Pediatric anti-glomerular basement membrane glomerulonephritis

Trivedi, Vipul A.; Malter, James S.; Guillery, Edward N.

doi:10.1002/(sici)1098-1101(1998)13:2<69::aid-jca4>3.0.co;2-6

Cited by 3 publications

(4 citation statements)

References 4 publications

(8 reference statements)

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“…Most cases of anti-GBM disease in pediatric patients have acute presentations with diffuse glomerular disease, including severe fibrinoid necrosis along with cellular crescent formation, with subsequent glomerular scarring leading to end-stage renal disease [6, 11, 20, 21, 22, 23, 24, 25]. More recent reports, where diagnosis and commencement of plasmapheresis has been prompt, have led to better outcomes [7, 26, 27, 28].…”

Section: Discussionmentioning

confidence: 99%

Anti-GBM disease after nephrectomy for xanthogranulomatous pyelonephritis in a patient expressing HLA DR15 major histocompatibility antigens: a case report

O’Hagan¹,

Mallett²,

Convery³

et al. 2015

CNCS

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Antiglomerular basement membrane (anti-GBM) antibody disease is uncommon in the pediatric population. There are no cases in the literature describing the development of anti-GBM disease following XGP or nephrectomy. We report the case of a 7-year-old boy with no past history of urological illness, treated with antimicrobials and nephrectomy for diffuse, unilateral xanthogranulomatous pyelonephritis (XGP). Renal function and ultrasound scan of the contralateral kidney postoperatively were normal. Three months later, the child represented in acute renal failure with rapidly progressive glomerulonephritis requiring hemodialysis. Renal biopsy showed severe crescentic glomerulonephritis with 95% of glomeruli demonstrating circumferential cellular crescents. Strong linear IgG staining of the glomerular basement membranes was present, in keeping with anti-GBM disease. Circulating anti-GBM antibodies were positive. Treatment with plasma exchange, methylprednisolone, and cyclophosphamide led to normalization of anti-GBM antibody titers. Frequency of hemodialysis was reduced as renal function improved, and he is currently independent of dialysis with estimated glomerular filtration rate 20.7 mls/min/1.73 m2. Case studies in the adult literature have reported the development of a rapidly progressive anti-GBM antibody-induced glomerulonephritis following renal surgery where patients expressed HLA DR2/HLA DR15 major histocompatibility (MHC) antigens. Of note, our patient also expresses the HLA DR15 MHC antigen.

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Section: Discussionmentioning

confidence: 99%

Anti-GBM disease after nephrectomy for xanthogranulomatous pyelonephritis in a patient expressing HLA DR15 major histocompatibility antigens: a case report

O’Hagan¹,

Mallett²,

Convery³

et al. 2015

CNCS

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“…However, the patient was left with 30% fibrous crescents [ 5 ]. Most cases of anti-GBM disease in paediatric patients have acute presentations with diffuse glomerular disease and severe fibrinoid necrosis along with cellular crescent formation with subsequent glomerular scarring and severe chronic disease leading to end-stage renal disease [ 4 ]. Being that there is direct antibody formation to the non-collagen domain of type IV collagen, the involvement is typically diffuse, with all glomerular lesions being of the same age.…”

Section: Discussionmentioning

confidence: 99%

“…Combination of rapidly progressive glomerulonephritis and pulmonary haemorrhage caused by this anti-GBM formation is known as Goodpasture’s syndrome [ 3 ]. Pulmonary haemorrhage is present in adult cases, yet children can develop isolated renal disease without pulmonary involvement [ 4,5 ]. Pulmonary involvement with Goodpasture’s syndrome is therefore less common in younger children [ 5 ].…”

Section: Introductionmentioning

confidence: 99%

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Rescue of renal function in a 3-year-old girl with Goodpasture's syndrome with a brief review of literature

Dixit

Kirschner

Bulimbasic

et al. 2010

Clinical Kidney Journal

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Goodpasture’s syndrome has been documented in only a handful of children under the age of four. We describe a 3-year-old girl presenting with anaemia and renal failure whose kidney biopsy showed anti-glomerular basement membrane (GBM) disease. She was treated aggressively with pulse steroids, plasmapheresis and monthly infusions of cyclophosphamide. After months of aggressive immunosuppression, her renal function normalized, and her anti-GBM antibody disappeared. A year after the onset, she underwent a second kidney biopsy for persistent proteinuria and hypertension that surprisingly showed focal sclerosing glomerulonephritis, an unreported finding at this age. The biopsy showed deposition of antibody on the GBM despite the fact that anti-GBM antibody had normalized in the serum 5 months earlier. Mycophenolate mofetil was added to the immunosuppression at that point. At her 3-year follow-up, creatinine clearance was 88.4 mL/min/1.73 m2, proteinuria was 408 mg/day and blood pressure was controlled with enalapril 0.2 mg/kg/day. She has not had a relapse or abnormal anti-GBM antibody for 30 months, but her renal prognosis remains guarded. To our knowledge, this is the youngest patient to have a successful rescue of renal function after isolated Goodpasture’s syndrome.

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Maternal alloimmune IgG causes anti-glomerular basement membrane disease in perinatal transgenic mice that express human laminin α5

Abrahamson

Steenhard

Stroganova

et al. 2019

Kidney International

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Pediatric anti-glomerular basement membrane glomerulonephritis

Cited by 3 publications

References 4 publications

Anti-GBM disease after nephrectomy for xanthogranulomatous pyelonephritis in a patient expressing HLA DR15 major histocompatibility antigens: a case report

Anti-GBM disease after nephrectomy for xanthogranulomatous pyelonephritis in a patient expressing HLA DR15 major histocompatibility antigens: a case report

Rescue of renal function in a 3-year-old girl with Goodpasture's syndrome with a brief review of literature

Maternal alloimmune IgG causes anti-glomerular basement membrane disease in perinatal transgenic mice that express human laminin α5

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