-Immune Glomerulonephritis (ANCA-Associated Glomerulonephritis) 18. 1.19 Anti-GBM Glomerulonephritis (Goodpasture Syndrome) 19. 1.20 Diseases with Structural GBM Changes 19. 1.21 Thin Basement Membrane Disease 21. 1.22 ...
Goodpastures disease is a fulminant rapidly progressive disease characterized by autoantibodies to the alpha-3 chain of type IV collagen (Goodpastures antigen). It can ..
Anti-glomerular basement membrane (GBM) disease is characterized by autoantibodies directed against the anti-GBM antigen, which is part of the non-collagenous domain of t..
While membranous nephropathy (MN) is one of the most common forms of nephrotic syndrome in adults, it is rarely associated with the pathologic finding of crescents on kidney biopsy. Most reported cases are in the context of concomitant anti-neutrophil cytoplasmic antibody (ANCA) or anti-glomerular basement membrane (anti-GBM) antibody disease, or were documented prior to the…
Hemoptysis ranging from blood-streaked sputum to massive hemorrhage is commonly the presenting feature. Patients may complain of dyspnea and cough. Pulmonary hemorrhage may be associated with severe hypoxemia and death. Intubation, assisted ventilation, and hemodialysis are often required in the acute phase. Renal function can range from normal to severe insufficiency, and the deterioration in renal function can occur rapidly. Some proteinuria is common, but nephrotic syndrome is rare. Hypertension is an unusual finding. Renal ultrasonography is usually normal. Pulmonary hemorrhage is often responsive to pulse ...
Analgesic nephropathy:. Analgesic nephropathy is a chronic kidney disease that gradually leads to end-stage renal disease and the need for permanent dialysis or a kidney transplant.. Diabetic nephropathy:. Nephropathy is the deterioration of the kidneys. Th final stage of nephropathy is called end-stage renal disease, or ESRD.. End Stage Renal Disease (ESRD):. Renal failure refers to temporary or permanent damage to the kidneys that results in loss of normal kidney function.. Glomerulonephritis: Glomerulonephritis is a type of glomerular kidney disease in which the kidneys filters become inflamed and scarred, and slowly lose their ability to remove wastes and excess fluid from the blood to make urine.. Goodpasture syndrome:. Goodpasture syndrome is a rare, autoimmune disease that can affect the lungs and kidneys.. Hematuria (blood in the urine):. Hematuria is the presence of red blood cells (RBCs) in the urine.. Hemolytic uremic syndrome:. Hemolytic uremic syndrome is a rare condition that ...
The main goal is to remove the harmful antibodies from the blood. A treatment called plasmapheresis removes whole blood from the body and replaces the plasma with fluid, protein, or donated plasma. Removing harmful antibodies may reduce inflammation in the kidneys and lungs.. Corticosteroid medications (such as prednisone) and other drugs that suppress or quiet the immune system may be used.. Controlling blood pressure is the most important way to delay kidney damage. You may get medicines to control high blood pressure, such as angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs).. You may be told to limit salt and fluids to control swelling. A low to moderate protein diet may be recommended in some cases.. You should be closely watched for signs of kidney failure. If kidney failure becomes severe, you may need ...
Learn about the causes, symptoms, diagnosis & treatment of Diffuse Alveolar Hemorrhage and Pulmonary-Renal Syndrome from the Professional Version of the Merck Manuals.
Dr. Bellot responded: Immunosuppression. Since the condition is produced by an abnormal immune response, the treatment is to reduce production of the |a href="/topics/antibody" track_data="{
View the Goodpasture surname, family crest and coat of arms. Discover the Goodpasture family history for the Dutch Origin. What is the origin of the name Goodpasture?
Radeke HH, Janssen-Graalfs I, Sowa EN, Chouchakova N, Skokowa J, Löscher F, Schmidt RE, Heeringa P, Gessner JE: Opposite regulation of type II and III receptors for immunoglobulin G in mouse glomerular mesangial cells and in the induction of anti-glomerular basement membrane (GBM) nephritis. J Biol Chem 2002, 277:27535-27544 ...
新製品、キャンペーン、カタログ、イベントなど、最新の情報を随時更新: メンブレン抗体アレイ Membrane Antibody Array
A lecture, conference and laboratory course on human pharmacology. Drug mechanisms, toxicities and kinetics are presented as a foundation to therapeutic application. This is a College of Medicine course that does not follow the regular academic calendar. Credit is not given for PCOL 501 if the student has credit for PCOL 425. Prerequisite(s): Grade of C or better in GCLS 501 and grade of C or better in GCLS 503; or consent of the instructor ...
Principal Investigator:MUROTA Sei-itsu, Project Period (FY):1987 - 1989, Research Category:Grant-in-Aid for Developmental Scientific Research, Research Field:Biological pharmacy
View: Main AbID Search Nested - start */ /* ----------------------------------------- */ .entry-content thead th a {padding:0!important;}tr{ -webkit-transition: all .35s ease-in-out; /* Safari 3.1 to 6.0 */ transition: all .35s ease-in-out; } /* ----------------------------------------- */ /* View: Main AbID Search Nested - end */ /* ----------------------------------------- */ /* ----------------------------------------- */ /* View: List of Antibodies from Antibody ID Ecomm - start */ /* ----------------------------------------- */ .entry-content thead th a {padding:0!important;} /* ----------------------------------------- */ /* View: List of Antibodies from Antibody ID Ecomm - end ...
Looking for definition of Goodpasture syndrome? Goodpasture syndrome explanation. Define Goodpasture syndrome by Websters Dictionary, WordNet Lexical Database, Dictionary of Computing, Legal Dictionary, Medical Dictionary, Dream Dictionary.
TY - JOUR. T1 - Diffuse alveolar hemorrhage due to antibasement membrane antibody disease appearing with a polyglandular autoimmune syndrome. AU - Moss, M.. AU - Neff, T. A.. AU - Colby, T. V.. AU - Schwarz, M. I.. AU - Zamora, M. R.. PY - 1994. Y1 - 1994. N2 - We describe a patient with type 3-C polyglandular autoimmune syndrome who presented with diffuse alveolar hemorrhage and normal renal function. The diagnosis of antibasement membrane antibody disease was established by immunofluorescent staining of transbronchial biopsy specimens. We suggest the incorporation of antibasement membrane antibody disease into the spectrum of diseases that define the polyglandular autoimmune syndromes.. AB - We describe a patient with type 3-C polyglandular autoimmune syndrome who presented with diffuse alveolar hemorrhage and normal renal function. The diagnosis of antibasement membrane antibody disease was established by immunofluorescent staining of transbronchial biopsy specimens. We suggest the ...
Medical definition of Goodpastures syndrome: an autoimmune disorder of unknown cause that is characterized by the presence of circulating antibodies…
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In studies of victims from the influenza pandemic of 1918-1919, Ernest Goodpasture described the coexistence of fatal pulmonary hemorrhage and proliferative glomerulonephritis in a young man (25)....
Conjugated linoleic acid (CLA) has been shown to reduce inflammation via Peroxisome Proliferator-Activated Receptor (PPAR)-γ in inflammatory disorders such as Crohns Disease and Inflammatory Bowel Disease. We sought to determine whether CLA isomers would reduce inflammation via PPAR-γ in cultured mesangial cells, and in murine models of anti-glomerular basement membrane (anti-GBM) glomerulonephritis and Systemic Lupus Erythematosus (SLE). SV40-transformed mouse mesangial cells (MES13) were cultured with pure CLA isomers (c9,t11 or t10,c12-CLA or a 50:50 mixture prior to immune stimulation with lipopolysaccharide and interferon-γ. Next, cultured mesangial cells were transfected with small interfering RNA (siRNA) targeting PPAR-γ and treated with CLA isomers prior to immune stimulation. ELISA, qPCR, Western blot, and Griess reaction were performed to measure cytokine production, mRNA expression, induced nitric oxide synthase (iNOS) and nitrite production, respectively. Next, myeloid-specific ...
106 patients (mean age 37 y, 74% men) with biopsy-proved IgA nephropathy, a serum creatinine level ≤ 265 µmol/L, and a urinary protein excretion rate ≥ 1 g/d or a 25% increase in serum creatinine level over the preceding 6 months. Exclusion criteria were systemic lupus erythematosus, chronic liver disease, antiglomerular basement membrane glomerulonephritis, pregnancy, and lactation. 75 patients (71%) continued to receive treatment throughout the study ...
Anti-neutrophil cytoplasmatic antibody (ANCA)-associated glomerulonephritis, anti-glomerular basement membrane (GBM) glomerulonephritis and lupus nephritis are the most common causes of rapid progressive glomerulonephritis (RPGN) in the Western world. These aggressive forms of autoimmune kidney diseases significantly contribute to end-stage renal disease and are associated with high morbidity and mortality. Moreover, patients show significant heterogeneity with respect to clinical outcome and response to therapy. T cell infiltration is a morphological hallmark of RPGN and it is a critical driver of kidney injury. Different CD4 T cell subsets that are endowed with distinct regulatory and effector functions are involved in this detrimental inflammatory process. In particular, the identification and functional characterization of IL-17-expressing CD4 Th17 cells have substantially advanced our understanding of organ-specific autoimmunity. In experimental models of crescentic and proliferative GN, ...
About Stanford Childrens Health and Lucile Packard Childrens Hospital Stanford. Stanford Childrens Health, with Lucile Packard Childrens Hospital Stanford at its center, is the Bay Areas largest health care system exclusively dedicated to children and expectant mothers. As a top-ranked childrens hospital by U.S. News & World Report, we are a leader in providing world-class, nurturing care and achieving extraordinary outcomes in every pediatric and obstetric specialty. Stanford Childrens Health provides everything from specialty care to general pediatrics and can be accessed through more than 60 locations across Northern California and 100 locations in the U.S. western region. As the pediatric and obstetric teaching hospital for the world-renowned Stanford University School of Medicine, were cultivating the next generation of medical professionals and are at the forefront of scientific research to improve childrens health outcomes around the world. We are a nonprofit organization ...
Immune-mediated nephritis contributes to disease in systemic lupus erythematosus, Goodpasture syndrome (caused by antibodies specific for glomerular basement membrane [anti-GBM antibodies]), and spontaneous lupus nephritis. Inbred mouse strains differ in susceptibility to anti-GBM antibody-induced and spontaneous lupus nephritis. This study sought to clarify the genetic and molecular factors that may be responsible for enhanced immune-mediated renal disease in these models. When the kidneys of 3 mouse strains sensitive to anti-GBM antibody-induced nephritis were compared with those of 2 control strains using microarray analysis, one-fifth of the underexpressed genes belonged to the kallikrein gene family, which encodes serine esterases. Mouse strains that upregulated renal and urinary kallikreins exhibited less evidence of disease. Antagonizing the kallikrein pathway augmented disease, while agonists dampened the severity of anti-GBM antibody-induced nephritis. In addition, nephritis-sensitive ...
Immune-mediated nephritis contributes to disease in systemic lupus erythematosus, Goodpasture syndrome (caused by antibodies specific for glomerular basement membrane [anti-GBM antibodies]), and spontaneous lupus nephritis. Inbred mouse strains differ in susceptibility to anti-GBM antibody-induced and spontaneous lupus nephritis. This study sought to clarify the genetic and molecular factors that may be responsible for enhanced immune-mediated renal disease in these models. When the kidneys of 3 mouse strains sensitive to anti-GBM antibody-induced nephritis were compared with those of 2 control strains using microarray analysis, one-fifth of the underexpressed genes belonged to the kallikrein gene family, which encodes serine esterases. Mouse strains that upregulated renal and urinary kallikreins exhibited less evidence of disease. Antagonizing the kallikrein pathway augmented disease, while agonists dampened the severity of anti-GBM antibody-induced nephritis. In addition, nephritis-sensitive ...
WIKI: Autoimmune diseases arise from an abnormal immune response of the body against substances and tissues normally present in the body (autoimmunity). This may be restricted to certain organs (e.g. in autoimmune thyroiditis) or involve a particular tissue in different places (e.g. Goodpastures disease which may affect the basement membrane in both the lung and the kidney). The treatment of autoimmune diseases is typically with immunosuppression--medication that decreases the immune response. A large number of autoimmune diseases are recognized. A major understanding of the underlying pathophysiology of happy autoimmune diseases has been the application of genome wide association scans that have identified a striking degree of genetic sharing among the autoimmune diseases.. This Webinar will also look into Immune-defficiency syndroms such as HIV/AIDS and into the root of auto-immune disorders.. Pricing information: Two webinars of EUR 19 € each or EUR 38 €. ...
This test has been cleared or approved by the U.S. Food and Drug Administration and is used per manufacturers instructions. Performance characteristics were verified by Mayo Clinic in a manner consistent with CLIA requirements ...
Pain management information for pain medicine healthcare professionals in treating and caring for their patients. Clinical Pain Advisor offers news, case studies and more.
Latest urology and nephrology news, research and treatment articles for urologists and nephrologists to stay updated. Clinical reviews on renal and urology treatments.
Carrieri, G and Murase, N and Woo, and Nalesnik, M and Azzarone, A and Funakoshi, Y and Thomson, AW and Todo, S and Starzl, TE (1991) Effect of FK 506 in the prophylaxis of autoimmune glomerulonephritis in NZB/WF1 mice. Transplantation Proceedings, 23. 3357 - 3359. ISSN 0041-1345 ...
Summary is not available for the mouse gene. This summary is for the human ortholog.] Type IV collagen, the major structural component of basement membranes, is a multimeric protein composed of 3 alpha subunits. These subunits are encoded by 6 different genes, alpha 1 through alpha 6, each of which can form a triple helix structure with 2 other subunits to form type IV collagen. This gene encodes alpha 3. In the Goodpasture syndrome, autoantibodies bind to the collagen molecules in the basement membranes of alveoli and glomeruli. The epitopes that elicit these autoantibodies are localized largely to the non-collagenous C-terminal domain of the protein. A specific kinase phosphorylates amino acids in this same C-terminal region and the expression of this kinase is upregulated during pathogenesis. This gene is also linked to an autosomal recessive form of Alport syndrome. The mutations contributing to this syndrome are also located within the exons that encode this C-terminal region. Like the ...
TY - JOUR. T1 - Una insolita microangioite a decorso protratto. T2 - sindrome di Goodpasture estesa successivamente al miocardio.. AU - Mori, R.. AU - Corvaglia, A. G.. AU - Frustaci, A.. PY - 1992/11. Y1 - 1992/11. N2 - We describe a disease, started in a female young adult patient as an apparent pulmonary siderosis, followed nine years later by an extracapillary proliferative nephritis, which developed to uremia in a few months. Later an intra-myocardial vasculitis, responsible of heart failure, appeared. Immune-histochemistry and serological tests exclude a disease mediated by anti-GMB antibodies, and pathologic features suggest a vasculitis mainly affecting lungs and kidneys.. AB - We describe a disease, started in a female young adult patient as an apparent pulmonary siderosis, followed nine years later by an extracapillary proliferative nephritis, which developed to uremia in a few months. Later an intra-myocardial vasculitis, responsible of heart failure, appeared. Immune-histochemistry ...
COL4A3 antibody (collagen, type IV, alpha 3 (Goodpasture antigen)) for ELISA, IHC-P, WB. Anti-COL4A3 pAb (GTX37323) is tested in Human, Mouse, Rat samples. 100% Ab-Assurance.
Inside a WBC we have a transcription factor called NFKB. In the cytosol, NFKB is normally inactivated by IKB. When a viral/bacteria protein stimulates an inflammatory response, the IKB is degraded and we have free NFKB. This translocates in the nucleus where is acts as a transcription factor, to increase cytokines, adhesion molecules, and COX-2. -Cytokines: fight pathogens but can also cause tissue damage. -Adhesion molecules: ICAM/VCAM: binds to the endothelial cells, which can then go into the tissue and fight the pathogen. -COX-2: AA is the subtrate for COX-2, which produces PGE. This causes dilation of the vessels, warmth, tenderness. ...
Vector database is a digital collection of vector backbones assembled from publications and commercially available sources. This is a free resource for the scientific community that is compiled by Addgene.. This page is informational only - this vector is NOT available from Addgene - please contact the manufacturer for further details. ...
Anti-GBM. , 7 EliA U/ml negativ 7 - 10 EliA U/ml grenzwertig , 10 EliA U/ml positiv. Quelle: PBL Flooroenzyme-Immunoassay FOR ANTI GBM ANTIBODIES Phadia GmbH 250-5514-021 ...
DefinitionTop. Hematuria is defined as an increased number of red blood cells (RBCs) in urine, namely, ,3 RBCs per high-power field (HPF) in a centrifuged urine sample. In microscopic hematuria the color of urine is unchanged. In gross hematuria the color of urine suggests the presence of blood.. Causes and PathogenesisTop. Causes of hematuria: The following classification is based on the origin of RBCs in the urinary tract:. 1) Glomerular hematuria (caused by glomerular disease): All types of acute or chronic glomerulonephritis, including IgA nephropathy, anti-glomerular basement membrane disease, and immune complex glomerulonephritis; hereditary causes, such as Alport syndrome; and benign causes, such as thin basement membrane disease. 2) Nonglomerular hematuria: a) Upper urinary tract: Nephrolithiasis, renal cysts, cancer (renal parenchyma, renal pelvis, renal calyces, ureter), hypercalciuria, hyperuricosuria, pyelonephritis, renal trauma, renal papillary necrosis, renal infarct, renal vein ...
Dr. Ernest William Goodpasture (October 17, 1886 - September 20, 1960) was an American pathologist and physician. Goodpasture advanced the scientific understanding of the pathogenesis of infectious diseases, parasitism, and a variety of rickettsial and viral infections. Together with colleagues at Vanderbilt University, he invented methods for growing viruses and rickettsiae in chicken embryos and fertilized chicken eggs. This enabled the development of vaccines against influenza, chicken pox, smallpox, yellow fever, typhus, Rocky mountain spotted fever, and other diseases. He also described Goodpasture syndrome. Goodpasture was born in Clarksville, Tennessee, in 1886. He received his B.A. from Vanderbilt University in 1908. In 1912, Goodpasture graduated from Johns Hopkins School of Medicine with an M.D. degree. There, under professors William H. Welch and George H. Whipple, he was subsequently appointed a Rockefeller Fellow in pathology; he held this position from 1912 to 1915. Thereafter, ...
I have one quibble with this otherwise excellent review in Chest. The authors decry eponyms as not being descriptive of pathology but preserve what may be the most inappropriate eponym in the history of medicine. Thus Wegeners Granulomatosis becomes ANCA-associated granulomatous vasculitis while anti-GBM disease is still referred to as Goodpasture syndrome. ...
Activation of p38 mitogen-activated protein kinase (MAPK) is known to be important in cytokine production and cell survival in inflammation. This study examined the effect of inhibiting p38 MAPK after onset of renal injury in an experimental model of crescentic glomerulonephritis. Furthermore, this study investigated whether p38 MAPK inhibition would cause widespread suppression of the cytokine network in vivo or uncontrolled apoptosis. In the in vivo studies, daily treatment with a p38 MAPKalpha/beta inhibitor was started 1 h (early treatment study) or 4 d (late treatment study) after induction of nephrotoxic nephritis in Wistar Kyoto rats. The treated rats remained healthy with normal weight gain during the study. Both early and late treatment with p38 MAPK inhibitor reduced renal monocyte chemoattractant protein-1 (MCP-1) levels, the number of glomerular macrophages, the severity of tissue injury, and proteinuria compared with the vehicle group. Unexpected, treatment with p38 MAPK inhibitor did not
This recently recognized variant of PAN52 is defined by inflammation that is largely confined to smaller vessels than in PAN - arterioles, capillaries and postcapillary venules. Angiograms are correspondingly normal. Major organ infarction is rare, glomerulonephritis is universal, and there is a high frequency of pulmonary hemorrhage. MPA is considerably more common than classic PAN and it is a considerably more common cause of a pulmonary-renal syndrome than Goodpastures syndrome. A forme-fruste of MPA is characterized exclusively by glomerulonephritis. Evidence of hepatitis B infection is usually absent. In contrast to classic PAN as well as such small vessel vasculitides as cryoglobulinemic vasculitis and Henoch-Schönlein purpura, there is little or no evidence of immune deposits. Fifty to 80% of patients with MPA have circulating ANCA - usually myeloperoxidase (perinuclear or p-ANCA)(see WG), a rare phenomenon in classic PAN. Some have antibodies to proteinase-3 (central or c-ANCA) as in ...
To the editor: In their article, Chalmers and associates (1) state that renal involvement is unusual in penicillamine-induced lupus erythematosus but that it has been described and give three literature citations (references 4, 8, 9). In their reference 4, Kirby and associates do describe renal disease in one of their four patients with penicillamine-induced lupus erythematosus; however, they also describe 17 additional patients with penicillamine-induced nephropathy, none of whom had lupus erythematosus. In reference 8, there is no mention of drug-induced lupus erythematosus among the various examples of penicillamine toxicity reported. Reference 9 refers only to penicillamine-induced Goodpastures syndrome, not ...
0058] It will be understood that the total daily usage of the compounds and compositions of the present invention will be decided by the attending physician within the scope of sound medical judgment. The specific therapeutically effective dose level for any particular patient will depend upon a variety of factors including the disorder being treated and the severity of the disorder; activity of the specific compound employed; the specific composition employed, the age, body weight, general health, sex and diet of the patient; the time of administration, route of administration, and rate of excretion of the specific compound employed; the duration of the treatment; drugs used in combination or coincidental with the specific polypeptide employed; and like factors well known in the medical arts. For example, it is well within the skill of the art to start doses of the compound at levels lower than those required to achieve the desired therapeutic effect and to gradually increase the dosage until ...
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Crescentic glomerulonephritis, a complication of severe immune glomerular injury, is the pathological correlate of rapidly progressive glomerulonephritis, mediated by both humoral and cellular effectors. In the current issue of the JCI, Chen et al. have implicated Bowmans capsule in functionally isolating potentially immune effectors, specifically antigen-specific CD8+ T lymphocytes, from podocytes. They suggest that, in crescentic glomerulonephritis, immune-mediated glomerular endothelial injury results in inside-out injury to the glomerulus, with subsequent leukocyte migration through a weakened or ruptured Bowmans capsule, resulting in outside-in injury. Effector T cells then recognize nephritogenic antigens presented by podocytes or other cells within the urinary space, enhancing injury and crescent formation.. ...
TY - JOUR. T1 - Effect of antibody charge and concentration on deposition of antibody to glomerular basement membrane. AU - Madaio, Michael P.. AU - Salant, D. J.. AU - Adler, S.. AU - Darby, C.. AU - Couser, W. G.. PY - 1984/1/1. Y1 - 1984/1/1. N2 - Fixed anionic sites within the glomerular capillary wall influence the permeation of serum proteins, the localization of various antigens, and the deposition of antibody in the subepithelial space. In anti-GBM nephritis antibody deposition occurs very rapidly to antigenic sites located relatively proximal in the glomerular capillary wall. We examined the influence of the glomerular charge barrier on anti-GBM antibody deposition by comparing the rate of deposition of antibodies with cationic and anionic isoelectric points. Purified sheep anti-rat GBM IgG was isolated from acid eluates of kidneys obtained 24 hr after rats were injected with sheep antiserum to rat GBM. Anti-GBM IgG was separated into cationic (pI 6.4-8.5) and anionic (pI 4.2-6.8) ...
Through the use of sophisticated apheresis machines, the transfusion specialists separate patient blood into its cellular and liquid fractions and, depending on the particular disease process, cleanse an individuals blood of either harmful cellular material or soluble plasma factors. For example, by removing plasma ("plasmapheresis") the Apheresis Unit treats a large number of antibody-mediated autoimmune diseases such as myasthenia gravis (a neurological disorder), Goodpastures syndrome (a kidney disorder), and TTP/HUS (a clotting disorder often associated with viral infection or the ingestion of bacterially contaminated food).. Other procedures include removing elevated levels of white cells ("leukapheresis") to prevent the neurological and pulmonary damage resulting from impeded blood flow that can be experienced by newly diagnosed leukemic patients (hyperleukocytic syndrome) or removing and exchanging red blood cells for fresh banked cells ("erythrocytapheresis") to prevent or treat the ...
Glomerulonephritis is a type of kidney disease in which the part of your kidneys that helps filter waste and fluids from the blood is damaged. Glomerulonephritis may be caused by problems with the bodys immune system. Often, the exact cause of glomerulonephritis is unknown. Damage to the glomeruli causes blood and protein to be lost in the urine. The condition may develop quickly, and kidney function is lost within weeks or months (called rapidly progressive glomerulonephritis). A quarter of people with chronic glomerulonephritis have no history of kidney disease ...
Credit points: 6 Teacher/Coordinator: A/Prof Paul Witting Session: Semester 1 Classes: Lectures (2 h/wk) and online lecturettes (3 x 20 min/wk); group focus tutorial (3 x 2 h over 2-3 weeks); guided museum session (1 h/wk); and preparation of online research notebooks (1 h/wk). Prerequisites: A mark of 70 or above in 12cp from {[ANAT2008 or ANAT2009 or (ANAT2010 or ANAT2910) or ANAT2011] or [BCHM2071 or BCHM2971) or BCHM2072 or BCHM2972) or BCHM2081 or BCHM2981) or BCHM2082 or BCHM2982)] or [(BCMB2001 or BCMB2901) or BCMB2002 or BCMB2902)] or [(BIOL2021 or BIOL2921) or (BIOL2022 or BIOL2922) or (BIOL2024 or BIOL2924) or (BIOL2030 or BIOL2930) or (BIOL2031 or BIOL2931)] or [(GEGE2001 or GEGE2901)] or [(IMMU2101 or MICR2021 or MICR2921 or MICR2022 or MICR2922 or MICR2031 or MICR2931 or MIMI2002 or MIMI2902)] or [(MBLG2071 or MBLG2971) or (MBLG2072 or MBLG2972)] or [(PCOL2011 or PCOL2021) or (PCOL2012 or PCOL2022)] or [(PHSI2005 or PHSI2905) or (PHSI2006 or PHSI2906) or (PHSI2007 or PHSI2907) or ...
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FibroStatin SL is a biotech company focused on the development of Goodpasture antigen-binding protein (GPBP) technology for research and medical purposes. FibroStatin SL was founded in 2005 by researchers from the ...
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One aspect of basement construction that is often overlooked is the waterproofing stage. Because basements are partially or completely underground, water will always find its way through the basement walls (concrete or block). There are several procedures available to the homeowner--sealing walls and floors or ...
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Human glomerulonephritis (GN) is characterized by sustained proteinuria, sodium retention, hypertension, and edema formation. Increasing quantities of filtered protein enter the renal tubule, where they may alter epithelial transport functions. Exaggerated endocytosis and consequent protein overload may affect proximal tubules, but intrinsic malfunction of distal epithelia has also been reported. A straightforward assignment to a particular tubule segment causing salt retention in GN is still controversial. We hypothesized that 1) trafficking and surface expression of major transporters and channels involved in volume regulation were altered in GN, and 2) proximal tubular endocytosis may influence locally as well as downstream expressed tubular transporters and channels. Effects of anti-glomerular basement membrane GN were studied in controls and megalin-deficient mice with blunted proximal endocytosis. Mice displayed salt retention and elevated systolic blood pressure when proteinuria had ...
... is a chapter in the book, Nephrology, containing the following 11 pages: Acute Glomerulonephritis, Glomerulonephritis Causes, Goodpastures Syndrome, Poststreptococcal Glomerulonephritis, Rapidly Progressive Glomerulonephritis, Nephrotic Syndrome, Orthostatic Proteinuria, Isolated Proteinuria, Focal Segmental Glomerulosclerosis, Membranous Nephropathy, Minimal Change Disease.
Looking for online definition of acute crescentic glomerulonephritis in the Medical Dictionary? acute crescentic glomerulonephritis explanation free. What is acute crescentic glomerulonephritis? Meaning of acute crescentic glomerulonephritis medical term. What does acute crescentic glomerulonephritis mean?
Collagen XVIII is a component of the highly specialized extracellular matrix associated with basement membranes of epithelia and endothelia. and capillary rarefaction. Anti-GBM BMS 378806 disease upregulated collagen XVIII/endostatin manifestation within the GBM and Bowmans capsule of wild-type mice. Collagen XVIII/endostatin-deficient mice developed more severe glomerular and tubulointerstitial injury than wild-type mice. Collagen XVIII/endostatin deficiency altered matrix redesigning enhanced the inflammatory response and advertised capillary rarefaction and vascular endothelial cell damage but did not impact endothelial proliferation. Supplementing collagen XVIII-deficient mice with exogenous endostatin did not affect the progression of anti-GBM disease. Taken together these results suggest that collagen XVIII/endostatin preserves the integrity of the extracellular matrix and capillaries in the kidney avoiding intensifying glomerulonephritis. The main constituents of most cellar membranes ...
In this model of crescentic GN, mice lacking endogenous IFN-γ developed less severe GN than genetically normal C57BL/6 mice. Crescent formation and elements of DTH were reduced in glomeruli of IFN-γ -/- mice, and functional injury, measured by serum creatinine and urinary protein excretion, was diminished in IFN-γ-deficient mice. Skin DTH to the nephritogenic antigen was reduced, consistent with the observed reductions in glomerular injury. Serum titers of antigen-specific IgG2a and IgG3, associated with IFN-γ and Th1 responses, were reduced in IFN-γ -/- mice, but splenocyte IL-2 levels were unaffected. As IL-2 is produced by Th1 cells (7), this result suggests that the effects of endogenous IFN-γ on Th1 responses were mediated directly by IFN-γ itself, and not by a generalized downregulation of all components of the Th1 response. Th2 elements of the immune response to sheep globulin were unaffected. There was a nonsignificant increase in the Th2-associated subclass IgG1, and total ...
Principal Investigator:YOSHIOKA Kazuo, Project Period (FY):1995 - 1996, Research Category:Grant-in-Aid for Scientific Research (C), Section:一般, Research Field:Pediatrics
VIDA: The Thomson "swinging bridge" came down with a splash on Monday. Originally built in the 1930s the bridge connected south bank residents with the outside world. Crews from Stayton Construction used cable cutters, chainsaws and an excavator to remove the privately owned structure around 10:15 a.m. in response to safety concerns.. From the November 29, 1985 issue of McKenzie River Reflections - "GOODPASTURE ROAD in 1940s" Courtesy Vida-McKenzie Neighborhood Watch Newsletter.. When the Goodpasture Bridge was built in 1938 the road only extended 1/2 mile or so beyond the bridge. There were only a few families living on the south side of the river that crossed on swinging foot bridges. Supples were packed, pulled and pushed across the foot bridges too.. ...
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Anti-GBM is an indirect solid phase enzyme immunoassay (ELISA) for the quantitative measurement of IgG class autoantibodies to glomerular basement membrane (GBM) in human serum or plasma. (KA1266) - Products - Abnova
Central to the development of glomerular inflammation and injury are alterations and abnormalities of various cytokines and signaling systems. There are four chapters in this book that deal with these aspects in the pathogenesis. The role of TGF-β in progressive glomerular disease is discussed in great detail in a chapter well written by Hyun Soon Lee, with particular reference to mesangial matrix accumulation, while the role of STAT3 activation in glomerulonephritis is elaborated in the well written chapter by Fumio Tsuji et al. ...
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The Basement membrane is a layer of fiber that is located under epithelium or endothelium. The epithelium is the tissue that lines the surfaces and cavities of
Basement membranes (BMs) are cell-associated extracellular matrices formed initially as laminin Dolymer scaffoldings. They act as solid-phase agonists for adher...
Basement membranes (BMs) are cell-adhesive scaffolds and agonists that are required for tissue growth, differentiation and adult functions. Elucidation of the m...
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Acute respiratory failure: Unlikely simple CA-PNA given worsening status while on appropriate antibiotic therapy. Active tuberculosis possible given history of chronic productive cough with hemoptysis, constitutional symptoms and imaging findings. IGRAs of limited utility in diagnosis of active disease, further, while three negative sputum AFB smears decreases the likelihood of TB, additional testing with NAAT and culture is required. Another possibility is a vasculitic process given concomitant hematuria and acute renal failure, with respiratory symptoms now 2/2 alveolar hemorrhage. This was evaluated with ANCA assay which was positive for p-ANCA with high titer. This is often suggestive of primary vasculitis (in this case likely microscopic polyangiitis vs. Churg-Strauss), however ELISA for target antigen is of particular importance as p-ANCA with specificity for antigens other than MPO can be associated with another condition on the differential: Goodpastures syndrome. This patient was ...
TY - JOUR. T1 - Radiologic manifestations of the systemic autoimmune diseases. AU - Primack, Steven. AU - Muller, N. L.. PY - 1998. Y1 - 1998. N2 - Advances in thoracic imaging during the past two decades, such as CT scans and MR imaging, have enhanced our understanding of the pleuropulmonary abnormalities that develop in the systemic autoimmune diseases. In this article, the thoracic radiologic manifestations of several connective tissue diseases (systemic lupus erythematosus, rheumatoid arthritis, Sjogrens syndrome, polymyositis/dermatomyositis, progressive systemic sclerosis, and anklyosing spondylitis), two granulomatous vasculitides, (Wegeners Granulomatosis and Churg-Strauss syndrome), and antiglomerular basement membrane disease are reviewed.. AB - Advances in thoracic imaging during the past two decades, such as CT scans and MR imaging, have enhanced our understanding of the pleuropulmonary abnormalities that develop in the systemic autoimmune diseases. In this article, the thoracic ...
TY - JOUR. T1 - Urine proteome scans uncover total urinary protease, prostaglandin D synthase, serum amyloid P, and superoxide dismutase as potential markers of lupus nephritis. AU - Wu, Tianfu. AU - Fu, Yuyang. AU - Brekken, Deirdre. AU - Yan, Mei. AU - Zhou, Xin J.. AU - Vanarsa, Kamala. AU - Deljavan, Nima. AU - Ahn, Chul. AU - Putterman, Chaim. AU - Mohan, Chandra. PY - 2010/2/15. Y1 - 2010/2/15. N2 - To identify potential biomarkers in immune-mediated nephritis, urine from mice subjected to an augmented passive model of antiglomerular basement membrane (GBM)-induced experimental nephritis was resolved using two-dimensional gels. The urinary proteome in these diseased mice was comprised of at least 71 different proteins. Using orthogonal assays, several of these molecules, including serum amyloid P (SAP), PG D synthase, superoxide dismutase, rennin, and total protease were validated to be elevated in the urine and kidneys of mice during anti-GBM disease, as well as in mice with spontaneously ...
Mortality at 1 and 5 years was 23% and 40%, respectively: standardized mortality ratio, 4.74 (95% CI, 3.62-6.32). End-stage renal disease was reached by 14% and 18% at 1 and 5 years, respectively. In multivariable analysis, serum creatinine level at biopsy and percentage of normal glomeruli in the initial biopsy specimen were the best predictors of kidney survival. C Statistics were 0.80 for creatinine level alone and 0.83 for creatinine level with normal glomeruli. In patients undergoing an additional biopsy, rapid progression in the index of chronic damage and serum creatinine level at the second biopsy were associated with kidney survival in multivariable analysis ...
Hyaline Membrane Disease. In: Hay, Jr WW, Levin MJ, Deterding RR, Abzug MJ. Hay, Jr W.W., Levin M.J., Deterding R.R., Abzug M.J. Eds. William W. Hay, Jr, et al.eds. Quick Medical Diagnosis & Treatment Pediatrics New York, NY: McGraw-Hill; . http://accesspediatrics.mhmedical.com/content.aspx?bookid=2196§ionid=166958030. Accessed December 12, 2017 ...

Anti-glomerular basement membrane disease superimposed on membranous nephropathy: a case report and review of the literature |...Anti-glomerular basement membrane disease superimposed on membranous nephropathy: a case report and review of the literature |...

Simultaneous anti-glomerular basement membrane disease and membranous nephropathy is very rare. There have been 16 previous ... The simultaneous occurrence of both anti-glomerular basement membrane disease and membranous nephropathy is rare. A 59-year-old ... Co-existence of membranous nephropathy and anti-glomerular basement membrane disease may be immune-mediated, although the exact ... Work-up included a kidney biopsy, which revealed anti-glomerular basement membrane disease with underlying membranous ...
more infohttps://jmedicalcasereports.biomedcentral.com/articles/10.1186/1752-1947-4-237/tables/1

Treatment of Steroid-sensitive Nephrotic Syndrome | Randomized Controlled Trial | Clinical TrialTreatment of Steroid-sensitive Nephrotic Syndrome | Randomized Controlled Trial | Clinical Trial

... and anti-glomerular basement membrane antibody glomerulonephritis.. Strength of recommendations and quality of supporting ... A Report of the International Study of Kidney Disease in Children. Kidney Int 20:765771 3. Bagga A, Ali U, Banerjee S, Kanitkar ... However, glomerular filtration rate is maintained with MMF while it falls during CNI therapy [50, 51]. In observational studies ... KDIGO kidney disease: improving global outcomes; SSNS steroid sensitive nephrotic syndrome; FR frequently relapsing; SO steroid ...
more infohttps://pt.scribd.com/document/193724359/Treatment-of-Steroid-sensitive-Nephrotic-Syndrome

Acute renal failure induced by acute interstitial nephritis secondary to cocaine | Nefrología (English Edition)Acute renal failure induced by acute interstitial nephritis secondary to cocaine | Nefrología (English Edition)

Basement membranes and the glomerular mesangium were normal. The interstitium displayed moderate mononuclear inflammatory ... He denied having taken non-steroidal anti-inflammatory drugs or other medication. The physical examination showed a good ... Cocaine-induced renal disease. Expert Opin Drug Saf 2004;3(5):441-8. [Pubmed] ... Molecular mimicry or direct binding of the drug to the tubular basement membrane are the main mechanisms involved,9 and this ...
more infohttps://www.revistanefrologia.com/en-acute-renal-failure-induced-by-articulo-X2013251413052705

Anti-glomerular basement membrane disease: MedlinePlus Medical EncyclopediaAnti-glomerular basement membrane disease: MedlinePlus Medical Encyclopedia

... anti-GBM diseases) is a rare disorder that can involve quickly worsening kidney failure and lung disease. ... Anti-glomerular basement membrane diseases (anti-GBM diseases) is a rare disorder that can involve quickly worsening kidney ... Anti-glomerular basement membrane disease and Goodpasture disease. In: Feehally J, Floege J, Tonelli M, Johnson RJ, eds. ... These substances are called antiglomerular basement membrane antibodies. The glomerular basement membrane is a part of the ...
more infohttps://medlineplus.gov/ency/article/000142.htm

Mesangial IgA deposits indicate pathogenesis of anti-glomerular basement membrane disease.  - PubMed - NCBIMesangial IgA deposits indicate pathogenesis of anti-glomerular basement membrane disease. - PubMed - NCBI

Anti-glomerular basement membrane (anti-GBM) disease is characterized by crescentic glomerulonephritis with immunoglobulin G ( ... Mesangial IgA deposits indicate pathogenesis of anti-glomerular basement membrane disease.. Wang A1, Wang Y, Wang G, Zhou Z, ... Anti-Glomerular Basement Membrane Disease/metabolism*. *Anti-Glomerular Basement Membrane Disease/pathology ... We report a rare case of a 31-year-old female who was diagnosed as having anti-GBM disease with extensive IgA deposits in the ...
more infohttps://www.ncbi.nlm.nih.gov/pubmed/22366925

Transforming growth factor-beta production in anti-glomerular basement membrane disease in the rabbit.  - PubMed - NCBITransforming growth factor-beta production in anti-glomerular basement membrane disease in the rabbit. - PubMed - NCBI

Transforming growth factor-beta production in anti-glomerular basement membrane disease in the rabbit.. Coimbra T1, Wiggins R, ... A model of antiglomerular basement (anti-GBM) disease in the rabbit was induced on day 0 by the injection of anti-GBM antibody ... suggesting the presence of substantial latent TGF-beta activity in control glomerular conditioned media. These same control- ... stimulatory activity in the kidney during immune-induced renal injury that results in severe fibrosis in both glomerular and ...
more infohttps://www.ncbi.nlm.nih.gov/pubmed/1987768?dopt=Abstract

Anti-Glomerular Basement Membrane Disease: Outcomes of Different Therapeutic Regimens in a Large Single-Center Chinese Cohort...Anti-Glomerular Basement Membrane Disease: Outcomes of Different Therapeutic Regimens in a Large Single-Center Chinese Cohort...

The low incidence and fulminant course of disease preclude a large randomized controlled study to define the benefits of any ... disease usually presents with rapidly progressive glomerulonephritis accompanied by pulmonary hemorrhage. ... Anti-Glomerular Basement Membrane Disease: Outcomes of Different Therapeutic Regimens in a Large Single-Center Chinese Cohort ... Anti-glomerular basement membrane (GBM) disease usually presents with rapidly progressive glomerulonephritis accompanied by ...
more infohttps://insights.ovid.com/crossref?an=00005792-201109000-00003

Videos • Anti-Glomerular Basement Membrane DiseaseVideos • Anti-Glomerular Basement Membrane Disease

Ranked list of possible diseases from either several symptoms or a full patient history. A similarity measure between symptoms ... Anti-Glomerular Basement Membrane Disease. On-line free medical diagnosis assistant. ... Anti-Glomerular Basement Membrane Disease. Goodpasture Syndrome - YouTube. Goodpasture Syndrome (Anti-GBM Antibody Disease) ... http://usmlefasttrack.com/?p=1930 anti, glomerular, basement, membrane, antibodies .... youtube.com - Tue, 18 Jun 2013 00:15. ...
more infohttps://lookfordiagnosis.com/videos.php?term=Anti-Glomerular+Basement+Membrane+Disease&lang=1

Cases reported • Anti-Glomerular Basement Membrane Disease; Anti-GBM Disease; Goodpasture SyndromeCases reported • Anti-Glomerular Basement Membrane Disease; Anti-GBM Disease; Goodpasture Syndrome

Anti-GBM Disease; Goodpasture Syndrome. On-line free medical diagnosis assistant. Ranked list of possible diseases from either ... A similarity measure between symptoms and diseases is provided. ... "Anti-Glomerular Basement Membrane Disease". Filter by keywords: ... On the first occasion, a diagnosis of anti-glomerular basement membrane (GBM) disease (with linear deposition of immunoglobulin ... Antiglomerular basement membrane (anti-GBM) disease is characterized by a linear deposition of immunoglobulins along the ...
more infohttps://lookfordiagnosis.com/cases.php?term=Anti-Glomerular+Basement+Membrane+Disease&lang=1

Anti-glomerular basement membrane disease superimposed on membranous nephropathy: a case report and review of the literature |...Anti-glomerular basement membrane disease superimposed on membranous nephropathy: a case report and review of the literature |...

Simultaneous anti-glomerular basement membrane disease and membranous nephropathy is very rare. There have been 16 previous ... The simultaneous occurrence of both anti-glomerular basement membrane disease and membranous nephropathy is rare. A 59-year-old ... Co-existence of membranous nephropathy and anti-glomerular basement membrane disease may be immune-mediated, although the exact ... Work-up included a kidney biopsy, which revealed anti-glomerular basement membrane disease with underlying membranous ...
more infohttps://jmedicalcasereports.biomedcentral.com/articles/10.1186/1752-1947-4-237

北京大学医学部机构知识库(IR@PKUHSC): Rapidly progressive glomerulonephritis due to anti-glomerular basement membrane disease accompanied by...北京大学医学部机构知识库([email protected]): Rapidly progressive glomerulonephritis due to anti-glomerular basement membrane disease accompanied by...

Anti-glomerular basement membrane (anti-GBM) disease is characterized by autoantibodies against antigenic site on type IV ... Gao, Bixia,et al."Rapidly progressive glomerulonephritis due to anti-glomerular basement membrane disease accompanied by IgA ... Rapidly progressive glomerulonephritis due to anti-glomerular basement membrane disease accompanied by IgA nephropathy: a case ... Rapidly progressive glomerulonephritis due to anti-glomerular basement membrane disease accompanied by IgA nephropathy: a case ...
more infohttp://ir.bjmu.edu.cn/handle/400002259/60985

A Case of Anti Glomerular Basement Membrane (GBM) Negative Goodpasture s Disease | OMICS InternationalA Case of Anti Glomerular Basement Membrane (GBM) Negative Goodpasture s Disease | OMICS International

Goodpastures disease is a fulminant rapidly progressive disease characterized by autoantibodies to the alpha-3 chain of type ... A Case of Anti Glomerular Basement Membrane (GBM) Negative Goodpasture?s Disease Megan Borkum1, Gregory L Calligaro2 and ... and anti glomerular basement membrane (GBM) antibodies were negative. Anti-myeloperoxidase antibodies (anti-MPO) (also known as ... 2002) Goodpastures disease in the absence of circulating anti-glomerular basement membrane antibodies as detected by standard ...
more infohttps://www.omicsonline.org/open-access/a-case-of-anti-glomerular-basement-membrane-gbm-negative-goodpastures-disease-2161-105X.1000213.php?aid=32718

Therapeutic Mechanism of Glucocorticoids on Cellular Crescent Formation in Patients With Antiglomerular Basement Membrane...Therapeutic Mechanism of Glucocorticoids on Cellular Crescent Formation in Patients With Antiglomerular Basement Membrane...

... basement membrane disease.Materials and MethodsThirty-four patients with biopsy-proven antiglomerular basement membrane ... and glomerular (r = 0.49, P = 0.007) macrophage infiltration.ConclusionsGCs might exert their therapeutic effects via ... in antiglomerular basement membrane disease.Materials and MethodsThirty-four patients with biopsy-proven antiglomerular ... Mechanism of Glucocorticoids on Cellular Crescent Formation in Patients With Antiglomerular Basement Membrane Disease☆,☆,☆☆ ...
more infohttps://insights.ovid.com/ajmeds/201708000/00000441-201708000-00008

Anti-glomerular basement membrane blood test: MedlinePlus Medical EncyclopediaAnti-glomerular basement membrane blood test: MedlinePlus Medical Encyclopedia

The glomerular basement membrane is the part of the kidney that helps filter waste and extra fluid from the blood. ... Anti-glomerular basement membrane disease and Goodpasture disease. In: Feehally J, Floege J, Tonelli M, Johnson RJ, eds. ... This test is used to diagnose certain kidney diseases, such as Goodpasture syndrome and anti-glomerular basement membrane ... Anti-glomerular basement membrane antibodies are antibodies against this membrane. They can lead to kidney damage. This article ...
more infohttps://medlineplus.gov/ency/article/003524.htm

The HLA-DRB1*1501 allele is prevalent among Japanese patients with anti-glomerular basement membrane antibody-mediated disease....The HLA-DRB1*1501 allele is prevalent among Japanese patients with anti-glomerular basement membrane antibody-mediated disease....

The HLA-DRB1*1501 allele is prevalent among Japanese patients with anti-glomerular basement membrane antibody-mediated disease. ... 1501 and anti-glomerular basement membrane (GBM) antibody-mediated disease in Japanese patients. ... Anti-Glomerular Basement Membrane Disease/genetics*. *Anti-Glomerular Basement Membrane Disease/immunology* ... The present study demonstrated that Japanese patients with anti-GBM antibody-mediated disease are very likely to carry the HLA- ...
more infohttps://phgkb.cdc.gov/PHGKB/phgHome.action?action=forward&dbsource=huge&id=35595

The association of HLA-DQB1, -DQA1 and -DPB1 alleles with anti- glomerular basement membrane (GBM) disease in Chinese patients....The association of HLA-DQB1, -DQA1 and -DPB1 alleles with anti- glomerular basement membrane (GBM) disease in Chinese patients....

The association of HLA-DQB1, -DQA1 and -DPB1 alleles with anti- glomerular basement membrane (GBM) disease in Chinese patients. ... Human leukocyte antigen (HLA) alleles are associated with many autoimmune diseases, including anti-glomerular basement membrane ... Anti-Glomerular Basement Membrane Disease/ethnology. *Anti-Glomerular Basement Membrane Disease/genetics* ... GBM) disease. In our previous study, it was demonstrated that HLA-DRB1*1501 was strongly associated with anti-GBM disease in ...
more infohttps://phgkb.cdc.gov/PHGKB/phgHome.action?action=forward&dbsource=huge&id=62889

Core Concepts in Parenchymal Kidney Disease | Fernando C. Fervenza | SpringerCore Concepts in Parenchymal Kidney Disease | Fernando C. Fervenza | Springer

Core Concepts in Parenchymal Kidney Disease provides comprehensive and state-of-the-art information on the diagnosis, treatment ... Anti-glomerular Basement Membrane Disease. Salama, Alan D.. Pages 125-135 Preview Buy Chapter $29.95 ... classification and pathogenesis of glomerular and tubulointerstitial diseases. Chapters feature various clinical scenarios and ... Core Concepts in Parenchymal Kidney Disease. Editors: Fervenza, F.C., Lin, J., Sethi, S., Singh, A.K. (Eds.) ...
more infohttp://www.springer.com/us/book/9781461481652

Rex F. Ochi, MD | Swedish Medical Center Seattle and IssaquahRex F. Ochi, MD | Swedish Medical Center Seattle and Issaquah

anti-glomerular basement membrane disease. *azotemia. *bartter syndrome. *calculus of urinary tract ...
more infohttp://www.swedish.org/swedish-physicians/profile.aspx?name=ochi+rex+ford&id=158166

Anthony M. Krajcer, M.D. | Seattle, WAAnthony M. Krajcer, M.D. | Seattle, WA

Anti-Glomerular Basement Membrane Disease. *Anti-Nuclear Antibody Measurement. *Antiphospholipid Syndrome. *Aortic Arteritis ... Sexually Transmitted Diseases Urinary Tract Infection Foot Pain Ankle Injury Hip Pain Knee Pain View More ...
more infohttps://www.swedish.org/swedish-physicians/profile.aspx?name=anthony+m+krajcer&id=158111

Jehan Zahid Bahrainwala | Faculty | About Us | Perelman School of Medicine | Perelman School of Medicine at the University of...Jehan Zahid Bahrainwala | Faculty | About Us | Perelman School of Medicine | Perelman School of Medicine at the University of...

Bahrainwala J, Stokes MB, Hannani A, Hogan J : Anti-Glomerular Basement Membrane Disease (Poster Presentation). American ... Jehan Z. Bahrainwala, M. Barry Stokes, Afshin K. Hannani, Jonathan J. Hogan: Atypical Antiglomerular Basement Membrane Disease ... Renal disease and pregnancy. Polycystic kidney disease. Kidney Donor transplant evaluation. Selected Publications. Reisinger, ... Bahrainwala J, Bern J: Diagnosis of Iron Deficiency Anemia in chronic kidney disease. Seminars in Dialysis. WB Saunders, 36(2 ...
more infohttps://www.med.upenn.edu/apps/faculty/index.php/g275/p8475115

Goodpasture Syndrome: Pathophysiology, Diagnosis, and Management. - Free Online LibraryGoodpasture Syndrome: Pathophysiology, Diagnosis, and Management. - Free Online Library

by Nephrology Nursing Journal; Health, general Acute kidney failure Care and treatment Acute renal failure Kidney diseases ... 1999). Anti glomerular basement membrane disease. Journal of the American Society of Nephrology, 10(11), 2446-2453. Madore, E, ... of anti-neutrophil cytoplasmic autoantibodies with myeloperoxidase specificity in anti-glomerular basement membrane disease. ... Course and prognosis of anti-basement membrane antibodymediated diseases: Report of 35 cases. Nephrology, Dialysis and ...
more infohttps://www.thefreelibrary.com/Goodpasture+Syndrome%3A+Pathophysiology%2C+Diagnosis%2C+and+Management-a076512453

Circulating anti-glomerular basement membrane autoantibodies against α3(IV)NC1 undetectable by commercially available enzyme...Circulating anti-glomerular basement membrane autoantibodies against α3(IV)NC1 undetectable by commercially available enzyme...

... disease have been reported with linear deposit of immunoglobulin G (IgG) along GBM, but have undetectable anti-GBM antibodies ... METHODS Sera from four patients were collected, with typical linear deposit of IgG along GBM but no anti-GBM reactivity by ... CONCLUSION Circulating anti-GBM antibodies undetectable by ELISA could recognize cryptic and conformation-dependent epitopes ... Circulating anti-GBM antibodies were detected by indirect immunofluorescence. Antigen specificity and its conformational ...
more infohttps://www.semanticscholar.org/paper/Circulating-anti-glomerular-basement-membrane-auto-Jia-Qu/92aea8a60167ced685ae4d3b214315af7ed192c2

Anti-GBM Antibody Disease Treatment & Management: Medical Care, Surgical Care, ConsultationsAnti-GBM Antibody Disease Treatment & Management: Medical Care, Surgical Care, Consultations

... in which circulating antibodies are directed against an antigen normally present in the GBM and alveolar basement membrane. The ... anti-GBM) antibody disease is a rare autoimmune disorder ... Anti-Glomerular Basement Membrane Disease. Clin J Am Soc ... linear staining of the glomerular basement membrane in a patient with anti-glomerular basement membrane (GBM) disease. Courtesy ... Anti-GBM Antibody Disease) and Anti-GBM Antibody Disease What to Read Next on Medscape. Related Conditions and Diseases. * Anti ...
more infohttps://emedicine.medscape.com/article/981258-treatment

Matthew GriffinMatthew Griffin

Spatial and Temporal Clustering of Anti-Glomerular Basement Membrane Disease.. Authors:. Mark Canney Paul V OHara Caitriona M ... Anti-donor immune responses elicited by allogeneic mesenchymal stem cells: what have we learned so far?. Authors:. Matthew D ... Monogenic causes of chronic kidney disease in adults.. Authors:. Dervla M Connaughton Claire Kennedy Shirlee Shril Nina Mann ... Patient reported health status and all-cause mortality in patients with coronary heart disease.. Authors:. Adam J N Raymakers ...
more infohttps://www.pubfacts.com/author/Matthew+Griffin

PDF] Complement deposition in renal histopathology of patients with ANCA-associated pauci-immune glomerulonephritis. | Semantic...PDF] Complement deposition in renal histopathology of patients with ANCA-associated pauci-immune glomerulonephritis. | Semantic...

RESULTS In direct immunofluorescence microscopy, C3c and C1q could be detected in glomerular capillary wall and/or mesangium in ... Characteristics and prognosis of Chinese patients with anti-glomerular basement membrane disease.. Zhao Cui, Ming-hui Zhao, ... Developments in anti-complement therapy; from disease to clinical trial.. Claire L. Harris, Richard B Pouw, David Kavanagh, ... Modified glomerular filtration rate estimating equation for Chinese patients with chronic kidney disease.. Ying-chun Ma, Li Zuo ...
more infohttps://www.semanticscholar.org/paper/Complement-deposition-in-renal-histopathology-of-Chen-Xing/72cef7c31e2696e497621d4c883bcc79aab61d92
  • r = −0.35, P = 0.046), the proportion of cellular crescents ( r = 0.67, P r = 0.64, P r = 0.72, P r = 0.50, P = 0.004) and glomerular ( r = 0.49, P = 0.007) macrophage infiltration. (ovid.com)
  • About the GBM, Alport,and anti-GBM - YouTube made with ezvid, free download at http://ezvid.com alports and anti-GBM. (lookfordiagnosis.com)
  • This clinical report adds new information to the spectrum of anti-GBM disease and suggests that neoplasia may be associated with unusual exposure of and/or immune response to epitopes in the GBM. (lookfordiagnosis.com)
  • Patients who are antineutrophilic cytoplasmic antibody (ANCA) positive with clinical presentations consistent with vasculitis are likely to benefit from aggressive therapy independent of the severity of disease. (medscape.com)
  • from disease to clinical trial. (semanticscholar.org)
  • Her special clinical interests include treating hypertension and kidney disease in pregnancy for conditions such as preeclampsia. (medstarhealth.org)
  • HLA-DPB1*0401 might be a protective allele to anti-GBM disease in Chinese patients. (cdc.gov)
  • Plasma dephosphorylated-uncarboxylated Matrix Gla-Protein (dp-ucMGP): reference intervals in Caucasian adults and diabetic kidney disease biomarker potential. (pubfacts.com)
  • Senescence marker activin A is increased in human diabetic kidney disease: association with kidney function and potential implications for therapy. (pubfacts.com)
  • Call for an appointment with your provider if you are producing less urine, or you have any other symptoms of anti-GBM disease. (medlineplus.gov)
  • The treatment with corticosteroids plus cyclophosphamide was found not to improve the renal outcome of disease (p = 0.73). (ovid.com)
  • The low incidence and fulminant course of disease preclude a large randomized controlled study to define the benefits of any given therapy. (ovid.com)
  • Dr. Phull recently completed his fellowship in pediatric pulmonary medicine where he provided the full scope of consultation, diagnostic testing and treatment of children and adolescents with chronic lung diseases. (medstarhealth.org)