At this year’s American Society of Nephrology (ASN) Kidney Week, two well-known kidney experts, Joel Topf, MD and Vlado Perkovic, MBBS, PhD, sat down to tackle a huge question: Can we ever truly “cure” kidney disease?

The short answer: we’re not there yet. But for conditions like diabetic kidney disease and IgA nephropathy, we may be entering a new phase where the goal is no longer just “slowing things down,” but pushing the disease into deep remission and maybe, one day, something close to a cure.

This conversation is full of hope, but also realism. Here’s what it means for you.*

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“Cure” vs. Remission: What Are Kidney Doctors Really Aiming For?

Dr. Perkovic explained that when kidney doctors talk about “curing” kidney disease, they don’t mean regrowing a new kidney or reversing all damage. Instead:

• Remission means your kidney function declines at the same slow rate as someone without CKD — usually about 1 mL/min per year — while on treatment.
• A true cure would mean reaching remission without ongoing treatment. That’s not possible today, but the field is inching closer to long-term remission for some patients.

For decades, nephrology has focused almost entirely on slowing CKD. Now, with new therapies and combination treatments, experts believe remission is becoming a realistic target.

Why Focus on Diabetic Kidney Disease and IgA Nephropathy?

Dr. Perkovic highlighted two major causes of kidney failure:

• Diabetic kidney disease (DKD) – the number one cause of kidney failure worldwide.
• IgA nephropathy (IgAN) – the most common primary glomerular disease leading to kidney failure, often affecting people in their 20s, 30s, and 40s.

For a long time, IgAN was thought of as “slow” or “mild” for many people. But long-term data tell a different story:

• Even people labeled “moderate risk” can end up on dialysis if they’re followed long enough.
• In some studies, many people with “only” 0.5–1 gram of protein in the urine per day (not even the highest range) eventually progressed to kidney failure over time.

The takeaway: both DKD and IgAN can be much more aggressive than they look at first, which is why better treatments – and earlier diagnosis – are so important.

The Problem With “Old” Treatment Targets

In earlier trials of ACE inhibitors and ARBs (the long-standing blood pressure and kidney-protective medicines), people with diseases like IgAN were still losing 5–8 mL/min of eGFR per year on average.

At that rate, someone can go from “okay” kidney function to needing dialysis in just a few years.

Nowadays, with new drug combinations, some groups of patients are seeing eGFR declines closer to 1 mL/min per year – much closer to normal age-related decline. That’s a huge shift.

Diabetic Kidney Disease: Why the Outlook Is Improving

DKD remains the number one cause of kidney failure worldwide. But combination therapy is changing the outlook.

Some patients who take:

• a RAS inhibitor,
• an SGLT2 inhibitor, and
• a GLP-1 agonist

…are now losing kidney function at close to 1 mL/min/year, the same rate seen in people without CKD.

This doesn’t reverse the disease, but it may dramatically slow progression and keep people off dialysis for many years longer.

Rethinking What’s “Really” Causing CKD

In many registries and older data, hypertension (high blood pressure) and “unknown cause” show up as major contributors to CKD and kidney failure.

Dr. Perkovic pushed back on that:

• He believes many of those cases may actually be IgA nephropathy or other specific kidney diseases that were never properly diagnosed, partly because:
  
  • There weren’t good treatment options before, and
  • If the result wouldn’t change management, doctors were often reluctant to do a kidney biopsy.

Now that targeted therapies for IgAN and other conditions are emerging, the thinking is shifting:

If we have better treatments, it becomes more important to get the right diagnosis, not just label everything “hypertension.”

New KDIGO guidelines also encourage more biopsies when IgAN is suspected, especially for people with protein in their urine. Over time, this may change how kidney disease is classified – and treated.

What About Non-Diabetic CKD and Blood Pressure Control?

Blood pressure control is still absolutely essential for:

• Reducing heart attack and stroke risk
• Protecting your overall health

But when it comes specifically to slowing kidney failure, intensive blood pressure lowering alone hasn’t always delivered the big improvements people hoped for.

That doesn’t mean it’s useless. It means:

• Blood pressure control is necessary, but not always sufficient on its own.
• We may need other targeted therapies (like SGLT2 inhibitors, new IgAN drugs, complement inhibitors, B-cell–targeting treatments, etc.) to truly change the long-term outlook.

Why “Hypertensive Nephropathy” May Be Overdiagnosed

One fascinating point raised: many people diagnosed with “hypertensive kidney disease” may actually have underdiagnosed IgAN or other glomerular diseases.

For years, the lack of available treatments meant biopsies weren’t done unless results would change management. Now, with new treatments available, guidelines are shifting and more biopsies may be recommended.

This is good news. It means more people may finally get an accurate diagnosis and access to effective treatment.

New Trials Generating Excitement

Two trials highlighted at Kidney Week caught the experts’ attention:

1. FINE-ONE

• Investigates finerenone in people with type 1 diabetes (not just type 2).
• Showed strong improvements in proteinuria, an encouraging early sign.

2. ORIGIN-3

• Evaluates atacicept, a therapy targeting APRIL and BAFF (proteins involved in IgAN).
• Significant reduction in proteinuria.
• Surprisingly strong safety profile so far, fewer infections than expected.

These aren’t cures, but they point to meaningful improvements in treatment options that may slow disease more effectively than ever before.

What This Means for You

If you’re living with CKD, DKD, or IgA nephropathy, here are a few practical takeaways from this conversation:

• Ask about your exact diagnosis.
  • Do your doctors know the underlying cause of your kidney disease?
  • Has a biopsy ever been considered, especially if you have protein in your urine and an unclear diagnosis?
    
• Review your medication “stack” and have conversations with your doctor.
  • Are you on:
    • A RAS blocker (ACE inhibitor or ARB)?
    • An SGLT2 inhibitor, if appropriate for you?
    • A GLP-1 agonist, especially if you have diabetes and weight or cardiovascular concerns?
  • If you have IgAN, ask whether newer targeted treatments or trials might be an option for you.
    
• Don’t underestimate proteinuria.
  • Even “moderate” protein levels can be a sign of higher long-term risk.
  • Reducing protein in your urine is now a major treatment goal, not just a lab number.
    
• Expect more progress.
  • The field is moving fast. Drugs once tested only in diabetes are now being used in people without diabetes.
  • Targeted immune therapies, complement inhibitors, and other new agents are being explored in broader types of CKD, not just one disease.

* Nephrology Times (November 13, 2025). “Curing Kidney Disease: What’s Changing in DKD and IgAN”. docwirenews.com

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