This review article focuses on the role of B cell activating factor (BAFF) and a proliferation-inducing ligand (APRIL) in the pathogenesis of IgA nephropathy (IgAN) and the value of targeting the two cytokines in the treatment of the disease.
Cheung CK et al. Front Nephrol. 2024;3:346769. doi: 10.3389/fneph.2023.1346769.
This retrospective cohort study of patients with IgAN analyzed the relationship among proteinuria, estimated glomerular filtration rate (eGFR) slope, and lifetime risk for kidney failure. Results show that few patients, even those considered “low risk,” are expected to avoid kidney failure in their lifetime.
Pitcher D et al. Clin J Am Soc Nephrol. 2023;18(6):727–738.
The IgAN Foundation is an organization that supports patients with IgAN and their caregivers. It promotes research and advances awareness efforts to improve outcomes for individuals with IgAN.
Immunoglobulin A nephropathy is characterized by anticommensal humoral immune responses
Currie EG et al. JCI Insight. 2022;7(5):e141289.
APRIL-dependent lifelong plasmacyte maintenance and immunoglobulin production in humans
Yeh T-W et al. J Allergy Clin Immunol. 2020;146(5):1109–1120.e4.
Serum levels of galactose-deficient immunoglobulin (Ig) A1 and related immune complex are associated with disease activity of IgA nephropathy
Suzuki Y et al. Clin Exp Nephrol. 2014;18(5):770–777.
Serum BAFF is elevated in patients with IgA nephropathy and associated with clinical and histopathological features
Xin G et al. J Nephrol. 2013;26(4):683–690.
Serum BAFF and APRIL might be associated with disease activity and kidney damage in patients with anti-glomerular basement membrane disease
Xin G et al. Nephrology (Carlton). 2013;18(3):209–214.
The level of galactose-deficient IgA1 in the sera of patients with IgA nephropathy is associated with disease progression
Zhao N et al. Kidney Int. 2012;82(7):790–796.
Patients with IgA nephropathy have increased serum galactose-deficient IgA1 levels
Moldoveanu Z et al. Kidney Int. 2007;71(11):1148–1154.
Microscopic hematuria as a risk factor for IgAN progression: considering this biomarker in selecting and monitoring patients
Zand L et al. Clin Kidney J. 2023;16(Suppl 2):ii19–ii27.
Glomerular hematuria: cause or consequence of renal inflammation?
Moreno JA et al. Int J Mol Sci. 2019;20(9):2205. doi: 10.3390/ijms20092205.
Persistent microscopic hematuria as a risk factor for progression of IgA nephropathy: new floodlight on a nearly forgotten biomarker
Coppo R et al. J Am Soc Nephrol. 2017;28(10):2831–2834.
Remission of hematuria improves renal survival in IgA nephropathy
Sevillano AM et al. J Am Soc Nephrol. 2017;28(10):3089–3099.
Long-term outcomes in IgA nephropathy
Pitcher D et al. Clin J Am Soc Nephrol. 2023;18(6):727–738.
Proteinuria reduction as a surrogate end point in trials of IgA nephropathy
Thompson A et al. Clin J Am Soc Nephrol. 2019;14(3):469–481.
The role of BAFF and APRIL in IgA nephropathy: pathogenic mechanisms and targeted therapies
Cheung CK et al. Front Nephrol. 2024;3:1346769. doi: 10.3389/fneph.2023.1346769.
High levels of gut-homing immunoglobulin A+ B lymphocytes support the pathogenic role of intestinal mucosal hyperresponsiveness in immunoglobulin A nephropathy patients
Sallustio F et al. Nephrol Dial Transplant. 2021;36(3):452–464.
BAFF is involved in the pathogenesis of IgA nephropathy by activating the TRAF6/NF κB signaling pathway in glomerular mesangial cells
Cao Y et al. Mol Med Rep. 2020;21(2):795–805.
Pathogenic role of a proliferation-inducing ligand (APRIL) in murine IgA nephropathy
Kim YR et al. PLoS One. 2015;10(9):e0137044.
TLR9 and BAFF: their expression in patients with IgA nephropathy
Li W et al. Mol Med Rep. 2015;10(3):1469–1474.
IgA Nephropathy
Wyatt R, Julian BA. N Engl J Med. 2013;368(25):2402–2414.
An update on the pathogenesis and treatment of IgA nephropathy
Boyd JK et al. Kidney Int. 2012;81(9):833–843.
Mice overexpressing BAFF develop a commensal flora-dependent, IgA-associated nephropathy
McCarthy DD et al. J Clin Invest. 2011;121(10):3991–4022.
Cutting edge: the dependence of plasma cells and independence of memory B cells on BAFF and APRIL
Benson MJ et al. J Immunol. 2008;180(6):3655–3659.
BAFF induces a hyper-IgA syndrome in the intestinal lamina propria concomitant with IgA deposition in the kidney independent of LIGHT
McCarthy DD et al. Cell Immunol. 2006;241(2):85–94.
New strategies and perspectives on managing IgA nephropathy
Selvaskandan H et al. Clin Exp Nephrol. 2019;23(5):577–588.
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