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PubMed This is a summary of 20 peer-reviewed journal articles Updated
Nephrology · IgA Nephropathy

Understanding Your IgA Nephropathy Diagnosis

At a Glance

IgA nephropathy is an autoimmune kidney disease in which abnormal IgA1 immune complexes collect in the kidney’s filters and cause inflammation. The disease can stay stable or worsen, so biopsy findings, kidney-filtering score (eGFR), and urine protein help estimate personal risk.

Finding out you have IgA Nephropathy (IgAN) can be a confusing experience, often because the diagnosis seems to appear out of nowhere. Many people first learn something is wrong during a routine physical when a urine test (urinalysis) picks up trace amounts of blood or protein that they never noticed [1]. For others, the discovery is more dramatic: after a simple cold, sore throat, or stomach bug, their urine suddenly turns the color of tea or cola—a symptom called gross hematuria [2].

This page explains the biology of what is happening inside your kidneys and why this condition affects people so differently.

What is IgA Nephropathy?

IgA Nephropathy is the most common form of primary glomerulonephritis (inflammation of the kidney’s filters) in the world [3]. It is an autoimmune disease, meaning your immune system accidentally damages your own healthy tissue—in this case, the glomeruli, which are the tiny cleaning units of your kidneys [4].

While IgAN can affect anyone, it is most frequently diagnosed in young adults in their 20s and 30s [1]. It is most common in people of East Asian and European descent and is less frequently reported in people of African descent, though this may partly be due to differences in how often kidney biopsies are performed in different regions [5][6][7].

The Proposed ‘4-Hit’ Model: How the Disease Starts

Researchers use a “4-hit” model as a proposed framework to explain how IgAN develops, though the actual biology involves complex immune and kidney factors.

  1. Hit 1: Abnormal IgA1 Production. Your body produces a version of an antibody called IgA1. In IgAN, this version is missing specific sugar molecules (galactose) on its surface. Doctors call this galactose-deficient IgA1 (Gd-IgA1) [4][8].
  2. Hit 2: Autoantibody Formation. Your immune system recognizes these exposed glycans on the Gd-IgA1 molecules as abnormal. In response, it creates new antibodies (autoantibodies) to target them [9][10].
  3. Hit 3: Immune Complex Creation. The altered IgA1 and the autoantibodies lock together in your bloodstream, forming clumps called immune complexes [11].
  4. Hit 4: Kidney Deposition and Damage. These clumps circulate and eventually get stuck in the mesangium, which is the central support structure of the kidney filters [12]. Once trapped, they can trigger inflammation and damage the surrounding tissue [13].

The Role of the Complement System

Once those immune complexes are stuck in your kidney, they can activate a part of your immune system called the complement system.

In IgAN, the stuck complexes activate two specific pathways of this system: the alternative pathway and the lectin pathway [14][15]. This localized immune response causes:

  • Inflammation: Recruiting white blood cells that irritate the kidney [16].
  • Proliferation: Causing kidney cells to multiply too quickly, which interferes with filtering [12].
  • Scarring: Over time, persistent inflammation leads to permanent scarring (fibrosis), which can reduce kidney function [17].

A Highly Variable Journey

One of the most challenging aspects of IgAN is its unpredictability. It is a “highly variable” disease, meaning the path it takes is different for every person [2].

  • Stable Course: For many, the disease remains quiet for decades. They may have microscopic blood in their urine but never develop high blood pressure or significant kidney damage.
  • Progressive Course: For others, the inflammation is more aggressive. Depending on the study cohort, roughly 30% to 45% of patients may progress toward kidney failure over a 20- to 25-year period if not effectively managed, meaning more than half do not progress to that point [18][19].

Because of this range, doctors use tests like your eGFR (estimated Glomerular Filtration Rate) and the amount of protein in your urine (proteinuria) to monitor your specific risk and tailor your care [20]. Even if you feel perfectly healthy, these markers tell the story of what is happening at the microscopic level.

Common questions in this guide

What exactly is IgA nephropathy?
IgA nephropathy is an autoimmune kidney disease in which abnormal IgA1-containing immune complexes collect in the glomeruli, the kidney’s tiny filters. The deposits can trigger inflammation and scarring, but the condition remains stable for some people and progresses in others.
How does IgA nephropathy develop?
A proposed four-step model begins with galactose-deficient IgA1, followed by autoantibodies, immune-complex formation, and deposition in the kidney’s mesangium. The deposits can activate complement pathways and cause inflammation, cell growth, and scarring.
Can a cold or stomach bug trigger IgA nephropathy symptoms?
Some people first notice visible blood in the urine after a cold, sore throat, or stomach illness, but this pattern does not by itself establish the cause of IgA nephropathy. Your doctor may also check whether another condition, such as liver disease, is contributing or whether the disease is primary.
What do eGFR and urine protein tell me about my IgA nephropathy?
eGFR estimates how well your kidneys filter blood, while proteinuria measures protein leaking into the urine. Their values and trends, considered with your biopsy findings, help your care team estimate the chance of kidney-function decline and tailor monitoring.
Does IgA nephropathy always cause kidney failure?
No; IgA nephropathy can remain quiet for decades, with some people having only microscopic blood in the urine. In study groups, about 30% to 45% progressed toward kidney failure over 20 to 25 years if not effectively managed, so your individual risk depends on findings such as eGFR, urine protein, and biopsy results.
What can my kidney biopsy tell me about IgA nephropathy?
A biopsy can show IgA deposits and whether the kidney has active inflammation, chronic scarring, or both. Those findings help your doctor judge whether the disease appears more likely to remain stable or progress, alongside eGFR and urine protein.

Questions For You

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Questions to Ask Your Doctor

Curated prompts to bring to your next appointment.

  1. 1.What does my kidney biopsy show besides IgA deposits, and do these findings suggest my case is likely to be stable or progressive?
  2. 2.Was my IgA Nephropathy triggered by another condition, such as a recent infection or liver issues, or is it considered 'primary'?
  3. 3.Based on my current proteinuria and eGFR, what is my estimated risk of kidney function decline over the next 10 years?
  4. 4.Does my biopsy show signs of active inflammation versus chronic scarring, and how does that influence my long-term outlook?
  5. 5.Since my diagnosis followed a cold/infection, should I expect my symptoms to flare every time I get sick?

References

References (20)
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    The incidence and prevalence of IgA nephropathy in Europe.

    Willey CJ, Coppo R, Schaefer F, et al.

    Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association 2023; (38(10)):2340-2349 doi:10.1093/ndt/gfad082.

    PMID: 37156519
  2. 2

    IgA Nephropathy in Adults: A Review.

    Stoneman S, Teh JW, O'Shaughnessy MM

    JAMA 2026; (335(9)):799-813 doi:10.1001/jama.2025.25020.

    PMID: 41587026
  3. 3

    Epidemiology of IgA Nephropathy: A Global Perspective.

    Schena FP, Nistor I

    Seminars in nephrology 2018; (38(5)):435-442 doi:10.1016/j.semnephrol.2018.05.013.

    PMID: 30177015
  4. 4

    Aberrantly Glycosylated IgA1 in IgA Nephropathy: What We Know and What We Don't Know.

    Ohyama Y, Renfrow MB, Novak J, Takahashi K

    Journal of clinical medicine 2021; (10(16)) doi:10.3390/jcm10163467.

    PMID: 34441764
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    Biopsy-proven glomerular diseases: a systematic review of global kidney biopsy registries.

    Covic A, Brinza C, Burlacu A, et al.

    Journal of nephrology 2025; (38(9)):2571-2585 doi:10.1007/s40620-025-02449-5.

    PMID: 41217595
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    IgA Nephropathy: Pleiotropic impact of Epstein-Barr virus infection on immunopathogenesis and racial incidence of the disease.

    Mestecky J, Julian BA, Raska M

    Frontiers in immunology 2023; (14()):1085922 doi:10.3389/fimmu.2023.1085922.

    PMID: 36865536
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    The prevalence of immunoglobulin A nephropathy in the European Union and the impact of the COVID-19 pandemic: an estimation approach utilizing the kidney biopsy frequency.

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    Clinical kidney journal 2025; (18(4)):sfaf068 doi:10.1093/ckj/sfaf068.

    PMID: 40236511
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    Autoantibodies Specific for Galactose-Deficient IgA1 in IgA Vasculitis With Nephritis.

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    PMID: 31844808
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    Glomerular Immunodeposits of Patients with IgA Nephropathy Are Enriched for IgG Autoantibodies Specific for Galactose-Deficient IgA1.

    Rizk DV, Saha MK, Hall S, et al.

    Journal of the American Society of Nephrology : JASN 2019; (30(10)):2017-2026 doi:10.1681/ASN.2018111156.

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    Serum galactose-deficient-IgA1 and IgG autoantibodies correlate in patients with IgA nephropathy.

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    PloS one 2018; (13(1)):e0190967 doi:10.1371/journal.pone.0190967.

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    Experimental evidence of pathogenic role of IgG autoantibodies in IgA nephropathy.

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    Journal of autoimmunity 2021; (118()):102593 doi:10.1016/j.jaut.2021.102593.

    PMID: 33508637
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    Molecular insight in intrarenal inflammation affecting four main types of cells in nephrons in IgA nephropathy.

    Zhang H, Deng Z, Wang Y

    Frontiers in medicine 2023; (10()):1128393 doi:10.3389/fmed.2023.1128393.

    PMID: 36968836
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    Glomerular deposition of galactose-deficient IgA1-containing immune complexes via glomerular endothelial cell injuries.

    Makita Y, Suzuki H, Nakano D, et al.

    Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association 2022; (37(9)):1629-1636 doi:10.1093/ndt/gfac204.

    PMID: 35746884
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    Current Understanding of the Role of Complement in IgA Nephropathy.

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    PMID: 25694468
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    Breaking tolerance in the glomerulus: complement as a driver and therapeutic target in IgA nephropathy.

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    Frontiers in medicine 2026; (13()):1896069 doi:10.3389/fmed.2026.1896069.

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    Collectin11 and Complement Activation in IgA Nephropathy.

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    IgA nephropathy: the lectin pathway and implications for targeted therapy.

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    Advances in Novel Biologics Targeting BAFF/APRIL in the Treatment of IgA Nephropathy.

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    Points of view in nephrology: personalized management of IgA nephropathy, beyond KDIGO.

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This page explains how IgA nephropathy develops and why its course can vary for informational purposes only; it does not constitute medical advice. Your nephrologist should interpret your biopsy, eGFR, proteinuria, and long-term risk.