A clinical constellation resulting from inflammatory injury of the glomeruli
Aetiology
Primary Causes
- Acute post-infectious (post-streptococcal) glomerulonephritis
- IgA nephropathy (Berger disease)
- Membranoproliferative glomerulonephritis
- Rapidly progressive glomerulonephritis (crescentic GN)
Secondary Causes
- Systemic lupus erythematosus (lupus nephritis)
- Vasculitides (ANCA-associated)
- Anti–glomerular basement membrane (anti-GBM) disease
- Infective endocarditis–associated GN
Pathophysiology

Clinical presentation
- Renal Manifestations
- Gross Hematuria
- Classically cola- or tea-colored urine
- Due to oxidation of hemoglobin in acidic urine
- Proteinuria (usually sub-nephrotic, <3.5 g/day)
- Oliguria
- Edema
- Periorbital edema (especially in the morning)
- Dependent edema (ankles, sacrum)
- Systemic Features
- Hypertension
- Malaise
- Headache
- Signs related to underlying systemic disease
Investigations
Bloods
- U+Es
Examination of urine
- Urinalysis - haematuria, proteinuria
- Urine microscopy - dysmorphic RBCs, RBC and granular casts, lipiduria
- Urine protein: creatinine ratio/24 hour urine to quantify proteinuria
Renal biopsy
Light microscopy
- Usually see hypercellularity - inflammatory and reactive proliferations
- Can see sclerosis - on-going damage
- May see crescents - bad, indicates rapidly progressive GMN
- Granulomas - GPA, sarcoid
Electon microscopy
- Can see immune complex depositions in the basement membrane
Immunoflourescence
- Shows what kind of antibody and what distribution e.g. linear IgG in Goodpasture's
Management
Non-immunosupressive
- Anti-hypertensives - target BP <130/80
- ACEi/ARBs
- Diuretics
- Statins
Immunosuppression
- Drugs e.g. corticosteroids, azathioprine
- Plasmapharesis - TPE (therapeutic plasma exchange)
- Antibodies - IV Ig, monoclonal T or B cell antibodies