New Ways of Understanding Membranous Nephropathy.

dc.contributor.authorTrujillo, Hernando
dc.contributor.authorAlonso, Marina
dc.contributor.authorPraga, Manuel
dc.date.accessioned2025-01-07T13:20:36Z
dc.date.available2025-01-07T13:20:36Z
dc.date.issued2020-03-31
dc.description.abstractIn the last decade, great advances have been made in the field of membranous nephropathy (MN). The autoimmune nature of the disease has been confirmed with the description of diverse antigens, and few but very important prospective trials regarding treatment alternatives have been published, changing profoundly the way we understand this entity. Nowadays, an individualized therapeutic scheme based on clinical and serologic data appears to be the most appropriate method to manage patients with MN. Although there is still a long way to go, it is expected that future scientific progress will enable a patient-centered medicine based on concept-driven therapies. MN is the most common cause of nephrotic syndrome (NS) in white adults. Approximately one-third of patients achieve spontaneous remission, one-third remain stable, and one-third have an aggressive course with persistent NS and deterioration of renal function. About 80% of patients have circulating autoantibodies to phospholipase A2 receptor 1. Numerous therapies have been described including alkylating agents, rituximab, and calcineurin inhibitors, but new drugs are currently being explored. Here, we review the most important aspects regarding MN with an emphasis on results of the most recent clinical trials and pathophysiologic advances. Key Messages: 1. Evolving pathophysiologic concepts and recently published clinical trials have deeply changed our view of MN. 2. Most patients with MN present autoantibodies against diverse glomerular antigens. 3. Currently, an individual patient-centered management based on clinical and serologic markers is the most adequate approach to treat patients with MN.
dc.identifier.doi10.1159/000506948
dc.identifier.essn2235-3186
dc.identifier.pmid32229730
dc.identifier.unpaywallURLhttps://www.karger.com/Article/Pdf/506948
dc.identifier.urihttps://hdl.handle.net/10668/25447
dc.issue.number6
dc.journal.titleNephron
dc.journal.titleabbreviationNephron
dc.language.isoen
dc.organizationSAS - Hospital Universitario Reina Sofía
dc.page.number261-271
dc.pubmedtypeJournal Article
dc.pubmedtypeReview
dc.rights.accessRightsopen access
dc.subjectAutoimmune diseases
dc.subjectGlomerulonephritis
dc.subjectMembranous nephropathy
dc.subjectNephrotic syndrome
dc.subjectPhospholipase A2 receptor
dc.subject.meshAdult
dc.subject.meshAutoantibodies
dc.subject.meshCalcium-Binding Proteins
dc.subject.meshComplement System Proteins
dc.subject.meshGlomerulonephritis, Membranous
dc.subject.meshHumans
dc.subject.meshKidney Function Tests
dc.subject.meshN-Acetylglucosaminyltransferases
dc.subject.meshReceptors, Phospholipase A2
dc.subject.meshThrombospondins
dc.titleNew Ways of Understanding Membranous Nephropathy.
dc.typeresearch article
dc.type.hasVersionVoR
dc.volume.number144

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