ArticleBMC nephrology2019
Recurrence of Goodpasture syndrome without circulating anti-glomerular basement membrane antibodies after kidney transplant, a case report.
Article in BMC nephrology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 16 citations in OpenAlex.
- Article
- Outcomes After Kidney Transplantation in Antiglomerular Basement Membrane Disease.Kidney international reports · 2025Article
- Unleashing the power of complement activation: unraveling renal damage in human anti-glomerular basement membrane disease.Frontiers in immunology · 2023Review
- Clinical outcomes and temporal trends of immunological and non-immunological rare diseases in adult kidney transplant.BMC nephrology · 2021Article
- Recurrence and Outcome of Anti-Glomerular Basement Membrane Glomerulonephritis After Kidney Transplantation.Kidney international reports · 2021Article
- SARS-CoV-2 infection and recurrence of anti-glomerular basement disease: a case report.BMC nephrology · 2021Article
- Long-term outcomes in kidney transplant recipients with end-stage kidney disease due to anti-glomerular basement membrane disease.Clinical transplantation · 2021Article
- Recurrent Glomerulonephritis after Renal Transplantation: The Clinical Problem.International journal of molecular sciences · 2020Review
- Article
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundGoodpasture Syndrome (GS) is an autoimmune disease caused by the development of auto-antibodies against the Glomerular Basement Membrane (GBM). Linear deposit of immunoglobulins G on the GBM detected by immunofluorescence analysis of renal biopsies is a GS pathognomonic finding. GS is commonly monophasic and its incidence is 1.6 case per million per year. CASE PRESENTATION: This report describes and discusses the case of a 40-year-old woman who one year after allograft kidney transplant, presented with acute pulmonary and renal symptoms of GS, leading to acute graft dysfunction, without circulating anti-GBM antibody detection in laboratory assays. She received a living donor kidney transplant 4 years after the first diagnosis of GS without circulating anti-GBM antibodies, when considered in remission.
conclusionsIn both episodes, the diagnosis of GS was based exclusively on the kidney biopsy that showed rapidly progressing glomerulonephritis with deposition of immunoglobulins G on the GBM. Although rare, the management of patients with GS without circulating anti-GBM antibodies is difficult due to the lack of standardized follow-up guidelines to reduce the risk of GS recurrence after kidney transplantation.
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