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C3 glomerulopathy associated with mycoplasma pneumoniae infection and positive IgA staining
Zhi-Yu Duan1, Ji-Jun Li1, Guang-Yan Cai1
1Department of Nephrology, First Medical Center of Chinese PLA General Hospital, National Key Laboratory of Kidney Diseases, Beijing Key Laboratory of Kidney Diseases Research, National Clinical Research Center for Kidney Diseases, Beijing, 100853, China.
Background:
Patients with C3 glomerulopathy (C3G) often have a history of infection, which implies that infection may lead to abnormal activation of the complement alternative pathway (CAP) and induce the development of C3G. However, patients with postinfectious glomerulonephritis (PIGN) often have a low serum C3 concentration and positive glomerular C3 staining, consistent with the activation of the CAP. PIGN, especially if it involves simultaneous IgA deposition, is often difficult to differentiate from C3G.
Case Presentation:
In this study, we report the consequences of Mycoplasma pneumoniae (MP) infection in a 66-year-old male Chinese patient, who developed persistent hypocomplementemia, gross hematuria, and rapidly progressive glomerulonephritis. The findings of the histologic examination of an initial renal biopsy were consistent with a diagnosis of IgA-dominant postinfectious glomerulonephritis. The sample was negative for Gd-IgA1 staining. After treatment with antibiotics, glucocorticoids, and mycophenolate mofetil, the patient's serum creatinine decreased from a peak of 387 µmol/L to 195 µmol/L prior to discharge, and there was a partial response in his urinary protein concentration. After 2 months, his serum C3 concentration had returned to normal. However, owing to reinfection with MP the patient's serum creatinine rapidly increased again to 475.07 µmol/L, and this was accompanied by a decrease in serum C3 concentration (> 8 months) and positivity for C3 nephritis factor. Examination of both renal biopsies showed stronger immunostaining for C3 than for IgA in the glomeruli.
Conclusion:
Thus, MP infection can cause sustained activation of the CAP, leading to C3G. For patients with MP infection, if there is an ongoing decrease in complement C3 levels and a progressive increase in serum creatinine, it is crucial to be vigilant for possible C3G and to consider the use of immunosuppressive therapy in conjunction with anti-infective treatment to prevent the ongoing activation of the CAP.
Insights
Mycoplasma pneumoniae infection can trigger sustained complement alternative pathway activation, leading to C3 glomerulopathy (C3G). Vigilance for C3G is crucial in MP-infected patients with declining C3 levels and rising creatinine, suggesting immunosuppressive therapy.
Area of Science:
- Nephrology
- Immunology
- Infectious Diseases
Background:
- Infection can trigger complement alternative pathway (CAP) activation, potentially leading to C3 glomerulopathy (C3G).
- Distinguishing C3G from postinfectious glomerulonephritis (PIGN) can be challenging due to overlapping clinical and histological features, including low C3 levels and C3 deposition.
- IgA-dominant PIGN may present similarly to C3G, complicating diagnosis.
Purpose of the Study:
- To investigate the link between Mycoplasma pneumoniae (MP) infection and C3 glomerulopathy (C3G).
- To highlight the role of sustained complement alternative pathway (CAP) activation in MP-induced kidney disease.
- To emphasize the diagnostic and therapeutic considerations for MP-associated C3G.
Main Methods:
- Case report of a 66-year-old male with Mycoplasma pneumoniae infection, hypocomplementemia, and rapidly progressive glomerulonephritis.
- Analysis of initial and subsequent renal biopsies, including immunofluorescence for C3 and IgA.
- Clinical monitoring of serum creatinine, C3 levels, and treatment response.
Main Results:
- Initial biopsy suggested IgA-dominant PIGN, but subsequent biopsies showed stronger C3 than IgA staining.
- MP reinfection led to recurrent renal dysfunction, decreased C3 levels, and C3 nephritis factor positivity.
- Treatment with antibiotics, glucocorticoids, and mycophenolate mofetil showed partial improvement, with normalization of C3 levels after initial treatment.
Conclusions:
- Mycoplasma pneumoniae infection can cause sustained CAP activation, resulting in C3G.
- Monitoring C3 levels and creatinine in MP-infected patients is crucial for early C3G detection.
- Consider immunosuppressive therapy alongside anti-infective treatment for MP-associated C3G to prevent CAP overactivation.
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