Search results for "glomerulonephritis"

showing 10 items of 45 documents

Reconstitution of the Complement Function in C1q-Deficient (C1qa−/−) Mice with Wild-Type Bone Marrow Cells

2001

Abstract Besides Ab-independent and Ab-dependent activation of the complement classical pathway in host defense, C1q plays a key role in the processing of immune complexes and in the clearance of apoptotic cells. In humans, C1q deficiency leads to systemic lupus erythematosus-like symptoms in over 90% of the cases, thus making this defect a strong disease susceptibility factor. Similarly, C1q-deficient mice (C1qa−/−) develop systemic lupus erythematosus-like symptoms, such as autoantibodies and glomerulonephritis. We have previously provided evidence that C1q is produced by cells of the monocyte-macrophage lineage. In this study, we have tested whether transplantation of bone marrow cells w…

Malemedicine.medical_treatmentImmunologychemical and pharmacologic phenomenaHematopoietic stem cell transplantationBiologyMiceClassical complement pathwayImmune systemimmune system diseasesY ChromosomemedicineAnimalsLupus Erythematosus SystemicImmunology and AllergyTissue DistributionRNA Messengerskin and connective tissue diseasesBone Marrow TransplantationMice KnockoutLupus erythematosusComplement C1qHematopoietic Stem Cell TransplantationGlomerulonephritismedicine.diseaseMice Inbred C57BLTransplantationKineticsmedicine.anatomical_structureImmunologyFemaleBone marrowStem cellThe Journal of Immunology
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Targeting transcription factor Stat4 uncovers a role for interleukin-18 in the pathogenesis of severe lupus nephritis in mice

2011

Polymorphisms in the transcription factor Stat4 gene have been implicated as risk factors for systemic lupus erythematosus. Although some polymorphisms have a strong association with autoantibodies and nephritis, their impact on pathophysiology is still unknown. To explore this further we used signal transducers and activators of transcription 4 (Stat4) knockout MRL/MpJ-Fas(lpr)/Fas(lpr) (MRL-Fas(lpr)) mice and found that they did not differ in survival or renal function from Stat4-intact MRL-Fas(lpr) mice. Circulating interleukin (IL)-18 levels, however, were elevated in Stat4-deficient compared to Stat4-intact mice, suggesting that this interleukin might contribute to the progression of l…

Malemusculoskeletal diseasesMice Inbred MRL lprchronic inflammationLupus nephritisKidneyInterleukin-23ArticleProinflammatory cytokineOligodeoxyribonucleotides AntisenseGene Knockout TechniquesInterferon-gammaMiceimmune system diseasesmedicineAnimalsskin and connective tissue diseasesSTAT4DNA PrimersAutoimmune diseaseMice Knockoutlupus nephritisMice Inbred BALB CBase Sequencebusiness.industryGene Transfer TechniquesInterleukin-18InterleukinGlomerulonephritishemic and immune systemsSTAT4 Transcription Factormedicine.diseaseInterleukin-12chronic glomerulonephritisNephrologyImmunologyInterleukin 18FemalebusinessNephritisKidney International
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A case of endocarditis with vasculitis due to Actinobacillus actinomycetemcomitans: a 16S rDNA signature for distinction from related organisms.

1998

Microbiology (medical)DNA BacterialVasculitisAggregatibacter actinomycetemcomitansMicrobiologyActinobacillus InfectionsGlomerulonephritisMedicineEndocarditisHumansRibosomal DNAbiologybusiness.industryPasteurellaceaeEndocarditis BacterialMiddle Aged16S ribosomal RNAmedicine.diseasebiology.organism_classificationInfectious DiseasesEndocardial diseaseImmunologyActinobacillusFemalebusinessVasculitisClinical infectious diseases : an official publication of the Infectious Diseases Society of America
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Metalloprotease meprin beta in rat kidney: glomerular localization and differential expression in glomerulonephritis

2008

Meprin (EC 3.4.24.18) is an oligomeric metalloendopeptidase found in microvillar membranes of kidney proximal tubular epithelial cells. Here, we present the first report on the expression of meprin beta in rat glomerular epithelial cells and suggest a potential involvement in experimental glomerular disease. We detected meprin beta in glomeruli of immunostained rat kidney sections on the protein level and by quantitative RT-PCR of laser-capture microdissected glomeruli on the mRNA level. Using immuno-gold staining we identified the membrane of podocyte foot processes as the main site of meprin beta expression. The glomerular meprin beta expression pattern was altered in anti-Thy 1.1 and pas…

Pathologymedicine.medical_specialtyNephrology/Acute Renal Failure10039 Institute of Medical GeneticsKidney GlomerulusFluorescent Antibody Techniquelcsh:MedicinePodocyte foot610 Medicine & health1100 General Agricultural and Biological SciencesBiologyurologic and male genital diseasesHeymann NephritisGlomerulonephritisWestern blot1300 General Biochemistry Genetics and Molecular BiologymedicineAnimalsRNA MessengerMicroscopy Immunoelectronlcsh:ScienceKidneyMetalloproteinase1000 MultidisciplinaryMultidisciplinarymedicine.diagnostic_testPodocytesReverse Transcriptase Polymerase Chain Reactionurogenital systemImmune Seralcsh:RNephrology/Chronic Kidney DiseaseMetalloendopeptidasesGlomerulonephritismedicine.diseaseMolecular biologyRats Inbred F344Ratsmedicine.anatomical_structureRats Inbred Lew570 Life sciences; biologylcsh:QNephritisImmunostainingResearch Article
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Acanthocyturia—A characteristic marker for glomerular bleeding

1991

Acanthocyturia—A characteristic marker for glomerular bleeding. Erythrocyte morphology by phase contrast microscopic examination (PCM) of the urine is widely employed in distinguishing glomerular from nonglomerular bleeding. The proposed percentages of dysmorphic red cells are significant for glomerular bleeding in the range of 10 to 80% in the literature, because there is no clear cut definition of “dysmor-phism.” In the present study midstream urine samples of 351 patients with hematuria (> 8 erythrocytes/μl) and of 33 healthy controls were examined. The various dysmorphic red cells were analyzed by PCM according to a detailed hematological classification. Most of the dysmorphic red cells…

Pathologymedicine.medical_specialtyRenal glomerulusKidney GlomerulusEchinocyteAcanthocytesHemorrhageUrineurologic and male genital diseasesBiopsymedicineHumansUrine cytologyKidneymedicine.diagnostic_testRed Cellurogenital systembusiness.industryOsmolar ConcentrationGlomerulonephritisHydrogen-Ion Concentrationmedicine.diseasefemale genital diseases and pregnancy complicationsProteinuriamedicine.anatomical_structureNephrologyKidney DiseasesAcanthocytebusinessBiomarkersKidney International
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New developments in IL-6 dependent biology and therapy: where do we stand and what are the options?

2005

Interleukin-6 (IL-6) is a four-helical protein which, on target cells, binds to a specific IL-6-receptor and two molecules of the promiscuous signal transducing protein gp130. Structure-function analysis defined three molecular contact sites between IL-6 and its receptor subunits. Using this information, competitive antagonistic proteins as well as hyperagonistic proteins were developed. Possible therapeutic applications of IL-6 antagonists are in IL-6 dependent haematological disorders (Castleman's disease, POEMS syndrome, multiple myeloma) and bone diseases (Paget's disease, osteoporosis). Designer IL-6 antagonists could suppress inflammatory activity in rheumatic and autoimmune diseases …

PharmacologySystemic lupus erythematosusbiologybusiness.industryUnstable anginamedicine.medical_treatmentGlomerulonephritisGeneral Medicinemedicine.diseaseGlycoprotein 130CytokineImmunologymedicinebiology.proteinPharmacology (medical)businessInterleukin 6ReceptorMultiple myelomaExpert opinion on investigational drugs
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Autoreactivity to mouse C1q in a murine model of SLE.

1995

A large proportion of systemic lupus erythematosus (SLE) patients develop glomerulonephritis, coincident with the appearance of autoantibodies to C1q, the Fc-recognizing collagen-like subcomponent of the first component of complement, C1. The MRL/lpr/lpr mouse is an established model for SLE, developing both antinuclear and anti-type II collagen autoantibodies, and rheumatoid factors(s), exhibiting reduced complement levels and later on developing glomerulonephritis and often arthritis. We report here an age-dependent decrease in serum C1q levels coincident with the development of IgG2b autoantibodies reactive with mouse C1q in MRL/lpr/lpr mice. Unlike IgG2b, although high levels of IgM, Ig…

Systemic diseaseImmunologyArthritischemical and pharmacologic phenomenaEnzyme-Linked Immunosorbent Assayurologic and male genital diseasesmedicine.disease_causeAutoimmunityMiceRheumatologyimmune system diseasesImmunology and AllergyMedicineAnimalsLupus Erythematosus Systemicskin and connective tissue diseasesAutoantibodiesLupus erythematosusbusiness.industryComplement C1qAutoantibodyGlomerulonephritismedicine.diseaseConnective tissue diseaseLupus NephritisDisease Models AnimalImmunologybusinessAnti-SSA/Ro autoantibodiesRheumatology international
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Angiotensin II Type 1 Receptor Antibodies Are Higher in Lupus Nephritis and Vasculitis than Other Glomerulonephritis Patients

2022

AbstractAngiotensin II type 1 receptor (AT1R) antibodies are considered non-HLA (human leukocyte antigen) antibodies connected with humoral rejection after kidney transplantation. The role of AT1R antibodies in the pathogenesis of glomerular diseases and systemic vasculitis is unknown. We assessed the level of AT1R antibodies in 136 patients with different types of glomerulonephritis and systemic vasculitis and we observed kidney function and proteinuria, serum albumin and total protein levels for 2 years. The mean levels of AT1R antibodies were the following: 6.00 ± 1.31 U/ml in patients with membranous nephropathy (n = 18), 5.67 ± 1.31 U/ml with focal and segmental glomerulosclerosis (n =…

VasculitisImmunologySystemic VasculitisGlomerulonephritis IGAGeneral MedicineGlomerulonephritis MembranousReceptor Angiotensin Type 1Angiotensin II type 1 receptor antibodiesAntibodies Antineutrophil CytoplasmicGlomerulonephritisLupus nephritisHLA AntigensCreatinineImmunology and AllergyHumansSerum AlbuminArchivum Immunologiae et Therapiae Experimentalis
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Extrahepatic Morbidity and Mortality of Chronic Hepatitis C

2015

Chronic hepatitis C virus (HCV) infection is associated with several extra-hepatic manifestations. Patients with HCV may develop mixed cryoglobulinemia and its sequelae, ranging from cutaneous and visceral vasculitis to glomerulonephritis and B cell non-Hodgkin’s lymphoma. HCV-infected patients have increased rates of insulin resistance, diabetes and atherosclerosis, which may lead to increased cardiovascular morbidity and mortality. Neurologic manifestations of HCV infection include fatigue and cognitive impairment. The mechanisms causing the extra-hepatic effects of HCV infection are likely multifactorial and may include endocrine effects, HCV replication in extra-hepatic cells, or a heig…

VasculitisLymphomaGlomerulonephritis/epidemiology/virologyLymphoma/epidemiology/virologyHepatitis C virusAlpha interferonHepacivirusddc:616.07Cryoglobulinemia/epidemiology/virologymedicine.disease_causeAntiviral AgentsAntiviral Agents/administration & dosage/pharmacology/therapeutic useHepacivirus/drug effects/pathogenicityLiver diseasechemistry.chemical_compoundGlomerulonephritisDiabetes mellitusRibavirinmedicineHumansGlucose Metabolism Disorders/epidemiology/virologyInterferon alfaGlucose Metabolism Disordersddc:616Hepatologybusiness.industryHepatitis C Chronic/drug therapy/epidemiology/immunology/mortality/virologyRibavirinVasculitis/epidemiology/virologyGastroenterologyInterferon-alphavirus diseasesHepatitis C Chronicmedicine.diseaseCryoglobulinemiadigestive system diseasesCryoglobulinemiachemistryRibavirin/pharmacology/therapeutic useHCVImmunologyMorbiditybusinessVasculitisInterferon-alpha/pharmacology/therapeutic usemedicine.drugGastroenterology
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Anti‐laminin auto antibodies in ANCA‐associated vasculitis

2000

Background. Endothelial cell damage occurs during vasculitic processes in vivo. With the alteration of the endothelium, exposure to basement membrane components may occur with induction of humoral immunity. Methods. In the present study, we evaluated the prevalence of antibodies against the basement membrane antigen laminin (LMN) in patients with ANCA-associated systemic vasculitis (AASV), pathologic controls (systemic lupus erythematosus, mixed cryoglobulinaemia, Henoch Schonlein purpura, primary glomerulonephritis) and normal individuals. Results. By ELISA, 21.6% of AASV (16/74) and 10% of pathologic controls (3/30), but only one of the normal controls (2.8%) had these antibodies (P = 0.0…

VasculitisPathologymedicine.medical_specialtyHenoch-Schonlein purpuraMyeloblastinEnzyme-Linked Immunosorbent AssayAntibodies Antineutrophil CytoplasmicEpitopesAntigenReference Valuesimmune system diseasesmedicineHumansReference Valuecardiovascular diseasesAutoantibodiesPeroxidaseAnti-neutrophil cytoplasmic antibodyTransplantationbusiness.industrySerine EndopeptidasesGranulomatosis with PolyangiitisGlomerulonephritismedicine.diseaseAutoantibodieSerine EndopeptidaseNephrologyImmunologyEpitopeLamininGranulomatosis with PolyangiitiGranulomatosis with polyangiitisVasculitisbusinessMicroscopic polyangiitisHumanSystemic vasculitisNephrology Dialysis Transplantation
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