What is IgA Nephropathy?

IgA nephropathy (IgAN), also known as Berger’s disease, is a type of glomerulonephritis — inflammation of the kidney’s small blood vessels (glomeruli), which normally filter waste and excess fluid from the blood. 

In IgAN, the immune system produces an abnormal form of immunoglobulin A (IgA). The body treats this abnormal IgA as foreign, creating antibodies against it. These form immune complexes that deposit in the glomeruli, leading to inflammation, scarring, and kidney damage. Over time, this weakens the kidney’s filtration barrier, causing proteinuria (protein in urine) and hematuria (blood in urine). In some cases, IgAN progresses to end-stage kidney disease (ESKD), also known as kidney failure. 

Common Symptoms of IgA Nephropathy

Many people with IgAN live with the disease for years before symptoms appear. In fact, up to 40% of patients show no symptoms at the time of diagnosis.¹ 

When present, IgA nephropathy symptoms may include: 

• Hematuria (blood in urine) — urine may appear dark brown or cola-colored, or microscopic blood may be detected on a urine test 
• Proteinuria (protein in urine) — which can cause urine to look foamy 
• Edema (swelling) in the legs, feet, or ankles 
• Hypertension (high blood pressure) 
• High cholesterol 
• Back or flank pain beneath the ribs on one or both sides 

How IgA Nephropathy is Diagnosed

A definitive IgAN diagnosis typically requires: 

• Blood tests to assess kidney function 
• Urinalysis to detect blood and protein 
• Kidney biopsy to confirm disease presence and severity 

IgA Nephropathy Progression & Treatment Goals

People with IgA nephropathy (IgAN) who have elevated proteinuria are at higher risk of progressive kidney damage and kidney failure. The severity of proteinuria strongly correlates with the likelihood of kidney failure within 10 years of diagnosis.² 

Because of this, the central focus of IgA nephropathy treatment is proteinuria reduction. The 2025 KDIGO clinical practice guidelines for IgAN recommend keeping proteinuria below 0.5 g/day, and ideally under 0.3 g/day, which is considered complete remission of proteinuria.³ 

Achieving and maintaining this target is associated with a slower loss of kidney function and better long-term outcomes. 

Treatment options for IgA nephropathy include renin–angiotensin system blockers, immunosuppressive therapies, targeted immunomodulatory therapies, sodium-glucose cotransporter-2 inhibitors, and dual endothelin–angiotensin receptor antagonists. 

How Common is IgA Nephropathy? 

Although IgAN is classified as a rare kidney disease (RKD), it is the most common type of primary glomerulonephritis worldwide.⁴ 

• Estimated incidence ranges from 1.29 to 2.5 per 100,000 people per year in the U.S.⁴ 
• Frequently IgAN appears when people are in their teens to late 30’s but can occur at any age⁵
• Geographic and ethnic patterns: most prevalent among people of East Asian ancestry, followed by white populations⁴
• Many people are diagnosed only after developing stage 3 or higher chronic kidney disease (CKD), with an estimated glomerular filtration rate (eGFR) ≤59 mL/min/1.73 m².⁶ ² 

Sources

1. Barratt & Feehally. J Am Soc Nephrol. 2005;16:2088-2097.
2. Pitcher. Clin J Am Soc Nephrol. 2023.
3. Rovin BH, Adler SG, Barratt J, et al. KDIGO 2025 Clinical Practice Guideline for the Management of Immunoglobulin A Nephropathy (IgAN) and Immunoglobulin A Vasculitis (IgAV). Kidney Int. 2025;108(4)(suppl):S1-S71.
4. McGrogan. Nephrol Dial Transplant. 2011.
5. National Organization for Rare Disorders. https://rarediseases.org/rare-diseases/iga-nephropathy/
6. Caster. Kidney Int Rep. 2023.