The short answer
IgA nephropathy (IgAN), also called Berger’s disease, is a kidney disease in which IgA-containing immune deposits build up in the glomeruli—the tiny filters that clean your blood. This can cause inflammation and allow blood and protein to leak into the urine. (NIDDK)
The disease varies considerably from person to person. Some people have mild disease that remains stable for years, while others gradually lose kidney function.
One of the most useful markers of future risk is persistent proteinuria. Under the 2025 KDIGO guideline, protein loss of 0.5 g/day or more is considered a clinically important marker of increased risk for progressive kidney-function loss. Lowering proteinuria is therefore an important treatment goal. (KDIGO)
What happens in IgA nephropathy?
IgA is an antibody involved in the immune system. In IgA nephropathy, abnormal immune processes result in IgA-containing immune complexes accumulating in the glomeruli.
This can trigger inflammation and damage the filtration barrier.
As a result, the kidneys may begin leaking:
- Red blood cells, causing hematuria
- Protein, causing proteinuria
- Sometimes increasing amounts of protein as kidney damage progresses
Over time, persistent inflammation and scarring can reduce the number of functioning filtering units and cause chronic kidney disease (CKD). (NIDDK)
The exact reason some people develop IgA nephropathy is not fully understood. Genetic and environmental factors appear to contribute. (NIDDK)
Early warning signs of IgA nephropathy
IgA nephropathy can be surprisingly quiet. Some people have no noticeable symptoms for years, and the condition is discovered through a urine test.
Blood in the urine
The classic clue is hematuria.
Sometimes blood is visible, making urine appear:
- Pink
- Red
- Brown or cola-colored
In other people, the blood is microscopic and can only be detected with urine testing.
Visible blood may occur around the time of a respiratory infection, although this pattern is not specific enough to diagnose IgA nephropathy by itself. Other kidney and urinary conditions can also cause hematuria. (NIDDK)
Protein in the urine
Proteinuria may cause urine to look unusually foamy, although foam in urine is not a reliable diagnostic test.
More importantly, protein can be measured with laboratory testing. Depending on the situation, clinicians may use:
- UACR — urine albumin-to-creatinine ratio
- UPCR — urine protein-to-creatinine ratio
- A timed urine collection in selected circumstances
Persistent protein loss is much more important for prognosis than simply noticing bubbles in the toilet.
Why protein loss matters so much
Proteinuria is not merely a laboratory abnormality.
When the glomerular filtration barrier is damaged, protein can cross into the urine. Persistent protein loss is associated with greater risk of kidney-function decline in IgA nephropathy.
The 2025 KDIGO guideline identifies proteinuria ≥0.5 g/day, or an equivalent measurement, as a marker of increased risk of progressive kidney-function loss. The guideline recommends aiming for proteinuria below 0.5 g/day, and ideally below 0.3 g/day, when achievable. (KDIGO)
This does not mean that someone with 0.6 g/day will inevitably develop kidney failure.
It means that persistent proteinuria provides important information about long-term risk and can help guide treatment.
What does eGFR tell you?
eGFR is an estimate of how well your kidneys are filtering blood.
A person with IgA nephropathy can initially have a normal or near-normal eGFR while still having significant kidney damage.
That is why doctors generally consider several pieces of information together:
Proteinuria + hematuria + eGFR + blood pressure + kidney biopsy findings + changes over time
A single eGFR result does not establish the entire prognosis.
Likewise, a falling eGFR deserves attention, but the rate and persistence of the decline are important.
Does everyone with IgA nephropathy develop kidney failure?
No.
The disease has a wide range of outcomes.
NIDDK reports that about 1 in 5 people with IgA nephropathy develop kidney failure within 10 years of diagnosis, but this population-level estimate should not be interpreted as an individual’s personal prediction. Many people have a much more stable course. (NIDDK)
Risk depends on factors such as:
- Persistent proteinuria
- Starting and changing eGFR
- Blood pressure
- The amount of kidney damage and scarring seen on biopsy
- How quickly kidney function changes
- Response to treatment
- Other health conditions
The KDIGO guideline emphasizes that even relatively low short-term risk does not necessarily mean low lifetime risk, particularly in younger people who may live with the disease for decades. (KDIGO)
What does a kidney biopsy tell you?
A kidney biopsy is the definitive way to diagnose IgA nephropathy.
A pathologist examines kidney tissue under a microscope and uses specialized testing to identify IgA deposits.
The biopsy can also show the extent and type of kidney injury, including inflammation and scarring. These findings can contribute to risk assessment and treatment decisions. (NIDDK)
Importantly, the biopsy is not simply a label saying “mild” or “severe.” Doctors interpret its findings together with proteinuria, eGFR, blood pressure, age, and the clinical course.
What can be done to protect kidney function?
Treatment depends on the individual’s risk and biopsy and laboratory findings.
Common components include:
- Blood-pressure control
- Reduction of persistent proteinuria
- Appropriate kidney-protective medication
- Avoiding unnecessary kidney stress
- Not smoking
- Maintaining a suitable dietary pattern, including attention to sodium intake
- Regular monitoring of eGFR and urine protein
The 2025 KDIGO guideline has expanded treatment options for IgA nephropathy, including supportive therapy and selected targeted treatments. Options can include renin-angiotensin system blockers, SGLT2 inhibitors, targeted-release budesonide, and sparsentan, depending on the individual’s circumstances and eligibility. (KDIGO)
These medications should be selected and monitored by a clinician rather than started or stopped based solely on an online article.
What should you monitor?
If you have IgA nephropathy, the most useful information is usually the trend.
Keep track of:
- Urine protein
- eGFR
- Serum creatinine
- Blood pressure
- Urinalysis/hematuria when clinically relevant
- Medication changes
- Other relevant laboratory results
For example:
UACR/UPCR six months ago → current result → direction of change → time interval
is more informative than asking whether one isolated value is “good” or “bad.”
Temporary increases in urine protein can occur with factors such as infection, exercise, fever, or other illness, so an unexpected result may need confirmation.
When should you contact your doctor promptly?
Seek medical evaluation if you develop:
- Clearly visible blood in the urine, especially if new or persistent
- Rapidly increasing swelling
- A substantial reduction in urine output
- Severe shortness of breath
- A significant or rapidly worsening rise in creatinine
- Very high blood pressure with symptoms
- New or rapidly increasing proteinuria
These findings do not automatically mean IgA nephropathy is suddenly progressing, but they deserve assessment.
Bottom line
IgA nephropathy can begin quietly, with microscopic blood or protein in the urine before noticeable symptoms or major loss of kidney function.
The most important prognostic issue is not simply whether IgA deposits are present. It is how much kidney damage exists, how much protein is being lost, what the eGFR is doing over time, and whether those risk factors can be reduced.
Persistent proteinuria—particularly ≥0.5 g/day—is an important warning marker, but it is not a guarantee of kidney failure. (KDIGO)
For someone diagnosed with IgA nephropathy, the practical goal is to measure urine protein and kidney function regularly, control blood pressure, use appropriate kidney-protective treatment, and watch the trend rather than fear a single abnormal result.