Kidney Week

Abstract: FR-PO0756

When ANCA Becomes Pathogenic: From Isolated Tubulointerstitial Nephritis to Pauci-Immune Crescentic Glomerulonephritis in Chronic Vascular Graft Infection

Session Information

• Glomerular Diseases: ANCA Vasculitis, Anti-GBM Disease, and Crescentic GN
  October 23, 2026 | Location: Exhibit Hall A, Convention Center
  Abstract Time: 10:00 AM - 12:00 PM

Category: Glomerular Diseases

• 1402 Glomerular Diseases: Clinical, Outcomes, and Therapeutics

Authors

• Sánchez Maure, Michelle, Centro Medico Nacional 20 de Noviembre, Mexico City, CDMX, Mexico

Michelle Sánchez Maure, MD

• Gonzalez-Fuentes, Carolina, Centro Medico Nacional 20 de Noviembre, Mexico City, CDMX, Mexico

Carolina Gonzalez-Fuentes, MD, MSc

• De La Torre, Juana Citlali, Centro Medico Nacional 20 de Noviembre, Mexico City, CDMX, Mexico

Juana Citlali De La Torre, DM

• Hopf, Karen, Centro Medico Nacional 20 de Noviembre, Mexico City, CDMX, Mexico

Karen Hopf, MD

• Hernandez, Regina Canade, Centro Medico Nacional 20 de Noviembre, Mexico City, CDMX, Mexico

Regina Canade Hernandez, DrMed, PhD, DrPH

• Alamilla-Sanchez, Mario, Centro Medico Nacional 20 de Noviembre, Mexico City, CDMX, Mexico

Mario Alamilla-Sanchez, MD, MSc

Introduction

ANCA-associated vasculitis (AAV) is characterized by necrotizing small-vessel inflammation and pauci-immune crescentic glomerulonephritis. Although ANCA positivity may occur in chronic infections, progression from isolated tubulointerstitial nephritis (TIN) to pauci-immune crescentic glomerulonephritis is rarely described. Distinguishing infection-related ANCA positivity from true AAV is essential, as immunosuppression during active infection may worsen outcomes.

Case Description

A 57-year-old man with prior thoracic aortic endoprosthesis placement presented with fever, constitutional symptoms, and weight loss. Laboratory studies showed acute kidney injury and subnephrotic proteinuria. PET imaging demonstrated active vascular graft infection, and blood cultures grew Pseudomonas aeruginosa. Serologic testing revealed PR3-ANCA positivity.
Initial kidney biopsy showed acute TIN with eosinophils and plasma cells, without glomerular involvement. Renal function improved after ceftazidime therapy, with serum creatinine decreasing from 2.6 to 1.2 mg/dL.
Six months later, the patient developed rapidly progressive kidney dysfunction, active urinary sediment and persistent PR3 positivity, requiring peritoneal dialysis. Repeat PET imaging showed no active graft infection. A second kidney biopsy demonstrated pauci-immune extracapillary proliferative glomerulonephritis with cellular and fibrocellular crescents. Treatment included methylprednisolone, intravenous cyclophosphamide and plasma exchange. Renal function improved, allowing dialysis discontinuation. At follow-up, serum creatinine was 2.4 mg/dL (eGFR 31 mL/min/1.73 m2).

Discussion

This case highlights the dynamic relationship between chronic infection, ANCA positivity, and progression to overt AAV. Initially, PR3-ANCA positivity likely represented an infection-related epiphenomenon, supported by biopsy findings of isolated TIN without glomerular involvement. Over time, the disease evolved to pauci-immune crescentic glomerulonephritis, suggesting transition to pathogenic ANCA-mediated autoimmunity, potentially driven by chronic antigenic stimulation, NETosis and molecular mimicry.
This report underscores the importance of repeat kidney biopsy in evolving renal syndromes and highlights the therapeutic challenge of balancing immunosuppression in patients with current or prior infection.

Acknowledgment

The authors used artificial intelligence–assisted tools exclusively for grammatical revision and language editing of the manuscript.