Abstract
Nephrotic syndrome is the most common glomerular disease in children. While the exact pathogenesis of nephrotic syndrome is not fully understood, recent research has shed light on some of the underlying mechanisms involved in it. Improvement by B cell depletion therapy using antiCD20 in nephrotic syndrome has led to a paradigm shift from immunoinflammatory disease influenced by T cell dysregulation to B cell involvement in the pathogenesis of nephrotic syndrome. The expression of the B cell activating factor (BAFF), an essential cytokine for the maturation and differentiation of B lymphocytes, in the podocytes of paediatric patients with nephrotic syndrome is known to be associated with worse renal outcomes. The pro-inflammatory cytokines and pathogenic antibodies produced by B cells allegedly cause podocyte injury leading to proteinuria due to effacement of foot processes. Considering the role of the BAFF in B cell proliferation and antibody production, BAFF signalling is a potential target for development as targeted therapy in nephrotic syndrome. Nevertheless, there is limited research regarding the role of BAFF in nephrotic syndrome, and the exact mechanism of BAFF involvement in the pathogenesis of nephrotic syndrome is still unknown. This review discusses the role of the BAFF in the pathogenesis of nephrotic syndrome and highlights the gap of knowledge for future research.