» Articles » PMID: 34200024

An Update on the Current State of Management and Clinical Trials for IgA Nephropathy

Overview
Journal J Clin Med
Specialty General Medicine
Date 2021 Jul 2
PMID 34200024
Citations 23
Authors
Affiliations
Soon will be listed here.
Abstract

IgA nephropathy remains the most common primary glomerular disease worldwide. It affects children and adults of all ages, and is a leading cause of end-stage kidney disease, making it a considerable public health issue in many countries. Despite being initially described over 50 years ago, there are still no disease specific treatments, with current management for most patients being focused on lifestyle measures and renin-angiotensin-aldosterone system blockade. However, significant advances in the understanding of its pathogenesis have been made particularly over the past decade, leading to great interest in developing new therapeutic strategies, and a significant rise in the number of interventional clinical trials being performed. In this review, we will summarise the current state of management of IgAN, and then describe major areas of interest where new therapies are at their most advanced stages of development, that include the gut mucosal immune system, B cell signalling, the complement system and non-immune modulators. Finally, we describe clinical trials that are taking place in each area and explore future directions for translational research.

Citing Articles

Real-world assessment of sparsentan's drug safety framework.

Fu W, Wang J, Xue Y, Pan D Ren Fail. 2025; 47(1):2461668.

PMID: 39972562 PMC: 11843636. DOI: 10.1080/0886022X.2025.2461668.


HDAC9-mediated deacetylation of CALML6 promotes excessive proliferation of glomerular mesangial cells in IgA nephropathy.

Zhuang X, Xiao F, Chen F, Ni S Clin Exp Nephrol. 2025; .

PMID: 39833449 DOI: 10.1007/s10157-024-02620-5.


Systematic review of the application of the Kidney Failure Risk Equation and Oxford classification in estimating prognosis in IgA Nephropathy.

Toal M, Fergie R, Quinn M, Hill C, ONeill C, Maxwell A Syst Rev. 2025; 14(1):16.

PMID: 39819700 PMC: 11737263. DOI: 10.1186/s13643-024-02739-2.


Post-transplant glomerular diseases: update on pathophysiology, risk factors and management strategies.

Regalia A, Abinti M, Alfieri C, Campise M, Verdesca S, Zanoni F Clin Kidney J. 2024; 17(12):sfae320.

PMID: 39664990 PMC: 11630810. DOI: 10.1093/ckj/sfae320.


State-of-Art Therapeutics in IgA Nephropathy.

Mathur M, Sahay M, Pereira B, Rizk D Indian J Nephrol. 2024; 34(5):417-430.

PMID: 39372635 PMC: 11450772. DOI: 10.25259/ijn_319_23.


References
1.
Jennette J . The immunohistology of IgA nephropathy. Am J Kidney Dis. 1988; 12(5):348-52. DOI: 10.1016/s0272-6386(88)80022-2. View

2.
Selvaskandan H, Cheung C, Dormer J, Wimbury D, Martinez M, Xu G . Inhibition of the Lectin Pathway of the Complement System as a Novel Approach in the Management of IgA Vasculitis-Associated Nephritis. Nephron. 2020; 144(9):453-458. DOI: 10.1159/000508841. View

3.
Goto T, Bandoh N, Yoshizaki T, Nozawa H, Takahara M, Ueda S . Increase in B-cell-activation factor (BAFF) and IFN-gamma productions by tonsillar mononuclear cells stimulated with deoxycytidyl-deoxyguanosine oligodeoxynucleotides (CpG-ODN) in patients with IgA nephropathy. Clin Immunol. 2008; 126(3):260-9. DOI: 10.1016/j.clim.2007.11.003. View

4.
Wyatt R, Julian B . IgA nephropathy. N Engl J Med. 2013; 368(25):2402-14. DOI: 10.1056/NEJMra1206793. View

5.
Allen A, Bailey E, Brenchley P, Buck K, Barratt J, Feehally J . Mesangial IgA1 in IgA nephropathy exhibits aberrant O-glycosylation: observations in three patients. Kidney Int. 2001; 60(3):969-73. DOI: 10.1046/j.1523-1755.2001.060003969.x. View