Lupus nephritis (renal involvement)
Renal involvement determines the severity of SLE. The pathogenesis is based on the formation of immune complexes (consisting of DNA and anti-DNA antibodies) directly in situ. These complexes are deposited in the mesangium and glomerular capillary basement membranes. The localization of deposits determines the specific clinico-morphological form of glomerulonephritis.
- Macroscopic appearance: kidneys are enlarged, mottled in appearance due to areas of petechial hemorrhages.
- Microscopic appearance: specific nuclear pathology — hematoxylin bodies — is revealed. The «wire loop» phenomenon is characteristic, representing a marked thickening of capillary basement membranes due to massive subendothelial deposits. Foci of fibrinoid necrosis and hyaline thrombi are also detected.
- Electron microscopy: virus-like inclusions are visualized in capillary endothelial cells.
In addition to glomeruli, tubulointerstitial changes develop in 50% of cases, caused by granular deposits in the tubular basement membrane.
Skin and joint changes
Skin involvement is a classic sign of SLE. The most well-known is well-demarcated erythema in the form of a «butterfly» pattern on the bridge of the nose and cheeks.
- In the acute phase: dermal edema, vasculitis with fibrinoid necrosis of vessel walls, and perivascular lymphomacrophage infiltration are observed.
- During remission/resolution: dermal sclerosis, epidermal atrophy and hyperkeratosis, and vacuolization of basal layer cells develop. Damage to hair follicles leads to hair loss.
Immunohistochemical examination reveals deposits of immunoglobulins and complement at the dermal-epidermal junction.
Acute, subacute, or chronic synovitis occurs in the joints. Its key feature is a non-erosive character: inflammation proceeds with desquamation of the lining synoviocytes and vasculitis, but without deformity of the joints themselves. Sclerioric villi are found in the tissue.
Cardiovascular system and CNS
The inflammatory process in SLE is generalized and affects vital life-support systems:
- Heart: inflammation can involve all layers (pericarditis, myocarditis). Abacterial verrucous Libman-Sacks endocarditis forms on the endocardium. Atherosclerosis develops more frequently in the coronary arteries.
- Vessels: arteriolitis, capillaritis, and venulitis occur in the microvasculature. In large vessels (including the aorta), elastolysis and elastofibrosis are observed due to damage to vasa vasorum.
- Central nervous system: neurological symptoms are associated with the action of antiphospholipid, antineuronal antibodies, and antibodies to the synaptic membrane. Morphologically, this manifests as productive or productive-destructive vasculitis, thrombosis without vasculitis, ischemic infarctions, hemorrhages, and neurocyte necrosis.
Spleen, lungs, and immune system
- Spleen: macroscopically enlarged. Microscopically, follicular hyperplasia and plasmacytic infiltration of the pulp are revealed. A specific sign is «onion-skin» periarterial fibrosis.
- Lungs: the most characteristic manifestation is pleuritis. Lupus pneumonitis with involvement of the lung tissue itself and vasculitis develops less frequently, ultimately leading to interstitial fibrosis and pulmonary hypertension syndrome.
- Lymphoid tissue: large follicles with germinal centers appear in the thymus (in expanded perivascular spaces) and enlarged lymph nodes.
Briefly: answers to topical questions
On which valves and leaflet surfaces do vegetations localize in Libman-Sacks endocarditis?
In atypical verrucous Libman-Sacks endocarditis, vegetations localize predominantly on left-sided valves: the mitral valve is most frequently affected, somewhat less often the aortic or tricuspid valve. A characteristic feature is the bilateral arrangement of deposits, i.e., involvement of both sides of the valve leaflets. The verrucous deposits themselves form directly in areas of endocardial ulceration.
How does joint damage in SLE morphologically differ from rheumatoid arthritis?
Systemic lupus erythematosus develops non-erosive synovitis without joint deformity. Microscopically, desquamation of lining synoviocytes, sclerosed villi, vasculitis with fibrinoid necrosis of walls, and perivascular infiltration are revealed. Morphological signs of joint involvement in rheumatoid arthritis are not detailed in the provided sources.
What specifically do hematoxylin bodies consist of in lupus nephritis?
Hematoxylin bodies represent freely lying destroyed nuclei.
The abbreviation WFH (Wire loops [membrane thickening], Hematoxylin bodies [nuclear pathology], Fibrinoid necrosis) will help remember the characteristic microscopic picture of lupus nephritis.
Class and exam questions
What type of necrosis is characteristic of vasculitis during SLE exacerbation?
During exacerbation of systemic lupus erythematosus, fibrinoid necrosis develops in the walls of blood vessels in the skin, joints, and other organs.
What is the «wire loop» phenomenon?
This is pathological thickening of the capillary basement membranes of renal glomeruli, which occurs as a result of massive subendothelial deposition of immune complexes.
Does joint involvement in SLE lead to their deformation?
No, systemic lupus erythematosus is characterized by the development of non-erosive synovitis, which proceeds without joint deformity.
What is the main cause of death in patients with SLE?
The most frequent severe outcome of the disease is acute or chronic renal failure with the development of uremia against the background of progressive lupus nephritis.
What else to study on this topic
- Classification of lupus glomerulonephritis (focal and diffuse proliferative)
- Morphological variants of glomerulonephritis (membranous, mesangioproliferative, fibroplastic)
- Pathogenesis of CNS involvement: the role of antiphospholipid and antineuronal antibodies
- Tubulointerstitial renal changes and their connection with immune complex deposits
- Changes in the thymus and lymph nodes in SLE
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