Anti-glomerular basement membrane (anti-GBM) glomerulonephritis is a rare cause of rapidly progressive glomerulonephritis in children. The case described is a 14-year-old girl who was admitted with an acute onset of generalized edema and elevated blood pressure. Initial investigations identified urinary abnormalities and systemic features of nephrotic and nephritic involvement: hematuria, proteinuria, and hypoalbuminemia. Laboratory evaluation also documented progressive impairment of renal function and positive circulating anti-GBM antibodies, supporting an immune-mediated glomerular process.
Early recognition of this presentation prompted further diagnostic evaluation because untreated anti-GBM disease can cause diffuse glomerular injury and rapid decline in kidney function. The presence of both nephritic and nephrotic features with rapid progression of renal impairment raised clinical concern for crescentic glomerulonephritis of an autoimmune etiology.
Definitive diagnosis was established by kidney biopsy. Histopathology demonstrated diffuse crescentic glomerulonephritis, a pattern characterized by extensive extracapillary cellular crescents reflecting severe glomerular injury. Immunofluorescence showed linear deposition of IgG along the glomerular basement membrane, a hallmark finding of anti-GBM disease and a key diagnostic feature that distinguishes it from other causes of crescentic glomerulonephritis.
The combination of positive circulating anti-GBM antibodies, the clinical picture of rapidly progressive renal dysfunction, and the biopsy demonstrating diffuse crescents with linear IgG deposition confirmed the diagnosis of pediatric anti-GBM crescentic glomerulonephritis in this patient.
Management was initiated promptly following diagnosis. The therapeutic regimen included high-dose corticosteroids and plasmapheresis to remove pathogenic circulating anti-GBM antibodies. Immunosuppression was continued with mycophenolate mofetil (MMF) as part of the maintenance strategy rather than a cyclophosphamide-based protocol.
Plasmapheresis is an established modality in anti-GBM disease to rapidly reduce circulating autoantibodies, while high-dose corticosteroids provide broad anti-inflammatory and immunosuppressive effects. Mycophenolate mofetil was used in this case as an alternative immunosuppressive agent to mitigate ongoing antibody production and inflammatory activity. The source does not report specific dosing schedules, number of plasmapheresis sessions, or exact corticosteroid regimens, so those treatment details were not available from the report.
During follow-up, clinical status and laboratory parameters improved over a three-month period. The patient experienced resolution of some clinical signs and laboratory trends consistent with disease control, and there was partial recovery of renal function. The report describes this as an improvement from the earlier progressive impairment, indicating that timely intervention achieved at least partial reversal of the acute injury.
The source provides no detailed serial laboratory values, kidney function metrics, or long-term outcomes beyond the three-month improvement, so the magnitude and trajectory of renal recovery beyond this interval are not reported.
This case highlights two principal clinical points: first, the importance of rapid recognition and early initiation of combined therapy in pediatric anti-GBM disease to limit irreversible glomerular damage; and second, the potential role of an MMF-containing combination regimen as an alternative to cyclophosphamide-based therapy in selected patients.
While cyclophosphamide is commonly used in severe anti-GBM disease to suppress autoantibody production, concerns about toxicity can prompt consideration of alternative agents. In this single pediatric case, MMF was used alongside corticosteroids and plasmapheresis, and the patient attained clinical and laboratory improvement with partial renal recovery at three months. The authors suggest this regimen may be feasible in selected patients, but the report is a single-case observation and does not provide comparative data, safety profiles, or long-term efficacy outcomes. Larger studies or series would be required to define the relative effectiveness and safety of MMF versus cyclophosphamide in pediatric anti-GBM disease.
Clinicians should continue to align management with existing guidelines and individualize therapy based on severity, comorbidities, potential toxicities, and available evidence. The KDIGO and other glomerular disease guidelines are referenced in the report bibliography, but the case itself does not provide guideline-derived protocol details.
The authors declared no conflicts of interest. Ethical approval was addressed in the report: given the nature of a case report, formal ethical approval was waived by the institutional Ethics Committee, and written informed consent for publication was obtained from the patient’s legal guardian. The article affirms that procedures followed applicable ethical standards and the principles of the Declaration of Helsinki.
Overall, this case report documents a pediatric presentation of anti-GBM crescentic glomerulonephritis with partial renal recovery after combined therapy including plasmapheresis and mycophenolate mofetil, and it raises the possibility that MMF-containing regimens could be considered as alternatives to cyclophosphamide in selected clinical scenarios. The source does not provide detailed dosing, the number of plasmapheresis sessions, or extended follow-up data beyond the three-month improvement.