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Expert views on IgAN care for nurses and NPs
Expert Guidance on Advancements in IgAN Care for Nurses and NPs in Nephrology

Released: July 18, 2025

Expiration: July 17, 2026

Wooin Ahn
Wooin Ahn, MD, PhD
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Key Takeaways
  • The emerging treatment approach for IgA nephropathy (IgAN) combines standard supportive care therapies to slow or halt progression of chronic kidney disease (CKD) with immunosuppressive treatments that address the underlying immunopathophysiology.
  • Proteinuria reduction is a key goal of IgAN treatment. Proteinuria is the result of glomerular damage, contributes to additional kidney damage, and correlates strongly with IgAN prognosis.
  • Multiple therapies with differing mechanisms of action are in late-stage clinical trials for IgAN.

In this commentary, Wooin Ahn, MD, PhD, addresses questions posed by nephrology healthcare professionals (HCPs) during a live symposium titled “Bridging IgAN Care: Nurse-Led Strategies for Management and Treatment With Novel Disease-Modifying Therapies” and highlights key points from the presentation. The submitted questions reflect nephrology nurses’ and nurse practitioners’ (NPs’) need for information on new therapies and evolving treatment recommendations to provide optimal care for their patients with IgA nephropathy (IgAN).

What Are Your Main Takeaways From the Symposium?

IgAN Treatment Goals
The main goal of IgAN treatment is proteinuria reduction. Proteinuria correlates with disease progression in almost all kidney diseases. It is the result of glomerular injury, but it can also cause additional damage to the kidneys, especially to the tubulointerstitial compartments. Increases in proteinuria activate the complement system, causing additional tubulointerstitial injury (ie, fibrosis and atrophy). The 2021 Kidney Disease: Improving Global Outcomes (KDIGO) practice guidelines for IgAN management identify proteinuria reduction to <1 g/day as a reasonable treatment target. However, the anticipated KDIGO guideline update is expected to recommend a target of <0.5 g/day, and preferably <0.3 g/day.

Emerging Treatment Strategy
There are 2 aspects of care to consider when managing patients with IgAN. First, HCPs should slow or halt the progression of CKD using supportive treatments, including lifestyle modifications and medications, that are appropriate for all people with glomerular kidney disease. HCPs should educate patients on lifestyle modifications such as smoking cessation and a low-sodium diet. Smoking cessation is critical because the glomerulus comprises capillaries that are lined by endothelial cells. Therefore, patients’ disease may progress if they choose to continue smoking. Lipid and blood pressure control are also general management approaches for all glomerular kidney diseases, and they are especially important in IgAN treatment. Medications that are part of supportive therapy include renin-angiotensin–aldosterone system inhibitors, which include angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs), SGLT2 inhibitors, and endothelin receptor antagonists. The second aspect of care is immunosuppressive therapy. The goal of this is to reduce pathogenic IgA immune complex production and glomerular inflammation, and agents indicated to achieve this are systemic glucocorticoids, targeted-release budesonide, and the complement Factor B inhibitor iptacopan. It is anticipated that the upcoming KDIGO guideline updates will incorporate this dual approach to IgAN management.

Emerging Therapies for IgAN
In addition to being identified as a treatment target, proteinuria reduction has been accepted by the FDA as a surrogate marker of IgAN progression in clinical trials. Use of proteinuria reduction as a clinical trial endpoint can reduce time to an approval, although initial approvals are currently identified as accelerated with continued approval based on results of confirmatory trial results. Since 2021, targeted-release formulation (TRF) budesonide, sparsentan, iptacopan, and atrasentan have received accelerated approvals for treatment of IgAN based on proteinuria reduction, with prescribing information subsequently updated to state that TRF budesonide is indicated to reduce loss of kidney function and sparsentan is indicated to slow kidney function decline in adults with IgAN who are at risk for disease progression.

Multiple additional agents in several classes are now in phase III trials for IgAN. Agents to block pathogenic antibody production include monoclonal antibodies (mAbs) that inhibit a proliferation-inducing ligand (APRIL) (sibeprenlimab, zigakibart), dual B-cell activating factor (BAFF/BLyS)/APRIL antagonists (atacicept, povetacicept, telitacicept), anti-CD38 mAbs (flezartamab, mezagitamab), and treatments that prevent kidney damage and/or reduce inflammation include an endothelin antagonist (SC0062), a mineralocorticoid receptor antagonist (finerenone), and several complement inhibitors (ravulizumab, sefaxersen, HRS-5965). Of these, the anti-APRIL mAb sibeprenlimab has been accepted for FDA priority review. Results of a prespecified interim analysis of the phase III VISIONARY study showed 50.2% reduction in 24-hour urinary protein-to-creatinine ratio (UPCR) with sibeprenlimab vs 2.1% increase with placebo. An FDA response is anticipated in 2025.

Questions Posed by HCPs

Can plasmapheresis be used as a treatment option for IgAN?
I think this is an interesting idea to test. Plasmapheresis has proven beneficial for thrombotic microangiopathies like thrombotic thrombocytopenic purpura (TTP), but data on plasmapheresis in IgAN have not demonstrated a clear benefit. Of note, the pathophysiology of IgAN is not the same as TTP, even though complement plays a role in both disease states.

How does IgAN affect a new kidney in patients after transplant?
This is an interesting question. IgAN can recur after kidney transplantation, and IgA deposition after kidney transplantation is quite common. But graft failure does not happen frequently, possibly because we would be using a lot of immunosuppression therapy after transplantation.

What proportion of patients on dialysis have end-stage renal disease (ESRD) because of IgAN?
It is hard to say because biopsies are not done for every patient with CKD. In addition, conditions often identified as causes of ESRD, such as hypertension and polycystic kidney disease, can also be the consequence of CKD rather than the cause. It is my opinion, though, that IgAN is an underappreciated cause of kidney failure and the prevalence of IgAN-associated kidney failure is higher than we think.

Your Thoughts
In your practice, how do nurses and nurse practitioners help patients incorporate new therapies into their IgAN treatment regimens? You can get involved in the discussion by answering the poll question and posting a comment below.

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In your practice, how do nurses and nurse practitioners help patients incorporate new therapies into their IgAN treatment regimens?

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