TextbookRheumatology & MusculoskeletalGranulomatosis with Polyangiitis

Granulomatosis with Polyangiitis

ANCA-associated small-vessel vasculitis (formerly Wegener granulomatosis) characterised by necrotising granulomatous inflammation of the upper and lower respiratory tract and necrotising glomerulonephritis. Strongly associated with c-ANCA/PR3 antibodies.

Key Facts

GPA (formerly Wegener granulomatosis) is characterised by necrotising granulomatous vasculitis affecting upper airway, lungs, and kidneys c-ANCA (anti-PR3): positive in >90% of generalised GPA; highly specific ENT: nasal crusting, epistaxis, sinusitis, saddle-nose deformity (nasal cartilage destruction), otitis media, subglottic stenosis Pulmonary: cavitating lung nodules, pulmonary haemorrhage, cough, dyspnoea Renal: pauci-immune crescentic GN (as with all AAV) Induction: rituximab (RAVE trial) or cyclophosphamide + prednisolone; maintenance: rituximab (MAINRITSAN) or azathioprine for ≥24 months Relapse rate: 50% within 5 years; PR3-ANCA positive patients have higher relapse risk than MPO Co-trimoxazole 960mg BD: may reduce ENT relapse rate (Stegeman trial)

Overview

Key Facts

GPA is the most common ANCA-associated vasculitis with distinctive upper respiratory tract involvement. PR3-ANCA is both diagnostic and prognostic.

Epidemiology

  • Incidence: ~10 per million/year in the UK
  • Peak age: 55-70 years; M=F
  • More common in Northern European populations

Pathophysiology

  • Anti-PR3 antibodies activate neutrophils → necrotising vasculitis
  • Granuloma formation in respiratory tract (distinctive feature vs MPA)
  • Pauci-immune crescentic GN in kidneys
  • Triad: upper airway granulomatous inflammation + lung involvement + renal vasculitis

Clinical Presentation

ENT (90%)

  • Nasal crusting, bloody discharge, epistaxis
  • Sinusitis (recurrent, destructive)
  • Saddle-nose deformity: nasal septal perforation and cartilage destruction
  • Subglottic stenosis: stridor, hoarseness (~15%)
  • Otitis media (serous or chronic)
  • Hearing loss (conductive or sensorineural)

Pulmonary (90%)

  • Cavitating lung nodules: multiple, bilateral; can mimic malignancy or TB
  • Pulmonary haemorrhage: dyspnoea, haemoptysis
  • Cough, pleurisy

Renal (80%)

  • Crescentic GN: haematuria, proteinuria, rapidly declining GFR
  • May present as RPGN

Other

  • Constitutional: fever, weight loss, fatigue
  • Eyes: scleritis, orbital pseudotumour (proptosis)
  • Skin: palpable purpura
  • Nervous system: mononeuritis multiplex, cranial nerve palsies

Red Flags

  • Haemoptysis + renal failure → pulmonary-renal syndrome
  • Subglottic stenosis → airway compromise
  • Rapidly rising creatinine → urgent treatment

Differential Diagnosis

DiagnosisKey FeaturesInvestigation
MPANo granulomata, no upper airway, p-ANCA/MPOANCA, biopsy
EGPAAsthma, eosinophiliaFBC (eosinophils), ANCA
TBCavitating lesions, AFB positiveSputum AFB, Mantoux
Lung cancerCavitating mass, smoking historyCT, biopsy
Anti-GBM diseaseLinear IgG, anti-GBM antibodiesAnti-GBM, biopsy
Cocaine-induced midline destructive diseaseCocaine use, ANCA can be positiveDrug history

Diagnosis / Investigation

Bloods

  • c-ANCA (anti-PR3): positive in >90% generalised GPA
  • p-ANCA (anti-MPO): positive in ~10% of GPA
  • CRP/ESR: elevated
  • U&Es: renal function
  • FBC: anaemia, leucocytosis
  • Urinalysis: haematuria, red cell casts, proteinuria

Imaging

  • CT chest: cavitating nodules (bilateral), ground-glass (haemorrhage)
  • CT sinuses: mucosal thickening, bony erosion
  • CT neck: subglottic stenosis

Biopsy

  • Renal biopsy: pauci-immune crescentic GN
  • Nasal/sinus biopsy: necrotising granulomatous vasculitis (may be non-diagnostic due to superficial sampling)
  • Lung biopsy: geographic necrosis with granulomata

Management

Induction (Generalised/Organ-Threatening)

  • Rituximab 375mg/m² weekly × 4 (RAVE trial) OR IV cyclophosphamide (CYCLOPS protocol) + prednisolone 1mg/kg tapering
  • Avacopan 30mg BD as steroid-sparing alternative (ADVOCATE trial)
  • Plasma exchange: for pulmonary haemorrhage

Maintenance (≥24 months)

  • Rituximab 500mg IV every 6 months (MAINRITSAN – superior to azathioprine)
  • OR azathioprine 2mg/kg/day

Limited Disease (ENT Only)

  • Methotrexate 20-25mg weekly + prednisolone (NORAM trial)
  • Co-trimoxazole 960mg BD: may reduce nasal/ENT relapse (Stegeman trial)

Subglottic Stenosis

  • Intralesional corticosteroid injection
  • Endoscopic dilation
  • May persist despite systemic treatment

Supportive

  • Co-trimoxazole for PCP prophylaxis
  • Bone protection
  • Annual influenza/pneumococcal vaccination

Referral

  • All GPA → rheumatology/nephrology
  • ENT involvement → ENT surgeon
  • Subglottic stenosis → airway specialist

Prognosis

  • 5-year survival: 75-80% with treatment
  • Relapse rate: ~50% within 5 years; PR3 > MPO
  • Renal survival: 70-80% at 5 years
  • Leading causes of death: infections (immunosuppression), renal failure, cardiovascular disease
  • Subglottic stenosis: may cause chronic morbidity; often refractory
  • Rituximab maintenance significantly reduces relapse rate vs azathioprine

Other Relevant Information

GPA vs MPA vs EGPA

FeatureGPAMPAEGPA
ANCAc-ANCA/PR3 (90%)p-ANCA/MPO (70%)p-ANCA/MPO (40%)
Upper airway+++-+
GranulomataYesNoYes (eosinophilic)
AsthmaNoNoYes (>95%)
EosinophiliaNoNoYes
RenalCrescentic GNCrescentic GNLess common
Relapse rateHigh (50%)LowerModerate