Lupus Nephritis; Pathogenesis and Treatment Update Review

Abstract

Lupus nephritis (LN) is a serious complication of systemic lupus erythematosus (SLE). LN is a leading cause of morbidity and mortality in SLE patients. LN presents with various symptoms and signs, ranging from asymptomatic renal involvement to End-Stage Renal Failure (ESRD). The pathogenesis of LN is not clearly understood, however, there are extra and intra-renal underlying factors that have been postulated in LN pathogenesis. Renal biopsy is crucial to stage LN and to rule out other causes. Histopathological studies have shown six different types of LN. Knowing the histopathological lesion, chronicity and the disease activity are essential to plan the LN treatment and to predict the outcome. There are different regimens for treating LN. In this review, LN pathogenesis and new advances in treatment will be briefly reviewed.

Treatment of Lupus Nephritis from Iranian Traditional Medicine and Modern Medicine Points of View: A Comparative Study

“…Among these factors, SLE, simply called lupus, is one of the most significant causes of nephritis, which is known as lupus nephritis (LN). In fact, sedimentation of inflammatory mediators in the kidney tissue as the main result of SLE leads to glomerulonephritis and tubulointerstitial inflammation [ 11 , 12 ].…”

“…Various studies have confirmed that the activation of nuclear factor kappa B (NF- κ B) signal pathway via upregulation of proinflammatory mediators such as cyclooxygenase-2 (COX-2) and tumor necrosis factor- α (TNF- α ) is responsible for LN [ 13 ]. Also, it has been demonstrated that B- and T-cell hyperactivity [ 14 ], increased T helper 1 (Th1) and T helper 17 (Th17) cytokines [ 15 , 16 ], activation of JAK/STAT-3 signaling [ 17 ], elevation of anti-double-stranded DNA (anti-dsDNA) antibodies [ 12 ], autoantibodies against proteins involved in clearing extracellular nuclear material such as pentraxin 3 or C-reactive protein [ 18 ], interleukin-6 (IL-6), interleukin-17 (IL-17), interleukin-23 (IL-23), TNF- α [ 19 , 20 ], oxidative stress [ 14 ], decreased T regulator cells (Tregs) [ 21 ], and complement system [ 22 ] play important roles in the pathophysiology of LN.…”