##plugins.themes.academic_pro.article.sidebar##

Submitted
Aug 15, 2023
Published
Oct 2, 2023
Download
PDF (Bahasa Indonesia)
Statistic
Read Counter : 412 Download : 404

Main Article Content

Abstract

Nephrotic syndrome is a glomerular disease characterized by severe proteinuria (≥3g/24 hours), hypoalbuminemia (≤25g/L), and oedema, with hyperlipidemia in some cases. This syndrome can affect both children and adults of all ages and can be caused by idiopathic or primary causes, or secondary causes due to infectious diseases, systemic diseases, malignancies, diabetes, and the effect of drugs. Specific therapy in nephrotic syndrome is determined by histopathology and the underlying cause. B cells or B lymphocytes are part of a key part of mammals' immune response called humoral immunity. Production of B cells in humans is lifelong, beginning in the fetal liver intrauterine and then in the bone marrow after birth. B cells developed from hematopoietic stem cells. The developmental stages of B cells include all stages of initial differentiation, maturation, antigen interaction, and ultimately antibody synthesis. Until recently, nephrotic syndrome was considered a T-cell-mediated disease, new insights point to the potential role of B cells in the pathogenesis of nephrotic syndrome. One of the mechanisms that occurs is that B cells produce antibodies that bind to antigens on the surface of podocytes which are special cells in the glomerulus and play a key role in the filtration process. In both SSNS and SRNS, the causal mechanism for both is still unclear but is thought to have a close relationship with immune system disorders, especially B cells.

Article Details

Creative Commons License
This work is licensed under a Creative Commons Attribution 4.0 International License.

How to Cite
Kristina, A., & Subandiyah, K. (2023). The Role Of B Cell Activating Factor (BAFF) In The Management Of Nephrotic Syndrome: A New Paradigm. Jurnal Klinik Dan Riset Kesehatan, 3(1), 33-44. https://doi.org/10.11594/jk-risk.03.1.5

References

1. Vallepu N, Velpula S, Kumar Dasari B, Kumar Thimmaraju M, Babu Gummadi S, Yelugam N, et al. Causes and Pathophysiology of Nephrotic Syndrome in Childhood. Ren Dis. 2020;1–13.
2. Trihono PP, Alatas H, Tambunan T, and Pardede SO. Tatalaksana sindrom nefrotik idiopatik pada anak. Ikatan Dokter Anak Indonesia. 2012. 349–352 p.
3. Hahn D, Samuel SM, Willis NS, Craig JC, and Hodson EM. Corticosteroid therapy for nephrotic syndrome in children. Cochrane Database Syst Rev. 2020;2020(8).
4. Colucci M, Oniszczuk J, Vivarelli M, and Audard V. B-Cell dysregulation in idiopathic nephrotic syndrome: What we know and what we need to discover. Front Immunol. 2022;13:47.
5. Forero-Delgadillo J, Ochoa V, Restrepo JM, Torres-Canchala L, Nieto-Aristizábal I, Ruiz-Ordoñez I, et al. B-cell activating factor (BAFF) and its receptors’ expression in pediatric nephrotic syndrome is associated with worse prognosis. PLoS One. 2022;17(11 November):1–13.
6. Jethwani P, and Krishnan N. Pathogenesis and Treatment of Refractory Oedema in Nephrotic Syndrome. EMJ Urol. 2021;(August):107–17.
7. Miner JH. Organogenesis of the kidney glomerulus. Organogenesis. 2011;7(2):75–82.
8. Wang C shi, and Greenbaum LA. Nephrotic Syndrome. Pediatr Clin North Am. 2019;66(1):73–85.
9. Pardede SO. Infeksi pada Ginjal dan Saluran Kemih Anak: Manifestasi Klinis dan Tata Laksana. Sari Pediatr. 2018;19(6):364.
10. Colucci M, Carsetti R, Rosado MM, Cascioli S, Bruschi M, Candiano G, et al. Atypical IgM on T cells predict relapse and steroid dependence in idiopathic nephrotic syndrome. Kidney Int. 2019;96(4):971–82.
11. Colucci M, Corpetti G, Emma F, and Vivarelli M. Immunology of idiopathic nephrotic syndrome. Pediatr Nephrol. 2018;33:573–84.
12. Althuwaiqeb SA, and Bordoni B. Histology, B Cell Lymphocyte. StatPearls. 2021;
13. Chapman J, and Zhang Y. Histology , Hematopoiesis Histochemistry and Cytochemistry. 2023;23–6.
14. Colucci M, Carsetti R, Rosado MM, Cascioli S, Bruschi M, Candiano G, et al. Atypical IgM on T cells predict relapse and steroid dependence in idiopathic nephrotic syndrome. Kidney Int. 2019;96(4):971–82.
15. Hoffman W, Lakkis FG, and Chalasani G. B cells, antibodies, and more. Clin J Am Soc Nephrol. 2016;11(1):137–54.
16. Eddy AA, and Symons JM. Nephrotic syndrome in childhood. Lancet. 2003;362(9384):629–39.
17. Davin JC. The glomerular permeability factors in idiopathic nephrotic syndrome. Pediatr Nephrol. 2016;31(2):207–15.
18. Hackl A, Zed SEDA, Diefenhardt P, Binz-Lotter J, Ehren R, and Weber LT. The role of the immune system in idiopathic nephrotic syndrome. Mol Cell Pediatr. 2021;8(1):1–11.
19. Benz K, Dötsch J, Rascher W, and Stachel D. Change of the course of steroid-dependent nephrotic syndrome after rituximab therapy. Pediatr Nephrol. 2004;19:794–7.
20. Althuwaiqeb SA, and Bordoni B. Histology, B Cell Lymphocyte. In: StatPearls [Internet]. StatPearls Publishing; 2022.
21. Moisini I, and Davidson A. BAFF: a local and systemic target in autoimmune diseases. Clin Exp Immunol. 2009 Nov;158(2):155–63.
22. Tangye SG, Bryant VL, Cuss AK, and Good KL. BAFF, APRIL and human B cell disorders. Semin Immunol. 2006 Oct;18(5):305–17.
23. Ahmadian E, Rahbar Saadat Y, Dalir Abdolahinia E, Bastami M, Shoja MM, Zununi Vahed S, et al. The Role of Cytokines in Nephrotic Syndrome. Mediators Inflamm. 2022;2022.