IgA nephropathy, also called Berger disease, is a kidney condition where treatment focuses on protecting kidney function, reducing protein loss in the urine, and slowing the disease’s progression. Today’s treatment landscape combines proven supportive measures with newly approved disease-specific medications and promising therapies being tested in clinical trials.

How Treatment Approaches Have Changed for IgA Nephropathy

For many years, doctors treating IgA nephropathy had to rely mainly on general kidney-protective measures rather than therapies that target the disease itself. The focus was on controlling symptoms and managing complications that arise when kidneys don’t work as well as they should. This approach, while helpful, didn’t directly address the underlying problem—the buildup of IgA antibodies (proteins that normally help fight infections) in the tiny filtering units of the kidneys called glomeruli.

Treatment decisions depend heavily on several factors unique to each patient. These include how much protein is leaking into the urine, how fast kidney function is declining, what the kidney biopsy shows under the microscope, and whether other health conditions like high blood pressure or diabetes are present. Some people with IgA nephropathy may have only small amounts of blood in their urine and stable kidney function for years, while others experience rapid progression toward kidney failure.

The past few years have brought significant changes. Medical societies now have clearer guidelines about when to start different treatments, and for the first time, several medications specifically designed for IgA nephropathy have received approval from health authorities. Meanwhile, researchers continue testing innovative approaches in clinical trials, offering hope for even more effective treatment options in the future.

Because IgA nephropathy affects people differently, there’s no single treatment plan that works for everyone. A young adult who was just diagnosed after a routine urine test might need a very different approach than someone in their fifties who has had the disease for years and is showing signs of worsening kidney function. The goal is always to preserve as much kidney function as possible while maintaining quality of life.

Standard Treatment: Protecting Your Kidneys

Every person diagnosed with IgA nephropathy should receive what doctors call “optimal supportive care.” This foundation of treatment helps protect the kidneys from further damage even if the disease itself isn’t directly targeted. The cornerstones of this approach include medications to control blood pressure and reduce protein in the urine, along with important lifestyle modifications.

The most commonly prescribed medications for IgA nephropathy belong to two closely related groups: angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs). These drugs work by affecting a hormone system in the body called the renin-angiotensin system, which plays a major role in controlling blood pressure and fluid balance. When this system is overactive, it can put stress on the kidneys and increase protein leakage.

ACE inhibitors and ARBs help relax blood vessels throughout the body, including the small vessels inside the kidneys. This reduces the pressure on the glomeruli, making it easier for them to filter blood without letting protein escape into the urine. Common ACE inhibitors include medications like enalapril and lisinopril, while popular ARBs include losartan and valsartan. Most people tolerate these medications well and take them once or twice daily for many years.

Side effects from ACE inhibitors and ARBs are generally mild but can include a dry cough (more common with ACE inhibitors), dizziness when standing up quickly, or elevated potassium levels in the blood. Doctors monitor kidney function and potassium levels with regular blood tests after starting these medications. Pregnant women cannot take these drugs because they can harm a developing baby, so alternative treatments must be used.

For patients with high blood pressure that isn’t controlled with ACE inhibitors or ARBs alone, doctors may add other blood pressure medications. Calcium channel blockers, beta blockers, or diuretics (water pills) are commonly used. Keeping blood pressure well-controlled is one of the most important ways to slow kidney disease progression, as high blood pressure damages the delicate blood vessels in the kidneys.

Some medical guidelines suggest that certain patients might benefit from omega-3 fatty acids, commonly found in fish oil supplements. These substances have anti-inflammatory properties and may help reduce kidney inflammation. However, the evidence supporting their use is mixed, and not all doctors recommend them routinely. When omega-3 supplements are used, they’re typically given at high doses (several grams per day) and may cause side effects like fishy aftertaste, digestive upset, or increased bleeding risk.

In recent years, a newer class of medications called SGLT2 inhibitors has shown promise for protecting kidneys in people with chronic kidney disease, including those with IgA nephropathy. These drugs were originally developed for diabetes but have proven benefits for kidney health even in people who don’t have diabetes. They work by helping the kidneys release excess sugar and sodium in the urine, which reduces stress on the kidneys. Examples include dapagliflozin and empagliflozin.

Until recently, corticosteroids (anti-inflammatory medications related to cortisone) were sometimes prescribed for IgA nephropathy patients with high levels of protein in their urine who were at risk of rapid disease progression. Drugs like prednisone or prednisolone reduce inflammation throughout the body, including in the kidneys. However, their use has become controversial because they can cause significant side effects, especially when taken for months at a time.

Common side effects of corticosteroids include weight gain, increased blood sugar (which can lead to diabetes), high blood pressure, mood changes, trouble sleeping, increased infection risk, bone thinning (osteoporosis), and changes in appearance such as a rounded face or increased body hair. Because of these risks, when corticosteroids are used, they’re typically prescribed for no more than six months and only for carefully selected patients. Many doctors now prefer the newer disease-specific treatments that target IgA nephropathy more directly.

For people who develop kidney failure—when the kidneys can no longer filter waste effectively on their own—treatment shifts to dialysis or kidney transplantation. Dialysis is a process that uses a machine or the body’s own lining (the peritoneum) to filter blood artificially. A kidney transplant involves receiving a healthy kidney from a living or deceased donor. About 20 to 40 percent of people with IgA nephropathy may eventually need one of these treatments within 20 years of diagnosis, though this varies widely.

Newly Approved Disease-Specific Treatments

The treatment landscape for IgA nephropathy changed dramatically when health authorities approved the first medications specifically designed to target this disease. These approvals came after clinical trials showed that the drugs could reduce protein in the urine—a key marker of kidney damage and a predictor of how quickly the disease will progress. Patients who might benefit most from these newer treatments are typically those with significant proteinuria who remain at high risk despite optimized supportive care.

One of the first disease-specific treatments approved is budesonide delayed-release capsules, sold under the brand name Tarpeyo. This medication is a corticosteroid, but unlike traditional prednisone that affects the whole body, budesonide is specially formulated to release its active ingredient in a specific part of the intestine. From there, it’s absorbed into the bloodstream and travels to areas of the immune system that may be producing the abnormal IgA antibodies.

Because budesonide targets the disease more specifically and much of it is broken down by the liver before it can cause widespread effects, it generally causes fewer side effects than traditional corticosteroids. However, side effects can still occur, including high blood pressure, swelling, and increased infection risk. The medication is taken once daily by mouth, typically for nine months. Clinical trials showed that people taking budesonide had significant reductions in their urine protein levels compared to those taking placebo.

Another recently approved medication is sparsentan, marketed as Filspari. This drug works through a unique dual mechanism—it blocks two different systems that contribute to kidney damage in IgA nephropathy. First, it blocks the angiotensin II receptor (similar to ARB medications), which helps lower blood pressure and reduce stress on the glomeruli. Second, it blocks the endothelin receptor, another pathway that promotes inflammation and scarring in the kidneys.

Endothelin is a substance in the body that causes blood vessels to narrow and promotes inflammation and fibrosis (scarring) in kidney tissue. By blocking both angiotensin and endothelin at once, sparsentan provides more comprehensive kidney protection than traditional ARBs alone. In clinical trials, patients taking sparsentan experienced greater reductions in proteinuria compared to those taking a standard ARB medication. The drug is taken once daily by mouth.

Common side effects of sparsentan include swelling (edema), low blood pressure, dizziness, and elevated potassium levels. As with ACE inhibitors and ARBs, sparsentan cannot be used during pregnancy. Patients need regular monitoring of their kidney function, blood pressure, and potassium levels while taking this medication.

A third approved medication is atrasentan, sold as Vanrafia. This is another endothelin receptor blocker, but unlike sparsentan, it specifically targets the endothelin-A receptor while having less effect on the endothelin-B receptor. This selective approach may offer a slightly different balance of benefits and side effects. Atrasentan also reduces proteinuria and helps slow kidney function decline. It’s taken once daily by mouth.

The most recent addition to approved treatments is iptacopan, marketed as Fabhalta. This medication represents a completely different approach—it’s a complement inhibitor. The complement system is part of the immune system that helps fight infections but can also cause inflammation when it becomes overactive. Research has shown that the complement pathway, particularly a component called factor B, plays an important role in causing kidney damage in IgA nephropathy.

Iptacopan works by blocking factor B, which reduces complement activation and the resulting inflammation in the kidneys. Clinical trials demonstrated that patients taking iptacopan had significant reductions in proteinuria. Because this medication affects the immune system, there’s an increased risk of certain infections, particularly from bacteria that are normally controlled by the complement system. Patients may need vaccinations before starting treatment and should watch for signs of infection.

Treatment Being Studied in Clinical Trials

While the recently approved medications represent major progress, researchers continue investigating additional therapies that might work even better or offer new options for patients. Clinical trials are carefully controlled research studies where new treatments are tested in human volunteers to determine if they’re safe and effective. These trials follow strict ethical guidelines and go through several phases before a treatment can be approved.

In Phase I trials, researchers test a new drug in a small group of people (typically 20 to 80) to evaluate its safety, determine a safe dosage range, and identify side effects. If the treatment appears safe, it moves to Phase II trials, which involve more participants (usually 100 to 300) and focus on determining whether the treatment actually works for the condition being studied. Phase III trials involve even larger groups (often 300 to 3,000 people or more) and compare the new treatment to standard treatments or placebo to definitively establish effectiveness and monitor side effects in a diverse population.

Several promising approaches are currently being tested in clinical trials for IgA nephropathy. One area of intense research focuses on medications that prevent the formation of the abnormal IgA antibodies that cause the disease in the first place. These include drugs that target B cells (the immune cells that produce antibodies) or block specific signaling pathways involved in IgA production. By stopping the problem at its source, these treatments might offer even more profound disease modification.

For example, some trials are testing medications that inhibit a protein called APRIL (A Proliferation-Inducing Ligand), which plays a key role in helping B cells survive and produce IgA antibodies. By blocking APRIL, researchers hope to reduce the production of the disease-causing IgA molecules. Early results from some of these trials have shown promising reductions in proteinuria with acceptable safety profiles.

Another investigational approach involves medications that target different parts of the complement system beyond factor B. Since complement activation appears to be a major driver of kidney inflammation and damage in IgA nephropathy, blocking this system at various points might provide benefits. Several complement inhibitors that target different complement components are in various phases of clinical trials.

Some researchers are exploring whether combining different treatment approaches might work better than any single therapy alone. For instance, trials might test whether using a complement inhibitor together with an endothelin blocker provides greater benefits than either drug alone. The idea is to simultaneously attack multiple mechanisms that contribute to kidney damage.

Trials are also investigating whether treatments that target kidney scarring (fibrosis) might help preserve kidney function even after inflammation has been reduced. Once the kidneys develop significant scarring, this tissue cannot be reversed, and it impairs kidney function. Medications that can slow or prevent fibrosis formation could be valuable for patients at all stages of the disease.

Clinical trials for IgA nephropathy are being conducted in many countries, including the United States, Canada, various European nations, and Asian countries where the disease is particularly common. Each trial has specific eligibility criteria that might include factors like age, how much protein is in the urine, current kidney function level (measured by estimated glomerular filtration rate or eGFR), and what other treatments the person is taking or has tried.

Participating in a clinical trial can offer potential benefits, including access to promising new treatments before they’re widely available, close monitoring by specialized medical teams, and the satisfaction of contributing to medical knowledge that might help future patients. However, trials also involve potential risks, such as unknown side effects from experimental treatments, the possibility of receiving placebo instead of active treatment (in some trial designs), and the time commitment required for frequent study visits and testing.

People interested in clinical trials for IgA nephropathy can search for opportunities through online registries, discuss options with their nephrologist, or contact patient advocacy organizations that maintain lists of current studies. It’s important to carefully review the informed consent documents, ask questions about what participation involves, and make sure the trial aligns with personal treatment goals and circumstances.

Most Common Treatment Methods

• Blood Pressure Medications (ACE Inhibitors and ARBs)
  • These are the foundation of treatment for nearly all IgA nephropathy patients
  • They help reduce protein leakage into urine by decreasing pressure on kidney filtering units
  • Common examples include enalapril, lisinopril, losartan, and valsartan
  • Taken daily, usually for life, with regular monitoring of kidney function and potassium levels
  • Side effects may include dry cough (more common with ACE inhibitors) and dizziness
• Disease-Specific Medications
  • Budesonide (Tarpeyo): A targeted-release corticosteroid that reduces production of abnormal IgA antibodies
  • Sparsentan (Filspari): A dual-action drug blocking both angiotensin and endothelin receptors to reduce kidney inflammation and damage
  • Atrasentan (Vanrafia): An endothelin receptor blocker that helps reduce proteinuria
  • Iptacopan (Fabhalta): A complement inhibitor that reduces immune system inflammation in the kidneys
  • These medications are typically used in patients with significant protein in the urine who remain at high risk despite supportive care
• SGLT2 Inhibitors
  • Medications originally developed for diabetes that also protect kidneys in chronic kidney disease
  • Examples include dapagliflozin and empagliflozin
  • They reduce stress on the kidneys by helping release excess sugar and sodium in the urine
  • Beneficial even for people without diabetes
• Omega-3 Fatty Acids
  • High-dose fish oil supplements with anti-inflammatory properties
  • Typically given at doses of several grams per day
  • Evidence for benefits is mixed, and not all doctors recommend them routinely
  • May cause side effects like fishy aftertaste and digestive upset
• Lifestyle Modifications
  • Reducing sodium intake to less than 2 grams per day (often lower)
  • Maintaining healthy weight through balanced diet and regular exercise
  • Avoiding tobacco products and limiting alcohol consumption
  • Managing stress and prioritizing mental health
  • These changes support kidney health and help control blood pressure
• Kidney Replacement Therapy
  • Dialysis: Used when kidneys can no longer filter waste effectively (kidney failure)
  • Hemodialysis: Blood is filtered through a machine several times per week
  • Peritoneal dialysis: The body’s own abdominal lining is used to filter blood
  • Kidney transplantation: Receiving a healthy kidney from a living or deceased donor offers the best long-term outcomes

Emerging Therapies in Clinical Development

Beyond the treatments already approved or in late-stage clinical trials, researchers are exploring entirely new therapeutic strategies for IgA nephropathy. Some of these approaches are still in early development but represent exciting possibilities for the future of treatment.

One innovative area involves therapies that directly target the abnormal structure of the IgA antibodies in IgA nephropathy. Scientists have discovered that the IgA molecules in this disease are missing a specific sugar called galactose in particular locations. This deficiency makes the IgA antibodies more likely to clump together and deposit in the kidneys. Researchers are investigating whether medications or other interventions that can either prevent the formation of these defective IgA molecules or break up the clumps might be beneficial.

Another approach being studied involves modulating the gut immune system. A large portion of the body’s IgA antibodies are produced in immune tissues associated with the intestines. Some research suggests that the intestinal immune system might be where the abnormal IgA production begins in many IgA nephropathy patients. Scientists are exploring whether treatments that modify the gut microbiome (the bacteria living in the intestines) or alter immune responses in the gut might reduce disease activity.

Gene therapy and other advanced biotechnology approaches are also being considered for IgA nephropathy, though these remain largely in preclinical or very early clinical investigation. The goal would be to correct the underlying immune system abnormalities that lead to defective IgA production. While these approaches are still years away from potential approval, they represent the frontier of what might be possible for treating this disease.

Some research groups are studying whether existing medications used for other immune system diseases might be repurposed for IgA nephropathy. This approach, sometimes called drug repurposing, can potentially speed up the development timeline since safety information for these drugs already exists. Medications used for conditions like lupus, rheumatoid arthritis, or other autoimmune diseases are being evaluated to see if they might also benefit IgA nephropathy patients.

The overall trend in IgA nephropathy research is toward personalized or precision medicine approaches. Not all patients have exactly the same disease mechanisms or respond to treatments in the same way. Researchers are working to identify biomarkers (measurable indicators in blood, urine, or kidney tissue) that can predict which patients are most likely to benefit from specific treatments. This could eventually allow doctors to tailor therapy based on each person’s unique disease characteristics rather than using a one-size-fits-all approach.