Lupus nephritis: current update

Abstract

Lupus nephritis is a major cause of morbidity and mortality in patients with systemic lupus erythematosus. The general consensus is that 60% of lupus patients will develop clinically relevant nephritis at some time in the course of their illness. Prompt recognition and treatment of renal disease is important, as early response to therapy is correlated with better outcome. The present review summarizes our current understanding of the pathogenic mechanisms underlying lupus nephritis and how the disease is currently diagnosed and treated.

Enhanced Activity of Akt in Teff Cells From Children With Lupus Nephritis Is Associated With Reduced Induction of Tumor Necrosis Factor Receptor–Associated Factor 6 and Increased OX40 Expression

“…The incidence of nephritis is greater in children with SLE than in adults (5), and though the prognosis has improved over the past decades, lupus nephritis remains a major cause of mortality and morbidity (6). The disease course of lupus nephritis in children is more severe than that in adults, requiring intensive immunosuppressive therapy that is associated with severe side effects (7,8).…”

The Pathogenesis of Lupus Nephritis

“…2,3 Second, the nuclear antigens used for immunization had to be accessible to antigen-presenting cells, a process that is normally avoided by the homeostatic mechanism of rapid dead cell clearance. In fact, SLE develops in individuals with unfortunate combinations of genetic variants that, among other immunoregulatory defects, compromise those mechanisms that normally assure low levels of chromatin in extracellular compartments, particularly mutations that alter apoptosis, 4,5 the opsonization of dead cells by complement, or their removal by phagocytes. 6 Neutrophils undergo NETosis, which releases nucleosomes into the extracellular extracellular space.…”

Antiinflammatory strategies, not just B cell depletion, are required for optimal therapy for severe proliferative lupus nephritis: Comment on the article by Rovin et al

“…However, we believe that the more likely explanation is that once kidney inflammation is initiated via immune complex deposition, the potential for damage progression is independent of autoantibody generation. Potential mechanisms likely involve inflammatory cytokine and chemokine production, as well as infiltration of the kidney by inflammatory cells and activation of kidney-resident cells (3).…”