| Feature | Minimal Change (MCD) | FSGS | Membranous Nephropathy | Amyloidosis | Diabetic Nephropathy |
|---|---|---|---|---|---|
| Trigger | Idiopathic; recent URI, NSAIDs, Hodgkin lymphoma | HIV, heroin, obesity, sickle cell, APOL1 variants | SLE, HBV/HCV, solid tumors, NSAIDs, anti-PLA2R autoAb | Multiple myeloma (AL); chronic inflammatory disease (AA) | Long-standing diabetes mellitus |
| Mechanism | Cytokine-mediated podocyte damage → loss of charge barrier → selective albumin leak. No IC deposition. | Podocyte injury & detachment → focal sclerosis. Primary (podocin/APOL1) or secondary (HIV, heroin, obesity, sickle cell). | Subepithelial IC deposition (anti-PLA2R Ab) → complement activation → podocyte injury → GBM thickening. | Misfolded protein (AL from myeloma, AA from chronic inflammation) deposits in mesangium & capillary walls. | Hyperglycemia → glycosylation of GBM → mesangial expansion → Kimmelstiel-Wilson nodules. Hyperfiltration injury. |
| HSR Type | TYPE IV T-cell cytokine–mediated podocyte injury |
NON-IMMUNE Podocyte structural damage; adaptive in secondary |
TYPE III In-situ IC (anti-PLA2R) → subepithelial deposits |
NON-IMMUNE Protein misfolding / deposition |
NON-IMMUNE Non-enzymatic glycosylation of GBM |
| Age / Demographics | Children #1 nephrotic in kids | Adults #1 nephrotic in African Americans | Adults European, Middle Eastern | Adults | Long-standing DM |
| Light Microscopy | Normal | Focal, segmental sclerosis with hyalinosis | Diffuse capillary wall thickening | Amorphous eosinophilic deposits | Mesangial expansion, nodular sclerosis (Kimmelstiel-Wilson) |
| Immunofluorescence | Negative | Negative or IgM/C1/C3 in sclerotic areas | Granular IgG and C3 | Apple-green birefringence with Congo red | Linear IgG along GBM |
| Electron Microscopy | Diffuse podocyte foot process effacement (only finding) | Foot process effacement + sclerosis | Subepithelial IC → "spike and dome" | Random fibrillar deposits (8–12 nm) | GBM thickening |
| Complement | Normal | Normal | Normal | Normal | Normal |
| Proteinuria | Highly selective | Non-selective | Non-selective | Non-selective | Non-selective |
| Steroid Response | Excellent | Poor | Variable | No | No |
| Prognosis | Very good | → ESRD | Variable | Progressive | Progressive |
| Feature | PIGN | IgA Nephropathy (Berger) | RPGN | Diffuse Prolif. GN (Lupus) | Alport Syndrome | MPGN |
|---|---|---|---|---|---|---|
| Trigger | 2–4 wks post Group A Strep pharyngitis / impetigo. Adults: Staph | URI or GI infection → hematuria within days (synpharyngitic) | Autoimmune disease, infection, ANCA+ vasculitis | SLE (autoimmune) | Inherited (X-linked collagen IV defect) | HBV, HCV, SLE, C3 nephritic factor |
| Mechanism | IC vs strep Ag (M protein) → subepithelial deposits → complement activation (↓C3) → GBM damage | Defective IgA1 glycosylation → mesangial IgA deposition → mesangial proliferation. | I: Anti-GBM Ab (Goodpasture if +lungs) II: IC (SLE, PIGN) III: Pauci-immune / ANCA+ (GPA, MPA) |
Anti-dsDNA + complement → subendothelial IC → severe inflammatory proliferation. Class IV. | X-linked defect in type IV collagen (α5 chain) → abnormal GBM → progressive deterioration. | I: subendothelial IC (HBV, HCV, SLE). II: C3NeF stabilizes C3 convertase → intramembranous dense deposits. |
| HSR Type | TYPE III Circulating IC → subepithelial deposits |
TYPE III IgA IC → mesangial deposition |
I: TYPE II anti-GBM II: TYPE III IC III: TYPE IV pauci-immune |
TYPE III Anti-dsDNA IC → subendothelial |
NON-IMMUNE Genetic collagen IV defect |
TYPE III I: IC. II: complement (C3NeF) |
| Onset | Acute (2–4 wk latency) | Episodic | Rapid (weeks) | Variable | Progressive | Subacute |
| Age / Demographics | Children & adults | Young adults | Any age | Young women | Children (X-linked boys) | Children & young adults |
| Light Microscopy | Enlarged, hypercellular glomeruli | Mesangial proliferation | Crescent formation (fibrin + macrophages) | "Wire-loop" capillaries | Normal early | "Tram-track" (GBM splitting) |
| Immunofluorescence | Granular IgG, C3 "starry sky" | Granular IgA (mesangial) | I: Linear (anti-GBM) II: Granular III: Negative |
IgG, IgA, IgM, C3 "full house" | Negative | Granular C3 ± IgG |
| Electron Microscopy | Subepithelial humps | Mesangial deposits | Usually no deposits (III); depends on type | Subendothelial deposits | GBM thinning / splitting → "basket-weave" | I: subendothelial IC II: intramembranous dense deposits |
| Complement | ↓ C3 | Normal | Normal | ↓ C3 | Normal | ↓ C3 |
| Key Clinical | Cola-colored urine, edema, HTN | Hematuria within days of URI | Rapid renal failure | Systemic SLE signs | Hearing loss, eye defects | Mixed nephritic / nephrotic |
| Anti-GBM Ab | No | No | Yes (Type I / Goodpasture) | No | No | No |
| Treatment | Supportive ± treat infection | ACEi ± steroids | Plasmapheresis + steroids (I); immunosuppression (II/III) | Immunosuppression | Supportive; transplant | Treat underlying cause |
| Prognosis | Kids: good. Adults: worse | Variable | Poor w/o Tx | Variable | Progressive | Often progressive |