When we think of kidney disease, we often picture dialysis or swelling. However, many kidney diseases show almost no symptoms in their early stages. One example, especially common among people of Asian descent, is IgA nephropathy. This chronic disease does not usually cause sudden severe discomfort, but over the years it may slowly lead to a decline in kidney function.

How does IgA nephropathy develop?
To understand IgA nephropathy, we first need to know about the glomerulus. The glomerulus is a tiny filter inside the kidney that continuously filters large amounts of blood every minute, removing extra water, electrolytes, and waste products to form urine. When the glomerulus becomes inflamed or damaged, its filtering function is impaired.
IgA is an antibody produced by our immune system. It is mainly found in the mucous membranes of the respiratory and digestive tracts, helping defend against invading bacteria and viruses. In some people, however, the structure of IgA is abnormal. When the body produces an excess of these abnormal IgA molecules, they combine with other proteins to form immune complexes. These complexes circulate in the bloodstream and deposit in the glomeruli, like tiny particles clogging a filter. This triggers local immune reactions and chronic inflammation. Over time, the glomeruli become scarred, and kidney function gradually declines.

Who gets it? What symptoms may appear?
IgA nephropathy often develops in young people. Many patients report having an upper respiratory infection, such as a cold or sore throat, before the disease is noticed. Some even find that their urine turns reddish every time they catch a cold—a classic feature of IgA nephropathy—though not everyone notices this.
Many others have no obvious symptoms at all and only find out during routine health checks, when tests reveal blood or protein in the urine. When such findings appear repeatedly, doctors will suspect a problem in the glomeruli and arrange further tests.

How is IgA nephropathy diagnosed?
Urine and blood tests can provide clues, but they cannot confirm the diagnosis, because other kidney diseases can also cause blood or protein in the urine.
The definitive method is a kidney biopsy. A small sample of kidney tissue is taken under local anesthesia and examined under a microscope with special staining. If there are significant deposits of IgA in the glomeruli, the diagnosis can be confirmed. Although the word “biopsy” may sound intimidating, this procedure is crucial for assessing disease severity and planning appropriate treatment.

Disease course and prognosis
The progression of IgA nephropathy varies widely.
Some people remain stable for many years, with only occasional abnormal urine tests. Others gradually develop significant proteinuria, declining kidney function, and eventually chronic kidney failure.
When heavy proteinuria appears or kidney function markers (such as eGFR) begin to worsen, the risk of needing dialysis becomes much higher.
Although IgA nephropathy does not always lead to dialysis, it should never be taken lightly. Regular monitoring of kidney function and urine protein, along with timely medical interventions, is the key to slowing the disease’s progression.

Treatment principles
At present, there is no way to completely remove IgA deposits in the kidneys. The goal of treatment is to reduce damage to the glomeruli.
Doctors often prescribe medications that control blood pressure, especially ACE inhibitors (angiotensin-converting enzyme inhibitors) or ARBs (angiotensin receptor blockers). These drugs not only lower blood pressure but also reduce the pressure within the glomeruli, lower proteinuria, and help protect the kidneys in the long term.
In addition, SGLT2 inhibitors, originally used to treat diabetic kidney disease, have been found to reduce proteinuria and provide protective effects for patients with IgA nephropathy as well.
If a biopsy shows active inflammation—such as crescent formation—doctors may use corticosteroids or other immunosuppressants for a short period to dampen the excessive immune attack. However, these drugs can have significant side effects and must be carefully evaluated.

New developments in treatment
In the past, treatment options for IgA nephropathy were limited. In recent years, as research into the disease mechanism has advanced, new therapies have been developed.
One major breakthrough targets the intestinal immune response. Because much of the body’s IgA originates from the intestinal and respiratory mucosa, scientists discovered that modulating gut immunity could reduce abnormal IgA production.
An oral medication called budesonide delayed-release capsules has been approved. This is a locally acting steroid that releases specifically in the lower small intestine, reducing the production of abnormal IgA. Clinical trials have shown that it can significantly lower proteinuria and slow the decline in kidney function, with fewer side effects compared to traditional systemic steroids. In 2025, Taiwan has also officially introduced this medication, though it is not yet covered by national health insurance.
Another promising direction is complement inhibitors. Complement proteins play an important role in immune reactions, and patients with IgA nephropathy often show overactivation of complement pathways. Several monoclonal antibodies targeting components such as C5 or C3 are currently in clinical trials, with the hope of precisely blocking this key inflammatory pathway.

Final thoughts
IgA nephropathy is a hidden chronic kidney disease. It arises from abnormal IgA production by the immune system, which keeps the kidneys in a prolonged state of inflammation. It tends to develop in younger people, with few early symptoms, yet it can cause irreversible kidney damage over time.
If routine check-ups reveal recurrent blood in the urine or proteinuria, do not ignore these findings. Follow up and undergo further testing if needed. Early detection, regular monitoring, and timely treatment can make a big difference—helping to preserve kidney function and maintain health for many years to come.