**1. Introduction**

Systemic lupus erythematosus (SLE) is a chronic multisystem autoimmune disease that frequently involve kidneys in women. The development of the disease is related to exposure to environmental factors in individuals with genetic predisposition. It is characterized by loss of tolerance against nuclear autoantigens, lymphoproliferation, polyclonal autoantibody production, immune complex disease and multiorgan tissue inflammation [1]. The affected organs include skin, joints, heart, lungs, kidneys, central nervous system and serous membranes. The disease involves a sequence of manifestations such as arthritis, serositis, chronic fatigue, skin rashes, glomerulonephritis, neurological involvement and hematological abnormalities [2]. SLE is the most frequent cause of secondary glomerular disease [3–5]. Lupus nephritis (LN) as a disease usually develops early in the clinical course of SLE in up to 50% of patients. The development of effective diagnostic tests and the introduction of new therapies has shown an improvement in the survival of patients with SLE. However, SLE patients still have a higher risk of death than the general population, especially patients with LN. Lupus glomerulonephritis with intense activity requires greater immunosuppression with increased risk of death from opportunistic infections. On the other hand, long-term treatment with high-dose

of corticosteroids is a risk factor for coronary atherosclerosis and cardiovascular disease [1, 6]. Glomerular immune complexes can activate complement and engage leukocyte Fc receptors to initiate renal inflammation and injury [1]. LN has very pleomorphic clinical and morphologic expressions. Clinical findings range from asymptomatic hematuria and proteinuria to nephrotic syndrome or rapidly progressive renal failure [7].
