CD80 Insights As Therapeutic Target in the Current and Future Treatment Options of Frequent-Relapse Minimal Change Disease

Overview

Journal Biomed Res Int

Publisher Wiley

Specialties Biomedical Engineering
Biotechnology
General Medicine

Date 2021 Jan 28

PMID 33506028

Citations 3

Authors

Yoong Mond Teh

Soo Kun Lim

Norhana Jusoh

Kahar Osman

Siti Aisyah Mualif

Affiliations

Soon will be listed here.

Abstract

Minimal change disease (MCD) is the most common cause of idiopathic nephrotic syndrome in children, and it is well known for its multifactorial causes which are the manifestation of the disease. Proteinuria is an early consequence of podocyte injury and a typical sign of kidney disease. Steroid-sensitive patients react well with glucocorticoids, but there is a high chance of multiple relapses. CD80, also known as B7-1, is generally expressed on antigen-presenting cells (APCs) in steroid-sensitive MCD patients. Various glomerular disease models associated with proteinuria demonstrated that the detection of CD80 with the increase of urinary CD80 was strongly associated closely with frequent-relapse MCD patients. The role of CD80 in MCD became controversial because one contradicts finding. This review covers the treatment alternatives for MCD with the insight of CD80 as a potential therapeutic target. The promising effectiveness of CD20 (rituximab) antibody and CD80 inhibitor (abatacept) encourages further investigation of CD80 as a therapeutic target in frequent-relapse MCD patients. Therapeutic-based antibody towards CD80 (galiximab) had never been investigated in MCD or any kidney-related disease; hence, the role of CD80 is still undetermined. A new therapeutic approach towards MCD is essential to provide broader effective treatment options besides the general immunosuppressive agents with gruesome adverse effects.

Citing Articles

Podocyturia an emerging biomarker for kidney injury.

Hanna C, Etry H, Ibrahim M, Khalife L, Bahous S, Faour W BMC Nephrol. 2025; 26(1):118.

PMID: 40045253 PMC: 11884025. DOI: 10.1186/s12882-025-04039-w.

The Potential of Naturally Derived Compounds for Treating Chronic Kidney Disease: A Review of Autophagy and Cellular Senescence.

Teh Y, Mualif S, Izzati Mohd Noh N, Lim S Int J Mol Sci. 2025; 26(1.

PMID: 39795863 PMC: 11719669. DOI: 10.3390/ijms26010003.

Research progress of CD80 in the development of immunotherapy drugs.

Li L, Yang L, Jiang D Front Immunol. 2024; 15:1496992.

PMID: 39575257 PMC: 11578925. DOI: 10.3389/fimmu.2024.1496992.

Understanding the podocyte immune responses in proteinuric kidney diseases: from pathogenesis to therapy.

Jiang H, Shen Z, Zhuang J, Lu C, Qu Y, Xu C Front Immunol. 2024; 14:1335936.

PMID: 38288116 PMC: 10822972. DOI: 10.3389/fimmu.2023.1335936.

Second and Third Generational Advances in Therapies of the Immune-Mediated Kidney Diseases in Children and Adolescents.

Grenda R, Obrycki L Children (Basel). 2022; 9(4).

PMID: 35455580 PMC: 9030090. DOI: 10.3390/children9040536.

References

Araya C, Diaz L, Wasserfall C, Atkinson M, Mu W, Johnson R . T regulatory cell function in idiopathic minimal lesion nephrotic syndrome. Pediatr Nephrol. 2009; 24(9):1691-8. PMC: 2785122. DOI: 10.1007/s00467-009-1214-x. View

Kerjaschki D . Caught flat-footed: podocyte damage and the molecular bases of focal glomerulosclerosis. J Clin Invest. 2001; 108(11):1583-7. PMC: 201002. DOI: 10.1172/JCI14629. View

Chembo C, Marshall M, Williams L, Walker R, Lynn K, Irvine J . Long-term outcomes for primary glomerulonephritis: New Zealand Glomerulonephritis Study. Nephrology (Carlton). 2015; 20(12):899-907. DOI: 10.1111/nep.12538. View

Yoshioka K, Ohashi Y, Sakai T, Ito H, Yoshikawa N, Nakamura H . A multicenter trial of mizoribine compared with placebo in children with frequently relapsing nephrotic syndrome. Kidney Int. 2000; 58(1):317-24. DOI: 10.1046/j.1523-1755.2000.00168.x. View

Szeto C, Lai F, Chow K, Kwan B, Kwong V, Leung C . Long-term outcome of biopsy-proven minimal change nephropathy in Chinese adults. Am J Kidney Dis. 2014; 65(5):710-8. DOI: 10.1053/j.ajkd.2014.09.022. View

Siu Y, Ka-Hang Tong M, Leung K, Kwan T, Au T . The use of enteric-coated mycophenolate sodium in the treatment of relapsing and steroid-dependent minimal change disease. J Nephrol. 2008; 21(1):127-31. View

Yoo T, Fornoni A . Nonimmunologic targets of immunosuppressive agents in podocytes. Kidney Res Clin Pract. 2015; 34(2):69-75. PMC: 4570600. DOI: 10.1016/j.krcp.2015.03.003. View

Guigonis V, Dallocchio A, Baudouin V, Dehennault M, Hachon-LE Camus C, Afanetti M . Rituximab treatment for severe steroid- or cyclosporine-dependent nephrotic syndrome: a multicentric series of 22 cases. Pediatr Nephrol. 2008; 23(8):1269-79. DOI: 10.1007/s00467-008-0814-1. View

Park S, Shin J . Another beneficial effect of rituximab on refractory ANCA-associated vasculitis: the role of interleukin-17 suppression?. Scand J Immunol. 2013; 77(3):221. DOI: 10.1111/sji.12025. View

10.

Francois H, Daugas E, Bensman A, Ronco P . Unexpected efficacy of rituximab in multirelapsing minimal change nephrotic syndrome in the adult: first case report and pathophysiological considerations. Am J Kidney Dis. 2006; 49(1):158-61. DOI: 10.1053/j.ajkd.2006.10.015. View

11.

Garin E, Diaz L, Mu W, Wasserfall C, Araya C, Segal M . Urinary CD80 excretion increases in idiopathic minimal-change disease. J Am Soc Nephrol. 2008; 20(2):260-6. PMC: 2637046. DOI: 10.1681/ASN.2007080836. View

12.

Endo A, Someya T, Nakagawa M, Murano Y, Sakuraya K, Hara S . Synergistic protective effects of mizoribine and angiotensin II receptor blockade on cyclosporine A nephropathy in rats. Pediatr Res. 2013; 75(1-1):38-44. DOI: 10.1038/pr.2013.169. View

13.

Peters H, van de Kar N, Wetzels J . Rituximab in minimal change nephropathy and focal segmental glomerulosclerosis: report of four cases and review of the literature. Neth J Med. 2008; 66(10):408-15. View

14.

Eddy A, Symons J . Nephrotic syndrome in childhood. Lancet. 2003; 362(9384):629-39. DOI: 10.1016/S0140-6736(03)14184-0. View

15.

Mudge S, Paizis K, Auwardt R, Levidiotis V, Fraser S, Power D . Corticosteroids worsen proteinuria and increase intraglomerular signaling by NF-ĸB in a model of membranous glomerulonephritis. Nephron Exp Nephrol. 2010; 116(2):e23-31. DOI: 10.1159/000317128. View

16.

Koyama A, Fujisaki M, Kobayashi M, Igarashi M, Narita M . A glomerular permeability factor produced by human T cell hybridomas. Kidney Int. 1991; 40(3):453-60. DOI: 10.1038/ki.1991.232. View

17.

Nolasco F, Cameron J, Heywood E, Hicks J, Ogg C, Williams D . Adult-onset minimal change nephrotic syndrome: a long-term follow-up. Kidney Int. 1986; 29(6):1215-23. DOI: 10.1038/ki.1986.130. View

18.

Waldman M, John Crew R, Valeri A, Busch J, Stokes B, Markowitz G . Adult minimal-change disease: clinical characteristics, treatment, and outcomes. Clin J Am Soc Nephrol. 2007; 2(3):445-53. DOI: 10.2215/CJN.03531006. View

19.

Ling C, Liu X, Shen Y, Chen Z, Fan J, Jiang Y . Urinary CD80 excretion is a predictor of good outcome in children with primary nephrotic syndrome. Pediatr Nephrol. 2018; 33(7):1183-1187. DOI: 10.1007/s00467-018-3885-7. View

20.

Cara-Fuentes G, Lanaspa M, Garcia G, Banks M, Garin E, Johnson R . Urinary CD80: a biomarker for a favorable response to corticosteroids in minimal change disease. Pediatr Nephrol. 2018; 33(7):1101-1103. PMC: 5990433. DOI: 10.1007/s00467-018-3886-6. View