Kidney Week

Abstract: FR-PO0744

Double-Positive Anti-GBM/Myeloperoxidase (MPO)-ANCA Crescentic Glomerulonephritis After Crohn Disease Flare with Renal Recovery

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

• Farouji, Abdelhadi, Henry Ford Hospital, Detroit, Michigan, United States

Abdelhadi Farouji, MD

• Pervez, Aqsa, Henry Ford Hospital, Detroit, Michigan, United States

Aqsa Pervez, MD

• Monk, Muhammad A., Henry Ford Hospital, Detroit, Michigan, United States

Muhammad A. Monk, MD

• Varghese, Vipin, Henry Ford Hospital, Detroit, Michigan, United States

Vipin Varghese, MD

Introduction

Anti-glomerular basement membrane (anti-GBM) disease is a rare autoimmune disorder, with 10–30% of cases demonstrating “double positivity” with concurrent anti-neutrophil cytoplasmic (ANCA) antibodies. Triggers for this overlap syndrome remain poorly defined.

Case Description

A 61-year-old man with a history of Crohn's disease in remission, not on therapy, presented with fatigue and acute kidney injury (creatinine 3.79 mg/dL; baseline 0.7–0.9 mg/dL).

Review of systems was notable for rhinorrhea, sore throat, headache, and productive cough with intermittent blood-tinged sputum. He also reported nasal crusting without epistaxis, congestion, and sinus pressure. He endorsed a recent flare of Crohn's disease 3–4 weeks prior, lasting one week and self-resolving, with diarrhea and hematochezia, raising concern for a systemic vasculitic process temporally associated with the flare.

Urinalysis demonstrated non-nephrotic range proteinuria (UPCR 1.21 g/g), dysmorphic red blood cells, and red blood cell casts. Serologic workup showed positive p-ANCA (1:80), elevated MPO antibodies (60 U/mL), and anti-GBM antibodies (113 U). Kidney biopsy showed extensive necrotizing crescentic glomerulonephritis with fibrinoid necrosis and cellular crescents involving most glomeruli. Immunofluorescence demonstrated linear IgG staining along the glomerular basement membrane without immune complex deposition, confirming double-positive anti-GBM/MPO-ANCA disease.

Treatment included high-dose intravenous methylprednisolone for 3 days, followed by an oral prednisone taper, plasmapheresis (10 sessions), and cyclophosphamide. Renal function improved, with creatinine decreasing from 3.98 to 1.68 mg/dL at one month.

Discussion

Double-positive disease is associated with severe renal injury, adverse renal outcomes, and increased relapse risk. Diagnosis relies on serologic findings, histopathology, and clinical correlation. Despite its aggressive course, early recognition and prompt therapy in our patient resulted in favorable renal recovery. The temporal association with a recent flare of Crohn's disease suggests immune dysregulation may have contributed to this overlap syndrome.

This case highlights the importance of recognizing double-positive disease in patients with autoimmune conditions presenting with rapidly progressive glomerulonephritis, as early diagnosis and aggressive therapy may improve renal outcomes.