ArticleBMC nephrology2013
Identical twins:one with anti-glomerular basement membrane glomerulonephritis,the other with systemic lupus erythematosus.
Article in BMC nephrology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 7 citations in OpenAlex.
- Atypical Antiglomerular Basement Membrane Disease in a Pregnant Patient with Systemic Lupus Erythematosus.Case reports in nephrology · 2023Article
- Absence of Anti-Glomerular Basement Membrane Antibodies in 200 Patients With Systemic Lupus Erythematosus With or Without Lupus Nephritis: Results of the GOODLUPUS Study.Frontiers in immunology · 2020Article
- Anti-glomerular basement membrane disease accompanied by systemic lupus erythematosus presenting central nervous system involvement.CEN case reports · 2017Article
- Establishing a tree shrew model of systemic lupus erythematosus and cell transplantation treatment.Stem cell research & therapy · 2016Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAnti-glomerular basement membrane (GBM) glomerulonephritis and systemic lupus erythematosus (SLE) are both disorders of the immune system; however, they are known as distinct diseases. Till now no clinical evidence suggests the genetic relationship between these two diseases. Herein, we present two identical twins; one was diagnosed as anti-GBM glomerulonephritis, the other SLE. This is the first clinical report on the genetic relationship between these two diseases. CASE PRESENTATION: A 25-year-old female was admitted complaining of intermittent gross hematuria for 6 months and elevated serum creatinine for 1 month. She denied hemoptysis. Laboratory examinations showed hemoglobin 7.4 g/dL, serum creatinine 7.15 mg/dL and albumin 2.8 g/dL. Urinalysis showed hematuria (484 RBCs per high-power field) and proteinuria 4+. Antinuclear antibody, complement levels and ANCAs were all normal. Renal ultrasound showed normal-sized kidneys without obstruction or masses. Serum anti-GBM antibody assay showed 119.70 RU/mL (normal range, <20 RU/mL). Chest X-ray was normal. She was diagnosed as anti-GBM glomerulonephritis and received plasma exchange (2000-3000 ml plasma/exchange, 5 turns), methylprednisolone 0.5 g for three days, plus cyclophosphamide. Although serum anti-GBM antibodies decreased gradually to a normal range, her renal function did not improve. One month later, her identical twin sister was diagnosed as SLE based on malar erythema, arthralgia, antinuclear antibody positive with liter 1:1000, and Anti-Smith (Sm) antibody ++. Anti-GBM antibody and complements were within normal ranges. Further study showed these twins were HLA-DRB1*1501 homozygotes.
conclusionThe presence of identical twins having anti-GBM nephritis and SLE respectively provides clinical evidence to support that anti-GBM nephritis and lupus may share a common genetic background to some extent, while environment may contribute to disease evolution in part.
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