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Sarah, a 25-year-old who graduated law school a few months ago and began working at a law firm, was recently diagnosed with immunoglobulin A nephropathy, or IgAN, also known as Berger’s disease.¹

Reference: 1. Rajasekaran A, et al. Am J Med Sci. 2021;361:176-194.

IgAN is a chronic, progressive, autoimmune kidney disease^1-3

A leading cause of chronic kidney disease
Most common primary glomerulonephritis worldwide

References: 1. Cheung CK, et al. Front Nephrol. 2024;3:1346769. 2. Cattran DC, et al. Kidney Int Rep. 2023;8(12):2515-2528. 3. Lai KN, et al. Nat Rev Dis Primers. 2016;2:16001.

IgAN

Typically manifests in adults 20-40 years of age^1,2

AND

Often leads to ESKD within 10-15 years of diagnosis^3,4

ESKD, end-stage kidney disease.

References: 1. Lai KN, et al. Nat Rev Dis Primers. 2016;2:16001. 2. Caster DJ, et al. Kidney Int Rep. 2023;8(9):1792-1800. 3. Pitcher D, et al. Clin J Am Soc Nephrol. 2023;18(6):727-738. 4. Wong K, et al. Lancet. 2024;403(10433):1279-1289.

IgAN leads to kidney injury through the pathogenic 4-hit cascade that starts in mucosal tissues where B cells reside.¹

Reference: 1. Cheung CK, et al. Front Nephrol. 2024;3:1346769.

B cells play an important role in IgAN pathogenesis¹

APRIL is a growth factor that, along with other growth factors, binds to receptors on B cells to promote B-cell development.^1,2

APRIL, a proliferation-inducing ligand.

References: 1. Cheung CK, et al. Front Nephrol. 2024;3:1346769. 2. Vazquez MI et al. Cytokine. 2015;74(2):318-326.

APRIL specifically acts at later stages of B-cell development and mediates the maturation of antibody-secreting B cells, also known as plasma cells.¹

APRIL, a proliferation-inducing ligand.

Reference: 1. Cheung CK, et al. Front Nephrol. 2024;3:1346769.

APRIL PROMOTES^1-3:

B-cell maturation
Antibody class switching and IgA production
Survival of antibody-producing B cells (plasma cells)

APRIL, a proliferation-inducing ligand; BCMA, B-cell maturation antigen; TACI, transmembrane activator and calcium-modulator and cyclophilin ligand interactor.

References: 1. Cheung CK, et al. Front Nephrol. 2024;3:1346769. 2. Chacko B, et al. ASN Kidney News. 2024;16(1):11-12. 3. Yeo SC, et al. Clin Kidney J. 2023;16 (suppl 2):ii9-ii18.

A genetic alteration in APRIL was identified as a risk factor for IgAN in a genome-wide study¹

APRIL levels correlate with galactose-deficient IgA1 (Gd-IgA1) levels²

AND

Patients with the highest serum APRIL levels had 10x higher risk of progressing to ESKD³

BCMA, B-cell maturation antigen; TACI, transmembrane activator and calcium-modulator and cyclophilin ligand (CAML) interactor.

References: 1. Kiryluk K, et al. Nat Genet. 2014;46(11):1187-1196. 2. Zhai YL, et al. Medicine (Baltimore). 2016;95(11):e3099. 3. Han SS, et al. J Am Soc Nephrol. 2016;27(11):3430-3439.

APRIL is an important initiating and sustaining factor of the 4-hit cascade — the pathological process that drives IgAN progression¹

Reference: 1. Mathur M, et al. J Clin Med. 2023;12(21):6927.

APRIL drives the production of Gd-IgA1, a pathogenic form of IgA that initiates the IgAN autoimmune cascade.¹

Reference: 1. Mathur M, et al. J Clin Med. 2023;12(21):6927.

Circulating Gd-IgA1 acts as an autoantigen, triggering the production of anti-Gd-IgA1 autoantibodies.¹

Reference: 1. Suzuki H, et al. J Am Soc Nephrol. 2011;22(10):1795-1803.

Autoantibodies bind to Gd-IgA1 and form pathogenic immune complexes.^1,2

References: 1. Novak J, et al. Kidney Dis (Basel). 2015;1(1):8-18. 2. Suzuki H, et al. J Am Soc Nephrol. 2011;22(10):1795-1803.

These circulating immune complexes deposit in the glomerular mesangium and lead to¹:

Proliferation of mesangial cells
ECM expansion
Activation of inflammatory cells and the complement system

ECM, extracellular matrix.

Reference: 1. Suzuki H, et al. J Am Soc Nephrol. 2011;22(10):1795-1803.

This can lead to kidney injury and possible ESKD.¹

Reference: 1. Lai KN, et al. Nat Rev Dis Primers. 2016;2:16001.

APRIL IS ASSOCIATED WITH^1-3:

Higher levels of Gd-IgA1
Higher risk of progression to ESKD
Recurrence of IgAN following kidney transplant

References: 1. Han SS, et al. J Am Soc Nephrol. 2016;27(11):3430-3439. 2. Zhai YL, et al. Medicine (Baltimore). 2016;95(11):e309 3. Jo HA, et al. BMC Nephrol. 2019;20(1):33.

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This website is for U.S. Healthcare Professionals Only

Sarah, a 25-year-old who graduated law school a few months ago and began working at a law firm, was recently diagnosed with immunoglobulin A nephropathy, or IgAN, also known as Berger’s disease.1

IgAN is a chronic, progressive, autoimmune kidney disease1-3

IgAN

B cells play an important role in IgAN pathogenesis1

APRIL PROMOTES1-3:

A genetic alteration in APRIL was identified as a risk factor for IgAN in a genome-wide study1

APRIL is an important initiating and sustaining factor of the 4-hit cascade — the pathological process that drives IgAN progression1

APRIL drives the production of Gd-IgA1, a pathogenic form of IgA that initiates the IgAN autoimmune cascade.1

Circulating Gd-IgA1 acts as an autoantigen, triggering the production of anti-Gd-IgA1 autoantibodies.1

Autoantibodies bind to Gd-IgA1 and form pathogenic immune complexes.1,2

These circulating immune complexes deposit in the glomerular mesangium and lead to1:

This can lead to kidney injury and possible ESKD.1

APRIL IS ASSOCIATED WITH1-3: