Systemic lupus erythematosus is more frequent in Asian women as well. The usual onset of SLE is between 15 and 45 years of age. Several trigger factors for SLE has been detected. The tissue injury is caused by immune complexes, deposition of which induces cell infiltration and damage to the tissue by proteolytic and collagenolytic enzymes. Histopathology of affected tissue reveals vasculitis with fibrinoid necrosis and deposition of immunoglobulin and complement in small vessels and capillaries.
Renal involvement begins with deposition of immune complexes in the glomeruli.
Mesangial proliferation, glomerular necrosis, hyaline thrombus formation, and interstitial damage determine the severity of kidney disease. Laboratory manifestation Patients with SLE produce wide spectrum of autoantibodies. The activity of the disease can be monitored by the levels of ANA, complement, cryoglobulins, and circulating immune complexes measured by the Raji cells assay. The patients with SLE may present with various systemic manifestations. Although almost in all cases deposits of immunoglobulin are found in the glomeruli, only one half has clinical nephritis.