| Class / examples | Initiating cause | Biopsy / serologic signature | Key genes / pathways | Typical clinical course | Current mechanism-aligned treatment |
|---|---|---|---|---|---|
| **Infection-related GN** (post-streptococcal GN; bacterial/viral/parasitic infection-associated GN) | Infection-triggered glomerular injury via immune-complex deposition, direct glomerular cell damage, molecular mimicry, and/or superantigen effects; control of infection is central (subtype-specific) (pqac-00000000, pqac-00000007) | Kidney biopsy required for subtype distinction in many cases; immune-complex/complement-associated patterns may be seen; supportive serologies depend on trigger (for example antistreptolysin O/anti-DNase B in post-streptococcal disease) (pqac-00000000, pqac-00000007) | Innate immunity, immune complexes, complement activation; immunopathogenesis-based GN framework classifies this separately from autoimmune GN (pqac-00000000, pqac-00000007) | Often acute nephritic presentation with hematuria, proteinuria, hypertension; may be self-limited or progress depending on pathogen, host factors, and delay in treatment (pqac-00000000, pqac-00000007) | **Treat infection first**; supportive nephritic care, then selective immunosuppression only when appropriate to subtype/severity (pqac-00000000, pqac-00000007) |
| **IgA nephropathy / IgA vasculitis nephritis** | Mucosal immune dysregulation with aberrant IgA biology and nephritogenic immune-complex deposition; genetic and environmental factors both contribute (subtype-specific) (pqac-00000001, pqac-00000002) | Mesangial IgA-dominant deposition on biopsy; mesangial proliferation is both diagnostic and prognostic in IgAN; clinical presentation ranges from asymptomatic urinary abnormalities to acute GN (pqac-00000001) | Multi-hit IgA pathway; podocyte injury marker **TCF21** upregulated in IgAN; vascular-development, adhesion, and extracellular-matrix programs enriched in proliferative IgAN; GWAS-informed susceptibility noted in recent reviews (pqac-00000001, pqac-00000002) | Usually chronic/indolent but heterogeneous; about **~20%** of IgAN patients progress to ESKD in the cited 2024 study summary; IgA vasculitis nephritis tends to be more severe in adults (pqac-00000001) | Optimized supportive care first; corticosteroids in selected higher-risk disease; emerging mechanism-based agents include **targeted-release budesonide**, B-cell/APRIL-directed therapies, SGLT2 inhibitors, endothelin receptor antagonists, and complement inhibitors (subtype-specific, evidence strength varies) (pqac-00000001, pqac-00000002, pqac-00000013) |
| **Lupus nephritis (LN)** | Autoimmune GN driven by systemic lupus with autoantibodies, immune complexes, complement activation, and kidney-resident/immune-cell interactions (subtype-specific) (pqac-00000000, pqac-00000011, pqac-00000012) | Kidney biopsy is the **gold standard**; creatinine and urinalysis are baseline tests; class III/IV ± V classification guides therapy; serologies are subtype specific to SLE/LN (pqac-00000011, pqac-00000012) | Autoantibodies, complement, inflammatory kidney-stroma/immune-cell crosstalk; biomarkers under development in serum/urine; ancestry-associated risk gradients noted in recent reviews (pqac-00000011, pqac-00000012) | Relapsing-remitting or chronic progressive; occurs in up to **50% of adult SLE** and **80% of juvenile-onset SLE**; about **30%** may progress to ESKD within 15 years in one 2024 consensus summary (pqac-00000012) | Induction: **MMF**, cyclophosphamide, **MMF+tacrolimus**, or **MMF+belimumab**; maintenance: **MMF** or azathioprine first line; rituximab for refractory disease; newer targeted agents include **voclosporin** and belimumab, with additional complement/B-cell pathway trials ongoing (pqac-00000011, pqac-00000012, pqac-00000014) |
| **ANCA-associated pauci-immune GN** | Autoimmune small-vessel vasculitis with pathogenic neutrophil-directed autoimmunity; severe crescentic GN phenotype is typical (subtype-specific) (pqac-00000000, pqac-00000009) | Pauci-immune necrotizing/crescentic GN on biopsy with supportive **ANCA** serology; histologic scores such as Berden, RRS, and MCCS help prognosis (pqac-00000009) | Th1/Th17/Tc1/Tc17 inflammatory programs; complement C5a axis is therapeutically relevant; spatial/single-cell data identified pathogenic cytokine-producing T cells (pqac-00000009) | Often rapidly progressive with AKI/RPGN; kidney failure risk remains substantial without prompt treatment (pqac-00000000, pqac-00000009) | Standard therapy remains glucocorticoids plus cyclophosphamide and/or rituximab; **avacopan** aligns with C5a-pathway biology; exploratory precision approach: **ustekinumab** in 4 relapsing ANCA-GN patients showed improvement over 26 weeks (pqac-00000009) |
| **Anti-GBM disease** | Autoimmune GN caused by antibodies to the glomerular basement membrane; classic severe crescentic GN/RPGN subtype (pqac-00000000) | Linear GBM-directed immunostaining on biopsy with circulating anti-GBM antibodies; biopsy remains central for confirmation and severity assessment (pqac-00000000) | Autoantibody-mediated injury to glomerular filtration barrier; downstream crescent formation and necroinflammation (pqac-00000000) | Typically acute, aggressive, rapidly progressive kidney failure; may include pulmonary involvement in Goodpasture spectrum (pqac-00000000) | Rapid immunosuppression plus **plasma exchange** to remove pathogenic antibodies, alongside corticosteroids/cytotoxic therapy (pqac-00000000) |
| **C3 glomerulopathy / C3 glomerulonephritis** | Autoinflammatory/complement-mediated GN from dysregulated alternative complement pathway (subtype-specific) (pqac-00000000, pqac-00000008) | C3-dominant biopsy pattern distinguishes this complement-mediated class; complement serologies/genetic workup may support diagnosis (pqac-00000000, pqac-00000008) | Strong disease-target associations include **CFH, C3, CFHR5, CFB, CFHR1, CFI**; complement dysregulation is the defining pathway (pqac-00000008) | Often chronic with recurrent/persistent hematuria-proteinuria and CKD progression; course is heterogeneous (pqac-00000000, pqac-00000008) | Mechanism-aligned therapy focuses on **complement inhibition** and complement-directed trial enrollment; supportive CKD/proteinuria management remains important (pqac-00000000, pqac-00000008) |
| **Monoclonal gammopathy-related GN** (for example MGRS-associated GN) | Nephrotoxic monoclonal immunoglobulin or light/heavy chain–related glomerular injury from plasma-cell or B-cell clone (subtype-specific) (pqac-00000000) | Biopsy pattern varies by deposit type; identification of a pathogenic monoclonal protein/clone is central to classification (pqac-00000000) | Monoclonal immunoglobulin-driven injury; clone biology rather than generic histology should drive treatment (pqac-00000000) | Often chronic/progressive unless the responsible clone is controlled; renal phenotype depends on deposit composition and location (pqac-00000000) | **Clone-directed therapy**: plasma-cell– or B-cell–targeted treatment rather than nonspecific GN immunosuppression alone (pqac-00000000) |
| **Alloimmune GN** (transplant-related alloimmune glomerular injury) | Alloimmune responses to non-self renal antigens after transplantation; distinct from autoimmune GN (pqac-00000000) | Diagnosis relies on biopsy plus transplant immunopathology context; antibody/complement staining patterns may support alloimmune injury (pqac-00000000) | Adaptive alloimmunity, antigen presentation, antibody-mediated injury, complement activation (pqac-00000000) | Variable; may be subacute or chronic and contribute to graft dysfunction/loss (pqac-00000000) | Mechanism-aligned approach is **suppression of adaptive immunity** with transplant-directed immunosuppression optimization (pqac-00000000) |


*Table: This table summarizes the major mechanistic glomerulonephritis classes and key subtype-specific features relevant to diagnosis, pathobiology, course, and treatment. It is useful as a compact knowledge-base scaffold because GN is heterogeneous and treatment increasingly follows mechanism rather than histology alone.*