Lupus Nephropathy
- In patients with SLE
- Autoimmune hyperactive circulating DNA-ANA
- Deposit in kidney ( glomerulus) ) and initiate inflam
- Genetic and environmental susceptibility
- Genes + UV rays → damaged DNA → Immune sys attacks DNA via ANA → ANA binds to Ag → forms IC →deposits in organs → causes inflam
Clinical features
- During flares – fever, WL, lymphadenopathy
- Skin – malar rash, SCLE
- Arthritis
- Raynaud’s phenomenon
- CDV – myocarditis, Libman-Sacks endocarditis (fibrin vegetations due to hypercoagulability assoc with anti-PL Ab)
- Lupus nephritis – proteinuria, hematuria, nephritic/nephrotic syn, mesangial + sub-epithelial deposits (cause glom inflam)
Stages of LN
- 1 – minimal mesangial LN – no change on biopsy, few deposits may be seen
- 2 – mesangial proliferation LN – deposits in mes
- 3 – focal LN – focal and segmental proliferation, necrosis + sclerosis, increased deposits
- 4 – diffuse LN – hypercellularity, membranous proliferation changes, necrosis + sclerosis
- 5 – membranous LN – cap wall expansion, deposits in sub epithelial area
- 6 – advanced sclerosing LN – glomerulosclerosis
Diagnosis
- Immunofluorescence – C3, IgG, M, A
- C1q antibodies indicates active nephritis
- Appear as lumps and bumps
- Presence of ANA, ↑ESR, anemia, low platelets, low WBC + ly
- Mesangioproliferative GN
Treatment
- Analgesics, NSAIDs, hydroxycholoroquine (200-400mg/day)
- CTST + IS (cyclophosphamide)
- ACEI /ARBs – for proteinuria
- Stages 1 and 2 require no treatment, only monitoring