Tap a disease → see the exam fingerprint

This is the core comparison from the PDF, tightened into Step 1 pattern recognition.

High-yield IF pattern ladder

Granular “lumpy-bumpy”Immune complex deposition: SLE, IgA vasculitis/HSP, mixed cryoglobulinemia.

Linear IgGAnti-GBM/Goodpasture. Pathognomonic along GBM.

Pauci-immuneANCA vasculitis: crescents, minimal to no deposits.

Congo red apple-greenAmyloidosis: fibrils in mesangium and capillary walls, nephrotic syndrome.

Nephritic: hematuria/RBC castsNephrotic: heavy proteinuriaRPGN: crescents + rapid renal failure

SLE: immune complexes with many faces

SLE kidney disease is mostly type III immune complex injury, with type II cytopenias and antiphospholipid overlap as classic systemic traps.

Specific antibodiesAnti-dsDNA and anti-Sm; ANA is sensitive but less specific.

MechanismImmune complexes deposit in mesangial, subendothelial, subepithelial, or intramembranous sites.

Diagnosis ruleAt least 4 criteria, including ≥1 clinical and ≥1 immunologic; they need not occur at the same time.

Kidney clueProteinuria, hematuria, hypertension; Class IV is most common/severe in many exam framings.

PDF pages 3–10

Lupus nephritis classes: mesangial → membranous

Minimal mesangialMildest, mesangial deposits only

mild

Mesangial proliferativeMesangial hypercellularity

mesangial

III

Focal proliferative<50% glomeruli involved

prolif

Diffuse proliferative>50% glomeruli; worst prognosis / high yield

most severe

MembranousSubepithelial deposits, thickened GBM

nephrotic

Advanced sclerosisESRD-like scarring

scar

PDF page 13

ANCA vasculitis: same renal pattern, different clues

All can give pauci-immune necrotizing crescentic GN. The exam differentiates them by airway, lung, eosinophils, granulomas, and ANCA type.

GPA / Wegenerc-ANCA / PR3. Upper airway + lower airway cavitary nodules + kidney. Necrotizing granulomas.

EGPA / Churg-Straussp-ANCA / MPO. Asthma, allergic rhinitis, lung infiltrates, eosinophilia, ↑IgE, granulomas.

MPAp-ANCA / MPO. Alveolar hemorrhage + kidney; no granulomas, no nasopharyngeal involvement.

Renal biopsyCrescents with minimal/no IF deposits; EM may show ruptures in GBM.

PDF pages 21–24

Two look-alikes in the same neighborhood

IgA vasculitis / HSPMost common vasculitis in children; post-URI/GAS. Palpable purpura on buttocks/legs + arthralgia + colicky abdominal pain + renal IgA/C3 mesangial deposits.

Mixed cryoglobulinemiaHepatitis C trigger. Palpable purpura + weakness + arthralgia; immune complex vasculitis; renal MPGN type I pattern.

Memory hookKids + IgA + belly = HSP. HCV + purpura/arthralgia/weakness = cryoglobulins.

PDF pages 17–20, 28

Anti-GBM / Goodpasture: the straight-line disease

Autoantibodies target the α3 chain of type IV collagen in GBM and alveolar basement membrane. That gives the classic kidney-lung syndrome.

α3

Antibody against NC1 domain of α3 chain of type IV collagen.

Type II hypersensitivity with complement/Fc-mediated injury.

Linear IgG deposits on immunofluorescence — pathognomonic.

⚠

Hemoptysis + pulmonary hemorrhage + hematuria/RBC casts + crescentic GN.

PDF pages 25–27

Amyloidosis: nephrotic protein spill

DepositMisfolded AL or AA amyloid fibrils in glomeruli, mesangium, and capillary walls.

StainCongo red positive with apple-green birefringence under polarized light.

MorphologyMesangial matrix thickening, uneven GBM widening, capillary obliteration, broad ribbons/masses.

ClinicalProteinuria and nephrotic syndrome are common; renal failure may occur.

PDF pages 15–16, 28

Diabetic nephropathy: AGE-RAGE → thick GBM → nodules

Hyperglycemia → ↑HbA1c and advanced glycation end products (AGEs).

AGEs bind RAGE on inflammatory cells → cytokines/growth factors like TGF-β and VEGF.

Excess basement membrane material → GBM thickening and protein leak.

Diffuse mesangial matrix expansion → PAS-positive Kimmelstiel-Wilson nodules.

Hyaline arteriolosclerosis, ischemia, tubular atrophy, interstitial fibrosis → small kidney.

PDF pages 29–33

Incipient vs overt diabetic nephropathy

Incipient

Hyperfiltration, early mesangial expansion
Mild GBM thickening
Microalbuminuria: 30–300 mg/day
GFR normal or increased
Potentially reversible with glycemic control

Overt

Persistent hyperglycemia injury
Advanced mesangial expansion
Macroalbuminuria: >300 mg/day
Progressive GFR decline
Kimmelstiel-Wilson nodules; irreversible progression risk

First EM change: GBM thickeningCommon: diffuse mesangial sclerosisPathognomonic: KW nodules

PDF pages 29, 31, 35

Checkpoint

Score 0/0

Fast exam traps

Goodpasture vs ANCABoth can be RPGN + lung. Linear IgG = anti-GBM; pauci-immune = ANCA.

Lupus class IVDiffuse proliferative, >50% glomeruli, severe; class V is membranous/nephrotic.

Diabetes timelineEarliest clinical sign is microalbuminuria; earliest morphologic EM change is GBM thickening.

HSP vs cryoHSP = child, IgA, abdominal pain. Cryo = HCV, purpura + weakness + arthralgia, MPGN.

Systemic diseases that scar the glomerulus

How to attack any renal-systemic vignette

Systemic Renal Lesions