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ANCA-associated pauci-immune glomerulonephritis in a patient with bacterial endocarditis: a challenging clinical
Andrea Cervi1, Dylan Kelly1, Iakovina Alexopoulou2
1Internal Medicine Residency Program.
Insights
Infective endocarditis (IE) can cause ANCA-associated glomerulonephritis (GN). This case highlights the diagnostic importance of kidney biopsy and the challenges in managing ANCA GN during active infection, especially with coinfections.
Area of Science:
- Nephrology
- Infectious Diseases
- Rheumatology
Background:
- Infective endocarditis (IE) typically causes glomerulonephritis (GN) through immune complex deposition.
- ANCA-associated vasculitis (AAV) is a rare complication of IE, often presenting with pauci-immune GN.
Observation:
- A 59-year-old man with chronic hepatitis B and C experienced acute kidney injury and Enterococcus faecalis IE.
- He presented with elevated proteinase-3 anti-neutrophil cytoplasmic antibodies (PR3-ANCA) and pauci-immune GN on kidney biopsy, indicative of ANCA-mediated GN.
- Literature review identified five prior cases of IE-related ANCA GN, predominantly associated with Streptococcus and Bartonella species.
Findings:
- All five previously reported cases of IE-related ANCA GN showed high PR3-ANCA levels and subacute or chronic infection.
- Treatment strategies varied, including immunosuppression (steroids and cyclophosphamide), antibiotics alone, and valve replacement.
- Renal function improved in 4 out of 5 patients.
Implications:
- Infection is a key factor in ANCA formation, but the specific role of PR3-ANCA in IE requires further elucidation.
- Kidney biopsy is crucial for distinguishing IE-related GN from ANCA vasculitis.
- This case underscores the rarity of IE-associated ANCA vasculitis and the complexities of treatment, particularly in patients with concurrent infections requiring immunosuppression.
Purpose:
We report the case of a 59-year-old man with chronic hepatitis B and C infection presenting with acute kidney injury and enterococcus faecalis-infective endocarditis (IE). An elevated proteinase-3 (PR3)-ANCA and pauci-immune glomerulonephritis (GN) on renal biopsy were discovered, corresponding to ANCA-mediated GN. We conducted a literature review to assess the role of ANCA in IE and treatment implications.
Methods:
On systematic review of the literature, we found five previous cases whereby IE caused by streptococcus and bartonella species were related to ANCA vasculitis-associated GN.
Results:
Most reports of IE-related GN are mediated by immune complex deposition and resolve following microbial clearance. Of the 5 cases of ANCA GN in the setting of IE, all had markedly elevated levels of PR3-ANCA with either a subacute or chronic course of infection. Patients were treated with a combination of steroids and cyclophosphamide (2/5), steroids and antibiotics alone (1/5), or with valvular replacement (2/5). Renal function was recovered in 4/5 patients.
Conclusion:
Infection is a major etiologic player in the formation of ANCA; however, the role of PR3-ANCA in IE remains unclear. Kidney biopsy is essential in differentiating IE-related GN due to infection and immune complex deposition versus ANCA-associated vasculitis. A paucity of reports on the development of GN in IE-associated ANCA vasculitis exists, highlighting the rarity of our case and lack of clear therapeutic strategies in a patient with active infection requiring immunosuppression. In this case, the patient's chronic hepatitis B and C coinfection presented a unique challenge.
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