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About IgA Nephropathy

IgA nephropathy is an immune complex-mediated glomerulonephritis
caused by IgA deposits in the glomeruli1-3

IgA nephropathy is an immune complex-mediated glomerulonephritis caused by the deposition of IgA in the glomerular mesangium and is often accompanied by persistent proteinuria, hypertension, and decreased kidney function.1-3

Epidemiology

IgA nephropathy is the most common primary glomerulonephritis worldwide, and prevalence varies by geographic region and population3,4

  • Globally, IgA nephropathy is estimated to occur at a rate of at least 2.5 cases per 100,000 individuals per year4
  • In the United States, the incidence has been estimated at ~1 per 100,000 individuals per year5,6
  • It is most prevalent among individuals of East Asian ancestry, followed by individuals of European descent, and is relatively uncommon among individuals of African ancestry3,4,7,8

IgA nephropathy can occur in individuals of any age, with diagnosis most commonly occurring in adulthood9:

  • The median age at diagnosis is approximately 40 years, and patients often already have impaired kidney function at diagnosis9

Long-term outcomes and disease burden

IgA nephropathy is associated with poor long-term outcomes.9 Findings from the UK National Registry of Rare Kidney Diseases (RaDaR) suggest that approximately 20%–30% of patients reach kidney failure within 10 years and >50% may progress to kidney failure within 20 years.9

Persistent proteinuria is a key prognostic biomarker in IgA nephropathy and is associated with increased lifetime risk of progressive kidney function loss and kidney failure.3,9,10

Even before kidney failure occurs, IgA nephropathy can negatively affect the physical health, mental health, and productivity of patients and their care-partners.11

  • Survey data from the United States show that nearly all patients and care-partners report fear and uncertainty about the future due to the disease, and many report symptoms of anxiety or depression11

    • Patients who progress to kidney failure often require years of dialysis, with more than half eventually receiving a kidney transplant.6

    Long-Term Outcomes in IgA NephropathyLong-Term Outcomes in IgA Nephropathy
    NephrologyIgAN

    Long-Term Outcomes in IgA Nephropathy

    Read about the UK National Registry of Rare Kidney Diseases (RaDaR) IgA nephropathy cohort and long-term outcomes

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    Pathophysiology

    IgA nephropathy is characterized by the deposition of immune complexes containing galactose-deficient IgA
    in the glomerular mesangium of the kidney, upregulating the production of endothelin-1 (ET-1) and angiotensin II (Ang II).12,13

    ET-1 and Ang II act in tandem via endothelin type A (ETA) and angiotensin II type 1 (AT1) receptors to stimulate the
    ongoing damage to the glomerular filtration barrier contributing to worsening proteinuria and progressive kidney damage.1,14

    As nephron loss progresses, intrarenal responses — such as glomerular hypertension, hyperfiltration, and
    tubulointerstitial response to persistent proteinuria — accelerate kidney function decline, ultimately leading to kidney failure.3

    The Role of Endothelin in IgANThe Role of Endothelin in IgAN
    Podcast Episode NephrologyIgAN

    The Role of Endothelin in IgAN

    Hear Professor Kohan provide an overview of the endothelin system and how it relates to the pathophysiology of chronic kidney disease and IgA nephropathy

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    Footnotes

    Ang II, angiotensin II; AT1, angiotensin II type 1; ET-1, endothelin-1; ETA, endothelin type A; IgA, immunoglobulin A; RaDaR, UK National Registry of Rare Kidney Diseases.

    1. Daehn IS et al. Nat Rev Drug Discov. 2021;20(10):770-788.
    2. Floege J et al. Kidney Int. 2025;107:640-651.
    3. Kidney Disease Improving Global Outcomes (KDIGO) Glomerular Diseases Work Group. Kidney Int. 2025;108(Suppl 4S):S1-S71.
    4. Rodrigues JC et al. Clin J Am Soc Nephrol. 12:677–686.
    5. Kwon CS et al. J Health Econ Outcomes Res. 2021;8(2)36-45.
    6. Bensink M et al. Kidney Med. 2024;6(2):100759.
    7. Barbour SJ et al. Kidney Int. 2013;84:1017–1024.
    8. Koratala A et al. JRSM Open. 2018;9(6):2054270418783902.
    9. Pitcher D et al. Clin J Am Soc Nephrol. 2023;18(6):727-738.
    10. Shimizu A et al. Clin Exp Nephrol. 2026;30:498–506.
    11. Szklarzewicz J et al. Qual Life Res. 2025;34:353–363.
    12. Kohan DE et al. Kidney Int Rep. 2023;8:2198–2210.
    13. Suzuki H et al. J Am Soc Nephrol. 2011;22:1795–1803.
    14. Komers R et al. Am J Physiol Regul Integr Comp Physiol. 2016;310:R877–R884.

    MA-DS-26-0031 | May 2026