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Ulcerative colitis in a renal transplant patient with previous Goodpasture disease
A M Hibbs1, B Bznik-Cizman, M Guttenberg
1Division of Nephrology, The Children's Hospital of Philadelphia, PA 19104, USA.
Insights
This case study describes a young boy with end-stage renal disease (ESRD) due to anti-glomerular basement membrane (anti-GBM) disease who later developed ulcerative colitis. His homozygosity for HLA DR2 may link these rare autoimmune conditions.
Area of Science:
- Nephrology
- Immunology
- Gastroenterology
Background:
- A 6-year-old boy presented with end-stage renal disease (ESRD) attributed to anti-glomerular basement membrane (anti-GBM) disease.
- He subsequently developed ulcerative colitis during immunosuppressive therapy for anti-GBM disease.
Observation:
- The patient underwent a renal transplant and later a pancolectomy for ulcerative colitis.
- At 14 years old, he remained asymptomatic for both conditions.
- Genetic analysis revealed homozygosity for HLA DR2.
Findings:
- The co-occurrence of anti-GBM disease and ulcerative colitis is a novel observation.
- The patient's HLA DR2 homozygosity is noted.
Implications:
- This case suggests a potential genetic predisposition, possibly linked to HLA DR2 homozygosity, for developing both anti-GBM disease and ulcerative colitis.
- Further research may elucidate shared etiological factors for these distinct autoimmune disorders.
Abstract:
A renal transplant was performed in a 6-year-old boy who developed end stage renal disease (ESRD) after presenting with antiglomerular basement membrane (anti-GBM) disease. At 10 years of age he developed ulcerative colitis while being immunosuppressed with cyclosporin, prednisone, and azothioprine. He had a pancolectomy, and at 14 years has no symptoms of ulcerative colitis or anti-GBM disease. HLA typing revealed that he was homozygous for HLA DR2. The co-occurrence of anti-GBM disease and ulcerative colitis has not previously been described. Although there is no known common etiology for these two autoimmune diseases, we propose that the patient's homozygosity at HLA DR2 may have predisposed him to both.