Synopsis
Recognise anti-glomerular-basement-membrane disease as a pulmonary–renal emergency, secure antibody and biopsy evidence rapidly, and support immediate specialist plasma exchange and immunosuppression decisions.
- Anti-GBM disease is caused by pathogenic antibodies against the alpha-3 chain of type IV collagen in glomerular and alveolar basement membranes.
- It typically produces rapidly progressive crescentic glomerulonephritis, pulmonary alveolar haemorrhage or both; isolated renal disease is common enough that absent lung symptoms do not reassure.
- Visible haemoptysis is not required for alveolar haemorrhage; hypoxia, new bilateral opacities and a falling haemoglobin may be the only bedside cluster.
Key red flags
Creatinine rising over days to weeks, glomerular haematuria, red-cell casts, proteinuria and oliguria is the characteristic renal emergency.
Investigation priorities
Detect the disease-defining circulating autoantibody and establish a baseline for clearance.
Management branches
Active GN accompanies haemoptysis, hypoxia, diffuse opacities or otherwise unexplained falling haemoglobin.
- Admit, support airway and oxygenation, stop avoidable anticoagulants after senior risk review, and treat life-threatening hyperkalaemia, acidosis or pulmonary oedema.
- Send anti-GBM antibody, ANCA, cultures and baseline immune-treatment tests immediately and arrange urgent renal biopsy when safe.
Key medicines
Plasma exchangeExchange volume, frequency, replacement fluid and stopping point follow the specialist renal protocol and antibody trend.
CyclophosphamideUse the centre's oral or intravenous induction regimen adjusted for age, kidney function, blood count and cumulative exposure.