Prognostic Significance of Clinical, Pathogenetic and Genetic Features Progression of Lupus Nephritis

Abstract

Systemic lupus erythematosus (SLE) is a heterogeneous autoimmune disease characterized by the presence of pathogenic autoantibodies, impaired immune regulation and chronic inflammation, which can lead to an increase in morbidity and early mortality from damage to end organs. More than half of all patients with SLE develop lupus nephritis. Genetic association studies have identified more than fifty polymorphisms that contribute to the pathogenesis of lupus nephritis, including genetic variants associated with altered programmed cell death and defective immune clearance of residues. These variants may contribute to the formation of immune complexes containing autoantibodies that contribute to the development of lupus nephritis. Genetic variants associated with lupus nephritis also affect the initial phase of innate immunity and the reinforcing, adaptive phase of the immune response. Finally, genetic variants associated with a kidney-specific effector response may affect damage to end organs and progression to end-stage renal failure and death. This review discusses the genetic understanding of key pathogenetic processes and pathways that can lead to lupus nephritis, as well as the clinical implications of these discoveries in connection with recent advances in biological therapy.