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IgA Nephropathy (IgAN) Progresses to ESKD in the Majority of Patients1

IgAN develops through the 4-hit cascade driven by Gd-IgA1. APRIL, a B-cell growth factor that promotes Gd-IgA1 production, is associated with progression to ESKD.2-4  

FEATURED CONTENT

IgAN Simulator

Dive into the molecular world of IgAN, and simulate IgAN progression using prognostic tools and patient risk factors.

The Role of APRIL in IgA Nephropathy

Learn about the pathogenic cascade that causes kidney injury and about APRIL, an initiating and sustaining factor in IgAN.2

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Understanding IgAN pathogenesis, progression, and management is critical for improving IgAN patient care. NephU has gathered expert-led resources and webinars to encourage ongoing disease education. Visit our Resource Center for more information.

Mechanism of Disease

Pathogenesis and the Role of APRIL

IgAN develops through the 4-hit cascade initiated by the production of Gd-IgA1. APRIL is an important initiating and sustaining factor in IgAN progression by promoting the production of Gd-IgA1 and immune complex formation.2

INFOGRAPHIC

APRIL and the 4-Hit Pathogenic Cascade of IgAN

This infographic highlights the role of APRIL in a
pre-hit 1 step that drives the 4-hit cascade.2

ON-DEMAND WEBINAR

The 4-Hit Cascade & The Role of APRIL in IgAN

Drs Rizk and Norouzi discuss the IgAN pathogenic cascade and APRIL, an important initiating and sustaining factor in this process.2

Hot Topics in Nephrology: Taking a Deeper Dive into the 4-Hit Cascade in IgA Nephropathy - The Role of APRIL - NephU

AUDIO/PODCAST

Hot Topics in Nephrology: Taking a Deeper Dive into the 4-Hit Cascade in IgA Nephropathy – The Role of APRIL – NephU

Dr Norouzi highlights the importance of APRIL in the initiation and progression of IgAN.2  

Disease Burden and Progression

IgAN Burden and Progression to ESKD

IgAN is the most common primary glomerulonephritis in the world and a leading cause of chronic kidney disease.5,6 In observational studies, most patients with IgAN develop ESKD within 10-15 years of diagnosis.1,7-9

INFOGRAPHIC

Overview of IgAN

This infographic focuses on IgAN diagnosis, prognosis, and disease management strategies.

INFOGRAPHIC

Risk of Progression to ESKD in IgA Nephropathy

This infographic highlights the risk of progression to ESKD, including in patients traditionally considered low risk.

Understanding the IgAN Patient Journey

WEBINAR

Understanding the IgAN Patient Journey

Listen as IgAN patient and nephrology healthcare provider Kelly Chen describes the physical, mental, and emotional toll of this chronic, progressive disease.

How Does IgAN Affect Individuals Based on Differences in Ethnicity, Race & Sex?

INFOGRAPHIC

How Does IgAN Affect Individuals Based on Differences in Ethnicity, Race & Sex?

Dr Murakami highlights how unique patient characteristics impact IgAN incidence and outcomes.

Disease Management

Risk Evaluation and IgAN Management

Despite treatment with optimized supportive care, many patients with IgAN remain at risk of developing ESKD.10

Utilization of the International IgA Nephropathy Prediction Tool

WEBINAR

Utilization of the International IgA Nephropathy Prediction Tool

What tools can you use to assess your patient’s risk of progression based on their individual characteristics? Dr Shah explains how to harness the Prediction Tool for a more thorough evaluation.

Role of the Renal Pathologist screenshot

WEBINAR

The Role of the Renal Pathologist

Dr. Hassler, renal pathologist and IgAN patient, offers insights into the histopathological features that are crucial for accurate diagnosis and risk stratification in IgA nephropathy, highlighting the significance of the renal biopsy and its interpretation.

Resource Center

As a member of the NephU community, you can access a complete resource library for ongoing education. Together, we can improve IgAN care and ease the burden of this chronic, progressive disease.

APRIL, a proliferation-inducing ligand; ESKD, end-stage kidney disease; Gd-IgA1, galactose-deficient IgA1; IgAN, IgA nephropathy; MEST-C, mesangial hypercellularity (M), endocapillary hypercellularity (E), segmental sclerosis (S), tubular atrophy and interstitial fibrosis (T), crescent (C).

References

1. Pitcher D, et al. Clin J Am Soc Nephrol. 2023;18(6):727-738. 2. Mathur M, et al. J Clin Med. 2023;12(21):6927. 3. Cheung CK, et al. Front Nephrol. 2024;3:1346769. 4. Han SS, et al. J Am Soc Nephrol. 2016;27(11):3430-3439. 5. Lai KN, et al. Nat Rev Dis Primers. 2016;2:16001. 6. Cattran DC, et al. Kidney Int Rep. 2023;8(12):2515-2528.  7. Wong K, et al. Lancet. 2024;403(10433):1279-1289.  8. Sim J, et al. Kidney Int Rep. 2024;9(4):S157-S158 (abstr WCN24-1268).
9. Barbour SJ, et al. Kidney Int. 2013;84(5):1017-1024. 10. Lafayette R, et al. Kidney Int Rep. 2023;8(3):S258 (abstr WCN23-0383).