Lowering immunoglobulin A (IgA) depends entirely on why it’s elevated. In most cases, high IgA signals an underlying condition, and the treatment targets that condition rather than IgA itself. The most common reason people need to lower IgA is IgA nephropathy, a kidney disease where abnormal IgA proteins deposit in the kidneys and cause damage. Other causes include liver disease, chronic infections, certain autoimmune conditions, and rare blood cell disorders. Each requires a different approach, but several medications, dietary changes, and supportive therapies can reduce IgA levels or limit the harm it causes.
Why IgA Becomes Elevated
IgA is an antibody your immune system produces to protect mucous membranes in your gut, lungs, and airways. It’s normally the most abundant antibody in your body. Problems arise when the immune system produces too much of it, produces a defective form, or when IgA accumulates where it shouldn’t.
In IgA nephropathy, the issue is a specific defective version of IgA1 that’s missing certain sugar molecules on its surface. These abnormal proteins clump together, circulate in the blood, and get trapped in the kidney’s filtering units. The cells that produce this defective IgA are concentrated in immune tissue lining the gut, particularly clusters called Peyer’s patches in the lower small intestine. This gut-kidney connection is central to newer treatment strategies.
Elevated IgA can also result from monoclonal gammopathy, where a single line of immune cells overproduces one type of IgA. This is a fundamentally different problem requiring therapies that target those specific cells. Liver disease, HIV, and chronic respiratory infections can raise IgA as well, and treating the underlying cause typically brings levels down.
Medications That Target IgA Production
The most direct pharmaceutical approach is a targeted-release form of budesonide (sold as Tarpeyo/Nefecon), which the 2025 KDIGO guidelines now recommend as the preferred first-line immunosuppressive treatment for high-risk IgA nephropathy. Unlike standard steroids that suppress the immune system broadly, this capsule is designed to release its medication specifically in the lower small intestine, right where those defective-IgA-producing immune cells live. By concentrating the drug at the source of the problem, it reduces production of the abnormal IgA while causing fewer side effects than systemic steroids. The standard course runs nine months.
When targeted budesonide isn’t available, the guidelines recommend a reduced-dose systemic corticosteroid regimen of roughly 0.4 mg/kg per day of methylprednisolone, tapered over time. In a large clinical trial of over 500 patients, this approach cut the risk of kidney failure or significant kidney function loss nearly in half compared to placebo. Systemic steroids carry more side effects, though, including infection risk, bone thinning, and blood sugar changes, so they’re reserved for cases where the targeted option isn’t accessible.
Supportive Therapies That Protect the Kidneys
Even before immunosuppressive drugs enter the picture, several medications form the foundation of managing elevated IgA in kidney disease. These don’t necessarily lower IgA levels directly, but they reduce the protein leaking into urine (proteinuria) that signals kidney damage, and they slow disease progression.
Blood pressure medications called ACE inhibitors or ARBs are recommended for all patients, pushed to the maximum tolerated dose. The 2025 guidelines set an aggressive blood pressure target of below 120/70 mmHg. The goal is to get proteinuria below 0.5 grams per day, ideally below 0.3.
SGLT2 inhibitors, originally developed for diabetes, have proven valuable for kidney protection in IgA nephropathy regardless of whether diabetes is present. In studies using dapagliflozin, both blood pressure and proteinuria dropped significantly over two years. These drugs reduce the workload on kidney filtering units through a separate mechanism from blood pressure medications, which is why they’re now recommended as add-on therapy.
Sparsentan (Filspari) is a newer drug that blocks two harmful pathways simultaneously. In a phase 3 trial, patients taking sparsentan achieved a 49.8% reduction in proteinuria after 36 weeks, compared to just 15.1% for patients on a standard ARB alone. The 2025 guidelines include it as a treatment option alongside SGLT2 inhibitors.
Dietary Changes That May Help
A gluten-free diet has shown promise for reducing IgA production, proteinuria, and blood in the urine in both animal and human studies. The IgA Nephropathy Foundation notes this connection, though the evidence is stronger for people who also have celiac disease or gluten sensitivity. Since the immune tissue in the gut plays such a central role in producing abnormal IgA, reducing dietary triggers that activate that tissue makes biological sense. If you’re considering this approach, it’s worth trying for several months to see if your markers improve.
Reducing sodium intake matters because it makes blood pressure medications work more effectively and directly reduces the pressure on kidney filters. High salt intake can partially cancel out the benefits of ACE inhibitors and ARBs. Most guidelines suggest keeping sodium below 2,000 mg per day.
Fish Oil and Omega-3 Fatty Acids
Fish oil has been studied extensively in IgA nephropathy, with mixed but generally encouraging results. The omega-3 fatty acids EPA and DHA reduce inflammation in the kidney, which can slow damage from IgA deposits even if they don’t lower IgA levels directly.
Dosing in clinical trials has varied widely. Several studies used approximately 1.9 grams of EPA plus 1.5 grams of DHA per day, which is a commonly tested middle range. One early trial using 1.6 grams of EPA and 1.0 gram of DHA daily showed improved kidney function. A Polish study found that even lower doses (0.54 grams EPA and 0.81 grams DHA daily for 12 months) improved kidney function and reduced urinary protein. Higher doses, up to 3.76 grams EPA and 2.94 grams DHA per day, have also been tested without clear superiority over moderate doses. For context, a standard over-the-counter fish oil capsule contains roughly 0.3 grams of combined EPA and DHA, so therapeutic doses typically require concentrated supplements or multiple capsules.
Tonsillectomy
Removing the tonsils is a more surprising intervention, but it has a rationale: the tonsils are another major site of IgA-producing immune tissue, and chronic tonsil infections can drive IgA overproduction. This approach remains common in Japan but is not recommended by international KDIGO guidelines due to inconsistent evidence across populations.
A retrospective study of 452 patients (half receiving tonsillectomy, half not) found that tonsillectomy was independently associated with higher rates of clinical remission and better long-term kidney survival. The eight-year kidney survival rate was 97% in the tonsillectomy group versus 79% in the non-tonsillectomy group. Patients who had their tonsils removed were 77% more likely to achieve clinical remission. However, the researchers noted these results came from a Chinese population, and European studies have not consistently replicated the benefit. Ethnic and genetic factors may play a role in who benefits most.
When Elevated IgA Comes From a Blood Cell Disorder
If high IgA is caused by a monoclonal gammopathy, where a single clone of plasma cells churns out excess IgA, the treatment approach shifts entirely. Standard immunosuppressive drugs that work for IgA nephropathy are often ineffective here. In a case series of five patients with IgA-related vasculitis driven by monoclonal gammopathy, three were resistant to multiple conventional treatments. Plasma cell-targeted therapies using combinations that included bortezomib (a drug that kills the overproducing plasma cells) achieved complete remission in four of five patients. This underscores why identifying the cause of elevated IgA matters so much: the wrong treatment for the wrong cause won’t work.
What Matters Most for Lowering IgA
The practical reality is that most people searching for ways to lower IgA have either been diagnosed with IgA nephropathy or received a blood test showing elevated levels. If you’re in the first group, the 2025 guidelines lay out a clear escalation path: maximize blood pressure medications first, add an SGLT2 inhibitor or sparsentan, then consider targeted budesonide or systemic steroids if proteinuria stays above 0.5 grams per day despite several months of supportive care. A gluten-free diet and fish oil supplementation are reasonable additions with low risk.
If you have elevated IgA without a clear diagnosis, the priority is figuring out what’s driving it. IgA levels alone don’t tell the full story. The type of IgA, where it’s depositing, and what’s triggering overproduction all shape which treatment will actually bring your levels down.