Vitamin D Receptor (VDR) Gene BsmI Polymorphisms in Lupus Nephritis

Document Type : Original Article(s)

Authors

1 Assistant Professor, Metabolic Research Center, Department of Rheumatology, Qazvin University of Medical Sciences, Qazvin, Iran.

2 Associate Professor, Rheumatic Diseases Research Center, Department of Rheumatology, Mashhad University of Medical Sciences, Mashhad, Iran.

3 Associate Professor, Immunology Research Center, Department of Immunology, Mashhad University of Medical Sciences, Mashhad, Iran.

4 Assistant Professor, Rheumatic Diseases Research Center, Department of Rheumatology, Mashhad University of Medical Sciences, Mashhad, Iran.

Abstract

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.

Keywords

References

  1. Edwolthy SM. Clinical manifestation of systemic lupus erythematosus. In: Harris E, Budd R, Firestein G, Genovese M, Sergent J, Ruddy S, et al. Kelley's text book of rheumatology. 7th ed. Philadelphia: WB. Saunders. 2005. p. 1105-23.
  2. Peterson K, Winchester R. Systemic Lupus Erythematosus: pathogenesis. In: Koopman WJ, Moreland LW, Editors. Arthritis and allied condition, a textbook of rheumatology. 15th ed. Philadelphia: Lippincott Williams and Wilkins; 2005. p. 1523-6.
  3. Albert PJ, Proal AD, Marshall TG. Vitamin D: the alternative hypothesis. Autoimmun Rev 2009; 8(8): 639-44.
  4. Lemire JM, Adams JS, Kermani-Arab V, Bakke AC, Sakai R, Jordan SC. 1,25-Dihydroxyvitamin D3 suppresses human T helper/inducer lymphocyte activity in vitro. J Immunol 1985; 134(5): 3032-5.
  5. Bhalla AK, Amento EP, Krane SM. Differential effects of 1, 25-dihydroxyvitamin D3 on human lymphocytes and monocyte/macrophages: Inhibition of interleukin-2 and augmentation of interleukin-1 production. Cell Immunol 1986; 98(2): 311-22.
  6. Müller K, Kriegbaum NJ, Baslund B, Sørensen OH, Thymann M, Bentzen K. Vitamin D3 me-tabolism in patients with rheumatic diseases: low serum levels of 25-hydroxyvitamin D3 in patients with systemic lupus erythematosus. Clin Rheumatol 1995; 14(4): 397-400.
  7. Ozaki Y, Nomura S, Nagahama M, Yoshimura C, Kagawa H, Fukuhara S. Vitamin-D receptor genotype and renal disorder in Japanese patients with systemic lupus erythematosus. Nephron 2000; 85(1): 86-91.
  8. Sakulpipatsin W, Verasertniyom O, Nantiruj K, Totemchokchyakarn K, Lertsrisatit P, Janwityanujit S. Vitamin D receptor gene BsmI polymorphisms in Thai patients with systemic lupus erythematosus. Arthritis Res Ther 2006; 8(2): R48.
  9. Huang CM, Wu MC, Wu JY, Tsai FJ. Associa-tion of vitamin D receptor gene BsmI polymorphisms in Chinese patients with systemic lupus erythematosus. Lupus 2002; 11(1): 31-4.
Journal of Isfahan Medical School
Volume 28, Issue 119 - Serial Number 119
November and December 2011
Pages 1311-1316

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History

  • Receive Date: 10 February 2011
  • Revise Date: 28 May 2024
  • Accept Date: 06 April 2022

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