New insights into the role of renal resident cells in the pathogenesis of lupus nephritis

Abstract

Systemic lupus erythematosus (SLE), an autoimmune disease of unknown etiology, is characterized by the production of autoantibodies and end-organ damage. Lupus nephritis affects up to 70% of patients with SLE and is the most critical predictor of morbidity and mortality. The immunopathogenesis of SLE is complex and most clinical trials of biologics targeting immune cells or their mediators have failed to show efficacy in SLE patients. It has therefore become increasingly clear that additional, local factors give rise to the inflammation and organ damage. In this review, we describe recent advances in the role of renal resident cells, including podocytes, mesangial cells, and epithelial cells, in the pathogenesis of lupus nephritis.

Keywords: Autoimmune diseases; Lupus nephritis; Podocytes; Systemic lupus erythematosus.

Figure 1.

Proposed model of the development of lupus nephritis. Autoimmunity persists from the asymptomatic stage to the stage marked by chronic kidney disease (CKD). Podocyte dysfunction ,may already occur at an early stage of the kidney damage process, ultimately leading to overt proteinuria and CKD. Identification of a common intracellular pathway that mediates not only aberrant immune cell activation related to autoimmunity but also podocyte dysfunction, will lead to a better understanding of the pathogenesis of lupus nephritis.