IgA Nephropathy: Prognosis and Current Therapies in 2025

When your kidneys start failing silently, you don’t always feel it. For many people with IgA Nephropathy, the first sign isn’t pain or fatigue-it’s blood in the urine after a cold or sore throat. This autoimmune kidney disease, first identified in 1968, is now the most common cause of primary glomerulonephritis worldwide. And in 2025, how we treat it has changed completely.

What IgA Nephropathy Actually Does to Your Kidneys

IgA Nephropathy, also called Berger’s disease, happens when your immune system makes too much of a specific antibody called IgA. Instead of fighting infections properly, this antibody clumps together and gets stuck in the filtering units of your kidneys-the glomeruli. These clumps trigger inflammation. Over time, that inflammation scars the filters. Once scarred, they can’t clean your blood anymore.

It often shows up in teens and young adults. Some people notice dark, cola-colored urine after an infection. Others never have symptoms until a routine blood test shows high protein or low kidney function. About 30-40% of cases are found this way-by accident. But here’s the scary part: up to half of those with persistent proteinuria will lose kidney function within 10 to 20 years. That means dialysis or a transplant could be coming.

The Big Shift in Treatment: KDIGO 2025 Guidelines

Before 2025, doctors treated IgA Nephropathy in steps. First, they’d give blood pressure meds-usually ACE inhibitors or ARBs-to reduce protein leakage. Wait three months. If protein didn’t drop enough, then they’d add steroids or other immune drugs. That approach let the disease keep damaging kidneys while waiting.

The KDIGO 2025 guidelines changed all that. Now, if you’re at high risk, you start multiple treatments at once. No more waiting. The goal isn’t just to slow things down-it’s to stop them before they get worse.

The new strategy has two parts. One targets the root cause: the bad IgA and the immune complexes that wreck your kidneys. The other targets the body’s response to the damage: high blood pressure, protein loss, and kidney stress. Both are treated together from day one.

What Works Now: The Four Key Therapies

Four main treatments are now standard for high-risk patients:

1. Nefecon - This is the first drug approved specifically for IgA Nephropathy. It’s a targeted-release steroid that acts in the gut, where IgA is made. Unlike regular steroids that flood your whole body, Nefecon reduces side effects like weight gain, mood swings, and bone loss. In patient surveys, 72% reported fewer side effects compared to traditional steroids.
2. Systemic glucocorticoids - Still used, especially where Nefecon isn’t available. But they come with risks: diabetes, infections, cataracts. Doctors now use lower doses for shorter times, and only for those with high proteinuria and fast-progressing disease.
3. RAS inhibitors + SGLT2 inhibitors - ACE or ARB drugs (like losartan or lisinopril) lower blood pressure and reduce protein in urine. Now, SGLT2 inhibitors (like dapagliflozin) are added. Originally for diabetes, they’ve proven to protect kidneys even in non-diabetics. They cut proteinuria and slow decline in kidney function.
4. DEARA drugs (like sparsentan) - A newer class that blocks two systems that cause kidney damage: endothelin and angiotensin. Approved in Europe in 2024 and under review in the U.S., it’s especially helpful for patients with heavy proteinuria who can’t tolerate steroids.

Proteinuria is now the main measure of success. The goal? Less than 0.5 grams per day. That’s half of what was considered acceptable just a few years ago. Studies show even patients with proteinuria between 0.44 and 0.88 g/g still had a 30% chance of kidney failure within 10 years. So lowering it further isn’t just a preference-it’s critical.

Regional Differences in Treatment

Not every treatment works the same everywhere. In Japan, removing the tonsils (tonsillectomy) is common. About 45% of eligible patients get it. The theory? Tonsils produce abnormal IgA. In China, mycophenolate mofetil and hydroxychloroquine are widely used. In Western countries, these aren’t standard-because the data doesn’t support them as strongly.

That’s a problem. A patient in South Africa or Nigeria might not have access to Nefecon, sparsentan, or even a nephrologist who knows how to use the new guidelines. Global access is the biggest gap. Only 22% of patients in low- and middle-income countries get guideline-recommended care. In high-income countries, it’s 85%.

The Cost Problem: Can You Afford to Live?

Nefecon costs $125,000 a year in the U.S. Sparsentan isn’t far behind. Insurance often denies coverage. Patients report spending months appealing denials. One Reddit user wrote: “I got approved after six letters, three phone calls, and a letter from my doctor. By then, my kidney function dropped 15%.”

Even if you get the drugs, managing them is hard. A 16-year-old on Nefecon, an SGLT2 inhibitor, an ARB, and a steroid has to take four pills at different times of day. One parent on Facebook said: “It’s overwhelming. He forgets, we panic, we double-check. It’s not just medicine-it’s a full-time job.”

What’s Next? Biomarkers and Personalized Treatment

Right now, doctors guess who will progress based on protein levels, blood pressure, and kidney biopsy results (MEST-C score). But that’s not enough. The field is racing toward biomarkers-blood or urine tests that tell you exactly which pathway is driving your disease.

Is it your gut? Your complement system? Your B-cells? If we can tell, we can pick the right drug: Nefecon for gut-driven IgA, complement blockers for inflammation-driven damage, APRIL inhibitors for B-cell overactivity.

Trials like TARGET-IgAN (expected to finish in 2027) are testing this. The hope? In five years, your treatment won’t be based on your age or protein level-but on your unique biology.

What Patients Really Care About

A survey of 1,200 IgA patients found that 83% said their top goal wasn’t just to live longer-it was to live well. They want to keep working, playing sports, traveling, being parents. They fear the side effects more than the disease sometimes.

That’s why the new guidelines stress minimizing treatment burden. No one wants to trade kidney failure for diabetes, depression, or a lifetime of steroid-related weight gain. The best therapy isn’t the one that lowers protein the most-it’s the one you can stick with without wrecking your life.

What You Should Do If You Have IgA Nephropathy

If you’ve been diagnosed:

• Ask for a full risk assessment using the KDIGO calculator-proteinuria, eGFR, blood pressure, and biopsy score.
• Don’t wait three months to start treatment if you’re high risk. Push for combination therapy now.
• Track your proteinuria monthly. Use a home dipstick test if available.
• Ask about SGLT2 inhibitors-even if you don’t have diabetes.
• If Nefecon or sparsentan are options, talk to your doctor about access, cost, and insurance appeals.
• Join a patient group. You’re not alone. The IgA Nephropathy Support Group on Facebook has over 8,500 members sharing tips, insurance hacks, and emotional support.

Progress isn’t guaranteed. But the tools to stop it are better than ever. The goal is simple: keep your kidneys working, keep your life intact, and avoid dialysis for as long as possible.

Final Thoughts: Hope, But Not Complacency

The future for IgA Nephropathy is brighter than it’s ever been. We have drugs that target the disease at its source. We have data that tells us exactly how to measure success. We have patients speaking up, demanding better care.

But progress isn’t automatic. It needs doctors who know the guidelines. It needs insurers that cover the drugs. It needs systems that deliver care equally, no matter where you live.

If you have IgA Nephropathy, your job is simple: know your numbers, ask the right questions, and don’t accept waiting as the default. The tools to protect your kidneys are here. Now it’s about using them-before it’s too late.