title: Identical twins:one with anti-glomerular basement membrane glomerulonephritis,the other with systemic lupus erythematosus.
abstract: BACKGROUND
  Anti-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.
  
  
  METHODS
  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.
  
  
  CONCLUSIONS
  The 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.
authors.forename: Xiaoxia
authors.initials: X
authors.lastname: Liu
authors.forename: Yu
authors.initials: Y
authors.lastname: Wu
authors.forename: Yuan
authors.initials: Y
authors.lastname: Yang
authors.forename: Jue
authors.initials: J
authors.lastname: Wang
authors.forename: Ye
authors.initials: Y
authors.lastname: Tao
authors.forename: Ping
authors.initials: P
authors.lastname: Fu
authors.affiliation: Department of Nephrology, Chengdu, Sichuan Province, China. hzxawy@scu.edu.cn.
authors.forename: Zhangxue
authors.initials: Z
authors.lastname: Hu
mesh_terms: D000328:Adult; D019867:Anti-Glomerular Basement Membrane Disease / Q000175:diagnosis* / Q000235:genetics*; D003937:Diagnosis, Differential; D005260:Female; D020022:Genetic Predisposition to Disease; D005820:Genetic Testing; D006801:Humans; D008180:Lupus Erythematosus, Systemic / Q000175:diagnosis* / Q000235:genetics*; D014430:Twins, Monozygotic / Q000235:genetics*