Define glomerulonephritis
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Glomerulonephritis (GN)
Definition
Glomerulonephritis is a spectrum of inflammatory disorders affecting the glomeruli (the filtration units of the kidney). It is defined as inflammation within the glomeruli, which can range from acute to chronic, and is characterized primarily by hematuria and proteinuria.
"Glomerulonephritis is an inflammatory process affecting the glomerulus... usually results from deposition of immune complexes within the glomeruli."
- Tintinalli's Emergency Medicine, p. 2066
"Inflammation within the glomeruli, or glomerulonephritis, which can range from acute or chronic, usually stems from humoral immune reactions."
- Junqueira's Basic Histology, p. 3430
Pathophysiology
The core mechanism involves the deposition of immune complexes within the glomeruli. These deposits trigger:
- Complement activation (notably C3 consumption)
- Leukocyte recruitment (neutrophils, monocytes, macrophages)
- Release of cytokines and growth factors
- Inflammation and glomerular injury → sclerosis within glomeruli → fibrosis in tubulointerstitial cells
There are two main humoral mechanisms by which antibodies accumulate in the glomerulus:
- Fixed antigen mechanism: Antibodies target natural structural elements of the glomerular basement membrane (GBM) - e.g., anti-GBM disease, where linear IgG deposition is seen on immunofluorescence. When coupled with pulmonary involvement (antibodies to alveolar membrane), this is called Goodpasture's syndrome.
- Circulating immune complex mechanism: Immune complexes formed in the circulation deposit in the GBM and mesangium, forming discontinuous "lumpy-bumpy" granular deposits.
(Smith and Tanagho's General Urology, p. 2458)
A third, pauci-immune group - the ANCA-associated nephritides - features necrotizing and crescentic lesions with minimal glomerular immunoglobulin deposition, despite circulating anti-neutrophil cytoplasmic antibodies (MPO/P-ANCA; PR3/C-ANCA).
Classification
GN is classified along two axes:
1. By Origin
| Type | Description |
|---|---|
| Primary GN | Disease isolated to the kidney |
| Secondary GN | Kidney involvement as part of a systemic disorder (e.g., SLE, vasculitis, infections) |
2. By Clinical Presentation
| Presentation | Features |
|---|---|
| Acute GN | Sudden onset hematuria, proteinuria, hypertension, oliguria |
| Rapidly Progressive GN (RPGN) | Severe injury with crescentic glomeruli; rapid decline to renal failure |
| Recurrent Macroscopic Hematuria | Episodes of gross hematuria (e.g., IgA nephropathy) |
| Chronic GN | Slow progressive course leading to end-stage renal disease |
(Tintinalli's Emergency Medicine, p. 2068)
3. By Immunologic Mechanism (based on immune deposit location)
| Class | Example |
|---|---|
| Subepithelial deposits | Post-streptococcal GN, membranous nephropathy |
| Subendothelial deposits | Lupus nephritis, type I MPGN |
| Mesangial deposits | IgA nephropathy, Henoch-Schonlein purpura |
| Anti-GBM (linear deposits) | Goodpasture's disease |
| Pauci-immune (no deposits) | ANCA-associated GN |
(Smith and Tanagho's General Urology, p. 2469-2482)
Key Subtypes
| Subtype | Key Features |
|---|---|
| Post-streptococcal GN | Most common in children; immune complex deposition after Group A strep infection; C3 complement low; usually self-limiting |
| IgA Nephropathy (Berger's disease) | Mesangial IgA deposits; recurrent hematuria; most common primary GN worldwide |
| Rapidly Progressive GN | Crescents in >50% of glomeruli; anti-GBM, immune complex, or pauci-immune types |
| Membranoproliferative GN | GBM thickening and mesangial hypercellularity; progressive course |
| Lupus Nephritis | Secondary GN due to SLE; subendothelial + mesangial immune complexes |
(Robbins & Kumar Basic Pathology, pp. 3040-3048)
Clinical Features
- Hematuria (most common; may be microscopic or macroscopic - "cola-colored" urine)
- Proteinuria (foamy urine)
- Hypertension
- Oliguria (in severe cases)
- Edema (periorbital, peripheral)
- Impaired renal function (raised creatinine, azotemia)
- Systemic symptoms: malaise, headache, anorexia, low-grade fever
(Tintinalli's Emergency Medicine, p. 2073)
Diagnostic Investigations
| Test | Finding in GN |
|---|---|
| Urinalysis | Hematuria, RBC casts, proteinuria, dysmorphic RBCs |
| Serum complement (C3, C4) | Low C3 in >90% of post-streptococcal GN; normal in IgA nephropathy |
| Anti-streptolysin O (ASO) | Elevated in post-streptococcal GN |
| ANCA (MPO/PR3) | Positive in ANCA-associated GN |
| Anti-GBM antibody | Positive in Goodpasture's disease |
| ANA / anti-dsDNA | Positive in lupus nephritis |
| Renal biopsy | Definitive diagnosis; reveals light microscopy, immunofluorescence, and electron microscopy patterns |
(Tintinalli's Emergency Medicine, p. 2078)
Prognosis
- Post-streptococcal GN: ~95% of patients recover renal function within 8-12 weeks.
- IgA nephropathy / minimal change disease: Generally good prognosis.
- Mesangiocapillary (membranoproliferative) GN: >70% progress to chronic renal failure.
- RPGN: Poor prognosis without prompt treatment; can rapidly lead to end-stage renal disease.
(Swanson's Family Medicine Review, p. 5638)
Sources: Tintinalli's Emergency Medicine; Junqueira's Basic Histology, 17e; Smith and Tanagho's General Urology, 19e; Robbins & Kumar Basic Pathology; Swanson's Family Medicine Review; Comprehensive Clinical Nephrology, 7th Edition; Brenner and Rector's The Kidney.
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