Examples of Glomerular Disease
Glomerular diseases encompass a diverse group of immune-mediated and non-immune kidney disorders affecting the glomeruli, with the most common examples being IgA nephropathy, membranous nephropathy, minimal change disease, focal segmental glomerulosclerosis, lupus nephritis, ANCA-associated vasculitis, and infection-related glomerulonephritis. 1, 2
Primary Glomerular Diseases
Most Common Adult Glomerulopathies
IgA Nephropathy (IgAN) is characterized by mesangial IgA deposits, typically presenting with hematuria and variable proteinuria, and represents one of the most frequent primary glomerular diseases worldwide 2
Membranous Nephropathy is an autoimmune disease where antibodies target podocyte antigens (particularly PLA2R in ~70% of primary cases), typically manifesting as nephrotic syndrome in adults 1, 2, 3
Focal Segmental Glomerulosclerosis (FSGS) features segmental sclerosis affecting some but not all glomeruli, can be primary (mediated by circulating factors amenable to immunosuppression) or secondary (where immunosuppression should be avoided) 1, 2
Minimal Change Disease (MCD) shows normal-appearing glomeruli on light microscopy but demonstrates podocyte foot process effacement on electron microscopy, commonly causing nephrotic syndrome particularly in children 2, 4
Systemic Diseases with Glomerular Involvement
Lupus Nephritis represents glomerular involvement in systemic lupus erythematosus, classified according to ISN/RPS criteria, and requires kidney biopsy for definitive classification and treatment planning 1, 2
ANCA-Associated Vasculitis includes microscopic polyangiitis, granulomatosis with polyangiitis, and eosinophilic granulomatosis with polyangiitis, often presenting with rapidly progressive glomerulonephritis 1, 2
Anti-GBM Antibody Glomerulonephritis (Goodpasture's Syndrome) is characterized by linear IgG deposits along the glomerular basement membrane, frequently with pulmonary involvement 1, 2
Complement-Mediated Diseases
C3 Glomerulopathy is characterized by dominant C3 deposits with minimal or no immunoglobulin deposits, including dense deposit disease and C3 glomerulonephritis 2
Immunoglobulin- and Complement-Mediated Glomerular Diseases with MPGN Pattern represents the updated classification replacing the older term "membranoproliferative glomerulonephritis" to better reflect disease pathogenesis 1, 2
Infection-Related Glomerular Disease
- Infection-Related Glomerulonephritis is associated with bacterial (including post-streptococcal), viral, or parasitic infections, with acute post-streptococcal glomerulonephritis being particularly common in children 2, 5
Hereditary Glomerular Diseases
Alport Disease is a genetic disorder affecting type IV collagen in the glomerular basement membrane, often diagnosed without biopsy when family history and genetic testing are confirmatory 1
Fabry Disease is an X-linked lysosomal storage disorder that can cause glomerular injury and may be diagnosed without biopsy when enzyme deficiency or genetic mutation is confirmed 1
Familial Focal Segmental Glomerulosclerosis in families with well-characterized mutations may not require biopsy confirmation when genetic diagnosis is established 1
Age-Related Epidemiologic Patterns
Minimal change disease is the leading cause of nephrotic syndrome in childhood, while membranous nephropathy and FSGS are more common in adults 4
IgA vasculitis demonstrates higher prevalence in pediatric populations compared to adults 4
ANCA-associated vasculitis shows female preponderance in children, with more acute presentations and higher percentages of cellular crescents on biopsy compared to older patients 4
Clinical Pitfalls and Diagnostic Considerations
The kidney biopsy remains the gold standard for diagnosis, but treatment may proceed without biopsy in specific circumstances including PLA2R-positive membranous nephropathy with normal eGFR, MPO or PR3-positive ANCA vasculitis, confirmed Alport disease, anti-GBM disease, Fabry disease, familial FSGS with known mutations, or when biopsy is contraindicated 1
Critical distinction: FSGS mediated by soluble factors may respond to immunosuppression, whereas secondary FSGS with similar histology should not receive immunosuppression—this differentiation is essential for appropriate management 1