Identical twins:one with anti-glomerular basement membrane glomerulonephritis,the other with systemic lupus erythematosus

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 presentationA 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.

• Publication year

  2013

• Venue

  BMC Nephrology

• Publication date

  2013-12-20

• Fields of study

  Medicine

• Identifiers
  DOI 10.1186/1471-2369-14-277PMID 24359316PMCID 3878216
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

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