Abstract: TH-PO1105
Granulomatous Interstitial Nephritis Associated with Bartonella Infection
Session Information
- Pathology and Lab Medicine
October 22, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Pathology and Lab Medicine
- 1700 Pathology and Lab Medicine
Authors
- Facal, Lucia, Hospital de Clinicas Doctor Manuel Quintela, Montevideo, Uruguay
- Yandian, Federico, Médica Uruguaya Corporación de Asistencia Médica (MUCAM), Montevideo, Uruguay
- Sethi, Sanjeev, Mayo Foundation for Medical Education and Research, Rochester, Minnesota, United States
Introduction
Granulomatous interstitial nephritis (GIN) is a renal lesion with a broad differential diagnosis, including infections, sarcoidosis, drug-induced reactions, and systemic inflammatory diseases.
Case Description
A 77-year-old woman with hypertension, presented with a one-year history of 20-kg weight loss, arthralgia, Raynaud's, and kidney dysfunction.
Laboratory showed bicytopenia, elevated erythrocyte sedimentation rate, severe hypocomplementemia with undetectable C4 levels, elevated rheumatoid factor, positive anticardiolipin and anti-β2 glycoprotein I IgM antibodies, polyclonal hypergammaglobulinemia and tubular-pattern proteinuria. Autoimmune serologies and serum ACE levels were negative.
Imaging studies demonstrated hepatosplenomegaly. Transesophageal echocardiography excluded infective endocarditis.
Kidney biopsy revealed non-necrotizing GIN with tubulitis, 30% interstitial fibrosis and tubular atrophy, and 53% globally sclerosed glomeruli. Immunostaining for IgG4, S100, CD1a, CD14, CD4, CD207 was negative.
Bone marrow biopsy demonstrated non-necrotizing granulomas. Urinary acid-fast bacilli smears and Warthin–Starry stain were negative.
Bartonella was confirmed by positive IgM and IgG serologies despite no cat exposure. Prolonged treatment with doxycycline plus rifampicin was initiated, resulting in marked improvement. Creatinine decreased from 5.2 to 1.9 mg/dL, with normalization of complement.
Discussion
Bartonella infection may induce GIN and profound systemic immune activation, mimicking autoimmune or lymphoproliferative disorders.
Bartonella infection is a recognized cause of culture-negative endocarditis-associated glomerulonephritis, and ANCA-associated glomerulonephritis has also been reported both with and without endocarditis. However, to our knowledge, GIN as the predominant renal lesion has not previously been described in association with Bartonella.