Search results for "lupus nephritis"

showing 10 items of 32 documents

Activation of the lectin pathway in murine lupus nephritis.

2004

In systemic lupus erythematosus (SLE), hypocomplementaemia and complement deposition have been described both in man and in experimental models. A major involvement of the classical pathway of complement activation has been demonstrated in this disease, however relatively little is known about the involvement of the lectin pathway. Therefore in the present study we have analyzed the activity of all three pathways of complement activation in murine models of SLE. In the mouse, MBL is expressed in two forms, namely MBL-A and MBL-C. In the present study young and old MRL-lpr and control MRL+/+ mice were compared for the levels of complement activity with specific attention for the lectin pathw…

Mice Inbred MRL lprImmunologychemical and pharmacologic phenomenaurologic and male genital diseasesmedicine.disease_causeAutoimmunityClassical complement pathwayMiceImmune systemimmune system diseasesMurine lupusLectinsmedicineAnimalsskin and connective tissue diseasesMolecular BiologyAutoantibodiesChemistrybacterial infections and mycosesmedicine.diseaseLupus NephritisComplement systemLectin pathwayImmunologyAlternative complement pathwayNephritisMolecular immunology
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Correlation of renal tubular epithelial cell-derived interleukin-18 up-regulation with disease activity in MRL-Faslpr mice with autoimmune lupus neph…

2002

Objective MRL-Faslpr mice spontaneously develop an autoimmune disease that mimics systemic lupus erythematosus in humans. Infiltrating T cells expressing interferon-γ (IFNγ) are responsible for the autoimmune kidney destruction in MRL-Faslpr mice, and interleukin-18 (IL-18) released by mononuclear phagocytes stimulates T cells to produce the IFNγ. Since MRL-Faslpr T cells are characterized by an overexpression of the IL-18 receptor accessory chain, we sought to determine the impact of IL-18 on the progression of lupus nephritis in MRL-Faslpr mice. Methods IL-18 expression in sera and kidney tissues from MRL-Faslpr mice was determined by enzyme-linked immunosorbent assay (ELISA), reverse tra…

Mice Inbred MRL lprmedicine.medical_treatmentImmunologyBlotting WesternLupus nephritisEnzyme-Linked Immunosorbent AssayBiologymedicine.disease_causeAutoimmunityAutoimmune DiseasesMiceRheumatologyimmune system diseasesInterferonmedicineImmunology and AllergyMacrophageAnimalsPharmacology (medical)Interferon gammaskin and connective tissue diseasesLupus erythematosusCell adhesion moleculeReverse Transcriptase Polymerase Chain ReactionCaspase 1Interleukin-18Epithelial Cellsmedicine.diseaseMolecular biologyImmunohistochemistryLupus NephritisUp-RegulationCytokineKidney TubulesImmunologymedicine.drugArthritis and rheumatism
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Interleukin 6 (IL-6) deficiency delays lupus nephritis in MRL-Faslpr mice: the IL-6 pathway as a new therapeutic target in treatment of autoimmune ki…

2009

Objective.To investigate the pathophysiological effect of interleukin 6 (IL-6) on lupus nephritis in MRL-Faslprmice.Methods.We generated IL-6-deficient MRL-Faslprmice using a backcross/intercross breeding scheme. Renal pathology was evaluated using immunohistochemistry detection for macrophages, lymphocytes, vascular cell adhesion molecule-1 (VCAM-1), and TUNEL (terminal deoxynucleotide transferase-mediated dUTP nick end-labeling) for apoptotic cells, and renal IgG and C3 deposition by immunofluorescence staining. Expression of inflammatory markers in the spleen was analyzed by quantitative real-time reverse transcription-polymerase chain reaction. Serum cytokine concentrations were detecte…

Pathologymedicine.medical_specialtyMice Inbred MRL lprImmunologyLupus nephritisVascular Cell Adhesion Molecule-1SpleenKidneyInterferon-gammaMiceLife ExpectancyRheumatologyImmunology and AllergyMedicineAnimalsHumansLupus Erythematosus Systemicfas ReceptorInterleukin 6InflammationMice KnockoutKidneyMice Inbred BALB CLupus erythematosusbiologybusiness.industryInterleukin-6Kidney metabolismmedicine.diseaseLupus NephritisInterleukin-10Proteinuriamedicine.anatomical_structureRenal pathologyImmunologybiology.proteinFemalebusinessBiomarkersSpleenKidney diseaseSignal TransductionThe Journal of rheumatology
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Segmented relationships to model erosion of regression effect in Cox regression

2010

In this article we propose a parsimonious parameterisation to model the so-called erosion of the covariate effect in the Cox model, namely a covariate effect approaching to zero as the follow-up time increases. The proposed parameterisation is based on the segmented relationship where proper constraints are set to accomodate for the erosion. Relevant hypothesis testing is discussed. The approach is illustrated on two historical datasets in the survival analysis literature, and some simulation studies are presented to show how the proposed framework leads to a test for a global effect with good power as compared with alternative procedures. Finally, possible generalisations are also present…

Statistics and ProbabilitybreakpointEpidemiologyProportional hazards modelLiver Cirrhosis BiliaryErosion (morphology)Lupus NephritisSet (abstract data type)Segmented regressionHealth Information ManagementNonlinear DynamicsRegression toward the meanCox modelCovariateStatisticsEconometricsHumansComputer SimulationSettore SECS-S/05 - Statistica SocialeSettore SECS-S/01 - Statisticaerosion of effectStatistical hypothesis testingMathematicsFollow-Up StudiesProportional Hazards Models
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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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Genetic predisposition—is lupus nephritis a question of copy numbers?**Copy number polymorphism in Fcgr3 predisposes to glomerulonephritis in rats an…

2006

TransplantationNephrologybusiness.industryImmunologyGenetic predispositionLupus nephritisMedicinebusinessmedicine.diseaseNephrology Dialysis Transplantation
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DNASE1L3 deficiency, new phenotypes, and evidence for a transient type I IFN signaling.

2022

Background: Deoxyribonuclease 1 like 3 (DNASE1L3) is a secreted enzyme that has been shown to digest the extracellular chromatin derived from apoptotic bodies, and DNASE1L3 pathogenic variants have been associated with a lupus phenotype. It is unclear whether interferon signaling is sustained in DNASE1L3 deficiency in humans. Objectives: To explore interferon signaling in DNASE1L3 deficient patients. To depict the characteristic features of DNASE1L3 deficiencies in human. Methods: We identified, characterized, and analyzed five new patients carrying biallelic DNASE1L3 variations. Whole or targeted exome and/or Sanger sequencing was performed to detect pathogenic variations in five juvenile …

VasculitisEndodeoxyribonucleasesImmunologyDNAInflammatory Bowel DiseasesLupus NephritisChromatinANCA Apoptosis DNASE1L3 Interferon-stimulated genes Nucleic acids Systemic lupus erythematosus Type I interferonAntibodies Antineutrophil CytoplasmicSettore MED/38 - Pediatria Generale E SpecialisticaPhenotypeInterferon Type IImmunology and AllergyHumansLupus Erythematosus SystemicInterferonsJournal of clinical immunology
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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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O33 Per-protocol repeat kidney biopsy portends relapse and long-term outcome in incident cases of proliferative lupus nephritis

2020

Background In patients with Lupus Nephritis (LN), clinical response to treatment and renal histopathology have been shown to be discordant. We investigated whether per-protocol repeat renal biopsies are predictive of LN relapses and long-term impairment of renal function. Methods Forty-two patients with an incident biopsy-proven active proliferative (class III/IV ± V) LN from the LN database of the Universite catholique de Louvain were included in the present retrospective study. Per-protocol repeat kidney biopsies were performed in all patients after a median time of 24.3 (IQR: 21.3–26.2) months. The NIH activity index (AI) and chronicity index (CI) scores were assessed in both baseline an…

medicine.medical_specialtyKidneyCreatinineProteinuriamedicine.diagnostic_testbusiness.industryLupus nephritisRenal functionRetrospective cohort studymedicine.diseaseResponse to treatmentGastroenterologychemistry.chemical_compoundmedicine.anatomical_structurechemistryInternal medicineBiopsymedicinemedicine.symptombusinessOral presentations
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Haemolytic-uraemic syndrome during severe lupus nephritis: efficacy of plasma exchange

2012

Systemic lupus erythematosus (SLE) has been described as a cause of thrombotic microangiopathy, especially thrombotic thrombocytopenic purpura (TTP). Haemolytic-uraemic syndrome (HUS) is less frequent in SLE. We report a case of such an association during an episode of severe lupus nephritis in a young woman, who was successfully treated with steroids, cyclophosphamide and especially plasma exchange with plasma replacement. This report highlights the importance of recognising atypical HUS in SLE patients by looking for schistocytes in case of haemolytic anemia with a negative antiglobulin test, in order to begin plasma exchange.

medicine.medical_specialtyThrombotic microangiopathyCyclophosphamidebusiness.industryAnemiaThrombotic thrombocytopenic purpuraLupus nephritismedicine.diseaseGastroenterologySchistocytePharmacotherapyimmune system diseaseshemic and lymphatic diseasesInternal medicineInternal MedicineMedicineskin and connective tissue diseasesbusinessAnti-SSA/Ro autoantibodiesmedicine.drugInternal Medicine Journal
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