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IgA Nephropathy

Also Known As: Berger’s Disease, Immunoglobulin A nephropathy, IgAN
System: Urinary System and Immune System
Autoantibodies:
  • Not classic autoantibodies

  • Involves galactose-deficient IgA1 and autoantibodies against it, forming damaging immune complexes

Primary Organ or Body Part Affected: Kidneys
Acceptance as Autoimmune: Confirmed
IgA Nephropathy - Berger's Disease

What is IgA Nephropathy?

IgA nephropathy is a chronic autoimmune kidney disease where a protein called immunoglobulin A (IgA) builds up in the kidneys’ filtering units (glomeruli). This buildup causes inflammation and damage, slowly impairing the kidneys’ ability to filter waste and excess fluid from the body.

What are the signs and symptoms of IgA Nephropathy?

Early stages often have no symptoms. When symptoms do appear, they may include:

  • Blood in urine (hematuria) – either visible or microscopic

  • Foamy urine – from excess protein

  • Swelling – especially in the feet, hands, or face

  • High blood pressure

  • Fatigue

  • Lower back or flank pain

Often triggered or worsened by respiratory or gastrointestinal infections.

What are the causes of IgA Nephropathy?

IgA nephropathy is believed to be caused by a faulty immune response involving abnormal IgA1, a type of antibody. This form of IgA is missing certain sugars (galactose-deficient IgA1), making it look “foreign” to the immune system. The body attacks it, forming clumps (immune complexes) that get stuck in the kidneys and cause inflammation.

Key contributors include:

  • Genetics – family history increases risk

  • Immune system abnormalities – production of galactose-deficient IgA1

  • Infections – particularly respiratory or GI tract infections can trigger flare-ups

  • Environmental factors – unclear, but may play a role

  • Autoimmune factors – not always classic autoimmunity, but involves auto-reactive processes

Diagnosis

Diagnosis typically involves:

  1. Urinalysis – shows blood and protein in urine

  2. Blood tests – check kidney function (creatinine, estimated GFR)

  3. Kidney biopsy – confirms IgA deposits in glomeruli

  4. Imaging – may rule out other kidney problems

Because symptoms can be subtle, diagnosis often happens after an unrelated urine test.

Treatment

There’s no cure, but treatments aim to slow disease progression and protect kidney function:

  • Blood pressure medications (ACE inhibitors or ARBs)

  • Corticosteroids or immunosuppressants (for high-risk patients)

  • Fish oil supplements (may reduce inflammation)

  • Low-salt, kidney-friendly diet

  • SGLT2 inhibitors (newer option in some patients)

  • Kidney transplant – for end-stage kidney disease

Prognosis

IgA nephropathy progresses slowly in most people. About 1 in 4–5 will develop kidney failure over 20 years. Others live with stable or mild disease for decades.

Controlling blood pressure and protein levels in urine are key to improving long-term outcomes.

Prevalence

  • Affects ~2 per 100,000 people per year

  • More common in men and young adults (teens to 30s)

  • Higher rates in East Asian and Caucasian populations

Citations

  • Wyatt RJ, Julian BA. IgA nephropathy. N Engl J Med. 2013;368(25):2402-14. doi:10.1056/NEJMra1206793

  • Kiryluk K, Novak J. The genetics and immunobiology of IgA nephropathy. J Clin Invest. 2014;124(6):2325-32.

  • KDIGO 2021 Clinical Practice Guideline for the Management of Glomerular Diseases. Kidney Int. 2021;100(4S):S1-S276.

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