Lupus nephritis (LN) is a major cause of morbidity in patients with systemic lupus erythematosus (SLE). Several cytokines and apoptotic markers such as IL-18 and soluble Fas (sFas) have been assumed to play a role in the pathogenesis of LN. Previous studies confirmed that serum concentrations of sFas and IL-18 are increased in SLE. However, only a few studies have suggested a possible correlation between IL-18 and sFas. This study was planned to continue our previous study on the correlation between those markers to evaluate this correlation in LN. Thirty-two patients with only LN and 46 patients without any major organ involvement participated in this study. SLEDAI score (except for scores related to nephritis) was the same in these two groups. In both groups, patients with any other major organ involvement were excluded. We found a significant rise in the serum concentrations of sFas ( ) and IL-18 ( ) in patients with proteinuria compared to those without it. This study showed that the correlation between sFas and IL-18 in LN ( , ) is significantly stronger than it is in mild SLE ( , ) with similar nonrenal SLEDAI score ( , ). Between these two serum markers, sFas is the only predictor of proteinuria. 1. Introduction Lupus nephritis is a serious complication of SLE. Proteinuria is the most frequently observed abnormality in lupus nephritis [1, 2]. Although the precise etiology of LN is not entirely known, several factors have been proposed in the initiation and progression of LN. Two important factors that are suggested to be involved in that are apoptosis imbalance [3] and overproduction of several cytokines like IL-18 [4]. Researchers have emphasized the pathogenic function of IL-18 and Fas/Fas ligand pathway in autoimmune-related diseases like lupus [5–7]. Besides, recent evidence suggests that IL-18- and Fas-mediated apoptosis may relate to each other by the proapoptotic effects of IL-18. IL-18 is able to enhance Fas/Fas ligand expression in specific cells [8, 9]. Fas (Apo/1-CD95) and its ligand belong to the tumor necrosis factor/nerve growth factor superfamily [10–16]. IL-18, a TNF-α inducer and Fas/Fas ligand expressor, is a crucial factor for the autoimmune process [5, 8, 9, 17–19]. Although the role of IL-18 and sFas has been elucidated separately, in the pathogenesis of LN [1, 4, 20], there is little evidence about the correlation between sFas and IL-18 in autoimmune diseases. Only a few studies mentioned that infections could raise serum sFas and IL-18 concentrations through increasing and/or enhancing apoptotic turnover of defensive cells
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