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Mycoplasma pneumoniae Infection Associated C3 Glomerulopathy Presenting as Severe Crescentic Glomerulonephritis
Lalani De Silva1, Dinesha Jayasinghe1, Priyani Amarathunga1
1Department of Pathology, Faculty of Medicine, University of Colombo, Colombo, Sri Lanka.
Insights
C3 glomerulopathy (C3GP) can rarely present as crescentic glomerulonephritis (CGN) following Mycoplasma pneumoniae infection. Early diagnosis and identification of triggers are crucial for managing this rare kidney disease.
Area of Science:
- Nephrology
- Immunology
- Infectious Diseases
Background:
- C3 glomerulopathy (C3GP) involves complement system dysregulation, typically presenting as proliferative glomerulonephritis.
- Crescentic glomerulonephritis (CGN) is an uncommon manifestation of C3GP.
Observation:
- A case of an adult South-Asian female with Mycoplasma pneumoniae infection developed CGN with systemic symptoms.
- Renal biopsy showed CGN with mesangial C3 deposits, excluding other immune deposits.
- Persistent proteinuria favored C3GP over infection-related glomerulonephritis (IRGN).
Findings:
- This case highlights a rare association between CGN and C3GP triggered by Mycoplasma pneumoniae.
- The patient progressed to end-stage renal failure despite immunosuppressive therapy.
Implications:
- Accurate diagnosis of CGN in C3GP is critical for patient outcomes.
- Identifying triggering factors like Mycoplasma pneumoniae is essential for managing CGN associated with C3GP.
Abstract:
C3 glomerulopathy (C3GP) is a group of diseases caused by a deregulated complement system, which encompasses both dense deposit disease and C3 glomerulonephritis. Renal manifestations of C3GP are primarily of proliferative glomerulonephritis, and only a few case reports of crescentic glomerulonephritis (CGN) in association with C3GP are available. Here is a case of an adult South-Asian female, who was diagnosed as seropositive acute Mycoplasma pneumoniae infection, with associated systemic manifestations, including immune-type extravascular haemolysis and nephrotic range proteinuria. Subsequent renal biopsy revealed CGN with disrupted Bowman's capsules and necrotizing lesions. Immunofluorescence showed coarse granular mesangial C3 deposits with negative IgM, IgG, IgA, and C1q. The immunomorphological phenotype raised two possibilities including C3GP and infection-related glomerulonephritis (IRGN). Persistent proteinuria with no evidence of resolution even after 6 months of follow-up favoured C3GP over IRGN. The patient proceeded to end-stage renal failure requiring renal replacement despite aggressive immunosuppression. This case illustrates the rare association of CGN with C3GP induced by Mycoplasma pneumoniae infection, highlighting the importance of correct diagnosis as well as timely identification of triggering factors in CGN on patient outcome.
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