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Background: Vitamin D has immunomodulatory function. Polymorphisms of the gene encoding the vitamin D receptor detected by BsmI may be source of diversity in its action. An association between vitamin D receptor gene BsmI polymorphisms and lupus nephritis has been reported. This study was performed to evaluate vitamin D receptor gene BsmI polymorphisms in lupus nephritis. Methods: Twenty nine patients with lupus nephritis enrolled in this study. Vitamin D receptor gene typing was performed based on polymerase chain reaction-restriction fragment length polymorphism. Finding: Vitamin D receptor genotyping of BsmI polymorphisms was 20.6% for BB, 51.7% for Bb, and 27.5% for bb without statistically significant difference (P = 0.090). In 21 patients that renal biopsy was done, the Bb genotype was the most (42.8%). There was not any correlation between renal histology and vitamin D receptor gene BsmI polymorphisms (P = 0.068). Conclusion: There was no relationship between vitamin D receptor gene BsmI polymorphisms and lupus nephritis. [ABSTRACT FROM AUTHOR]

Background: Soluble FAS (sFAS) is an apoptosis "programmed cell death" marker and results from shedding of FAS molecules during activation of FAS mediated apoptosis. There are several important reasons that Apoptosis is deregulated in active systemic lupus erythematosus and FAS is over expressed by T-cells; although the role of its soluble form (sFas) is unclear. We have investigated the correlation between serum levels of sFAS and active organ damages in lupus patients. Methods: Our study was performed on 114 systemic lupus erythematosus patients, compared with 50 randomly selected sex-, age- and race-matched healthy controls. The patients were randomly selected in different phases of disease activity. All the physical examinations and laboratory parameters were collected for determination of the SLEDAI index. sFAS, AntidsDNA, C3, and C4 levels were determined using a commercially available ELISA kit. Findings: There was a significant difference between serum levels of sFAS in the case and control groups (P = 0.001). We found a significant correlation coefficient between the sFAS and SLEDAI2K variables (P = 0.001, r= 0.494). It was a significant statistical difference between serum levels of sFAS in patients with rising in amount of proteinuria more than 0.5 g/l in 24h urine sample collection and without it (P = 0.04), and central nervous system (CNS) damage versus normal CNS patients (P = 0.006). It was not difference between sFAS and cardiac damage (P = 0.05) but it was near significant difference. Conclusion: We found a correlation between sFAS serum levels and central nervous system involvement and rising in amounts of proteinuria in systemic lupus erythematosus patients. [ABSTRACT FROM AUTHOR]