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Granulomatosis with polyangiitis (GPA) and IgA vasculitis are both capable of causing rapidly progressive glomerulonephritis and purpura. Characteristic manifestations of GPA include sinusitis, pulmonary and kidney involvement, accompanied by elevated PR3-ANCA titers, whereas abdominal pain is uncommon. We present a case of GPA that initially manifested with abdominal pain and IgA deposition in the walls of cutaneous vessels, complicating the diagnosis.
Case Description
A 61-year-old male patient with a one-year history of chronic sinusitis presented with symptoms including fever, abdominal pain, arthralgia, and palpable purpura in the lower extremities. Additionally, glomerular hematuria and proteinuria were observed. Computed tomography revealed pulmonary nodules, kidney enlargement, and diffuse thickening of the small intestinal wall. The skin biopsy revealed necrotizing vasculitis characterized by granulomatous inflammation and IgA deposition within the vessel walls, findings that are indicative of IgA vasculitis. Oral prednisolone was initiated, which improved abdominal pain and arthralgia. However, within a week, kidney function deteriorated rapidly, with serum creatinine rising from 1.0 mg/dL to 6.3 mg/dL, requiring hemodialysis. Laboratory tests revealed a markedly elevated PR3-ANCA level (315 U/mL). Kidney biopsy revealed that 11 out of 19 glomeruli exhibited prominent cellular crescent formation, while mesangial matrix expansion or endocapillary hypercellularity was subtle in non-crescentic glomeruli. Immunofluorescence staining showed weak mesangial deposition of IgA and C3. Electron microscopy revealed only a small number of electron-dense deposits in the paramesangial area. Taken together with the histological findings, the patient was diagnosed with GPA rather than IgA vasculitis. The patient was treated with high-dose intravenous steroids, avacopan, rituximab, and plasma exchange therapy. Following treatment, kidney function improved, with serum creatinine decreasing to 1.7 mg/dL, allowing discontinuation of dialysis. The purpura and intestinal wall thickening also resolved.
Discussion
Notably, the patient presented with abdominal pain and IgA deposition in cutaneous vessels, complicating the differentiation between GPA and IgA vasculitis. There have been only a limited number of reported cases of GPA mimicking IgA vasculitis in pediatric patients, and this represents the first documented instance in adults. The abdominal pain and the presence of strong IgA deposition in the skin were atypical features for GPA. According to the previous reports, gastrointestinal involvement is observed in only 5% to 10% of GPA cases. The mechanism of IgA deposition in the skin remains unclear; however, chronic mucosal inflammation, as seen in patients with chronic sinusitis or allergic rhinitis, may lead to alterations in IgA structure or metabolism, which could in turn contribute to its deposition within small dermal vessels.
This case highlights that GPA can present with abdominal pain and IgA deposition in the skin, findings that are atypical for GPA and mimic IgA vasculitis. In such cases, kidney biopsy is crucial for accurate diagnosis and timely initiation of appropriate immunosuppressive therapy.
