Sle pathology
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"systemic lupus erythematosus" AND pathology
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systemic lupus erythematosus pathology lupus nephritis ISN RPS classification 2018 review
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Systemic lupus erythematosus (SLE): pathology
SLE is a multisystem autoimmune immune-complex disease. Loss of self-tolerance causes production of antinuclear antibodies, particularly anti-dsDNA. Antigen-antibody complexes deposit in tissues, activate complement, and produce inflammation, vasculitis, necrosis, and later fibrosis. The principal mechanism is a type III hypersensitivity reaction.
Brenner and Rector's The Kidney, 2-Volume Set, p. 1452.
Brenner and Rector's The Kidney, 2-Volume Set, p. 1452.
Characteristic pathological lesions
- Hematoxylin bodies (LE bodies): Round/smudgy lilac structures composed of denatured nuclear material complexed with ANA. They are highly characteristic but rare in tissue biopsies.
- Vasculopathy/vasculitis: Immune-complex mediated vessel-wall injury, fibrinoid necrosis, thrombosis, and thrombotic microangiopathy. Antiphospholipid antibodies can cause arterial or venous thrombosis.
- Libman-Sacks endocarditis: Sterile verrucous vegetations, usually on either surface of mitral or aortic valve leaflets.
- Serositis: Fibrinous pleuritis, pericarditis, or peritonitis, sometimes with immune-complex deposition.
- Skin: Interface dermatitis, basal-cell vacuolar degeneration, perivascular/periadnexal lymphocytic infiltrates, and immune deposits at the dermoepidermal junction, called the lupus band.
Lupus nephritis
Renal disease is the key pathology and an important prognostic feature. Glomerular immune deposits activate complement and inflammation. Biopsy may also show tubulointerstitial inflammation/fibrosis and vascular lesions, including thrombotic microangiopathy.
Goldman-Cecil Medicine, p. 2817.
Goldman-Cecil Medicine, p. 2817.
Immunofluorescence
Typical finding is “full-house” immunofluorescence:
- IgG
- IgA
- IgM
- C3
- C1q
Strong C1q staining supports lupus nephritis. On electron microscopy, deposits may occur in mesangial, subendothelial, and subepithelial sites.
ISN/RPS classes of lupus nephritis
| Class | Lesion |
|---|---|
| I | Minimal mesangial LN: normal light microscopy, mesangial immune deposits on IF/EM |
| II | Mesangial proliferative LN: mesangial hypercellularity and matrix expansion |
| III | Focal LN: active/chronic proliferative lesions in <50% glomeruli |
| IV | Diffuse LN: active/chronic proliferative lesions in ≥50% glomeruli |
| V | Membranous LN: diffuse subepithelial deposits with capillary-wall thickening |
| VI | Advanced sclerosing LN: predominantly globally sclerosed glomeruli |
Classes III and IV can show:
- Endocapillary proliferation
- Wire-loop lesions from extensive subendothelial immune deposits
- Hyaline thrombi
- Necrosis
- Cellular crescents
- Hematoxylin bodies
The 2018 revision emphasizes separate assessment of activity and chronicity indices. A high chronicity burden, including glomerulosclerosis, tubular atrophy, and interstitial fibrosis, implies worse renal prognosis. The ISN/RPS classification is summarized in this renal pathology review.
One-line exam summary
SLE is an immune-complex-mediated multisystem disease characterized by ANA-associated tissue injury, hematoxylin bodies, vasculitis/thrombosis, Libman-Sacks endocarditis, lupus-band dermatitis, and full-house immune-complex lupus nephritis.
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