IgA nephropathy, also known as Berger disease, is a kidney disorder in which immunoglobulin A deposits accumulate in the glomeruli, the kidney’s filtering units. These deposits can trigger inflammation and gradually affect how the kidneys handle blood filtration. One of the best-known signs is blood in the urine, but the condition can also be discovered because of proteinuria, rising blood pressure, or abnormal kidney function tests. ^[1][2][3]

Some people first notice cola-colored or tea-colored urine after a respiratory infection, while others have microscopic blood in the urine detected only on testing. Not every patient has symptoms in the early stages. Because the course is variable, a person may feel well for years while silent kidney injury slowly progresses. This is one reason regular follow-up matters once the diagnosis is suspected or confirmed. ^[1][2][4]

In addition to hematuria, patients may develop foamy urine from protein loss, swelling in the legs or around the eyes, elevated blood pressure, or reduced kidney function over time. Some remain stable for many years, while others move toward chronic kidney disease. The degree of proteinuria, blood pressure control, kidney biopsy findings, and baseline kidney function all influence prognosis. ^[1][2][3]

The disorder is linked to abnormal immune handling of IgA, but the exact reason it develops is not fully understood. Family history may be relevant in some cases, and the disease is not the same as a simple urinary tract infection. Patients should not assume that visible blood in the urine is benign, especially when it recurs. ^[1][2]

Evaluation usually includes urine testing, blood pressure measurement, kidney function tests, and assessment of urinary protein. A kidney biopsy is often required to confirm the diagnosis because many conditions can produce hematuria or proteinuria. The biopsy can also provide information about the extent of inflammation and scarring, which helps with long-term risk assessment. ^[1][2][3]

Treatment depends on disease severity and the risk of progression. Blood pressure control is central, and medications that reduce protein leakage from the kidneys are often part of standard care. Some patients need more advanced therapy, while others are managed with supportive treatment and monitoring alone. Decisions about immunosuppressive therapy require individualized assessment of kidney function, biopsy findings, infection risk, and expected benefit. ^[1][2][4]

Long-term management focuses on preserving kidney function. This may include controlling blood pressure, limiting additional kidney stressors, monitoring urine protein, and reviewing medications that could worsen kidney injury. Patients with progressive disease may ultimately require dialysis or kidney transplantation, although this does not happen in every case. ^[1][2][3]

Medical review is important if there is visible blood in the urine, persistent swelling, rising blood pressure, or decreased urine output. Anyone already diagnosed with IgA nephropathy should keep follow-up visits even when symptoms are mild, because worsening can occur gradually and may be detected first in laboratory monitoring rather than symptoms alone. ^[1][4]

FAQ

Is blood in the urine always caused by IgA nephropathy?

No. Blood in the urine can be caused by many conditions, including infection, stones, tumors, and other kidney disorders. IgA nephropathy is only one possible cause. ^[1][2]

Does IgA nephropathy always cause symptoms?

No. Some patients have no clear symptoms early on and are diagnosed because of microscopic blood or protein in the urine. ^[1][3]

How is IgA nephropathy confirmed?

A kidney biopsy is often needed to confirm the diagnosis and assess the degree of inflammation and scarring. ^[1][2]

Can IgA nephropathy lead to kidney failure?

It can in some patients, especially when proteinuria, high blood pressure, and reduced kidney function are present. However, the course varies widely. ^[1][3][4]

What should patients monitor over time?

Blood pressure, kidney function, urine protein, and episodes of visible hematuria are all important during follow-up. ^[1][2]