Shikha Wadhwani, MD, MS

This is a deep dive into one segment of a recent episode of 

Kidney Compass: Navigating Clinical Trials

, HCPLive's podcast co-hosted by Shikha Wadhwani, MD, and Brendon Neuen, MBBS, PhD. In this episode, Neuen steps out of his usual co-host role to join as a guest, discussing the FIND-CKD trial results he presented at the European Renal Association (ERA) Congress.

Inside FIND-CKD: Can Finerenone Pair With Immunosuppression in GN?

Finerenone, a nonsteroidal mineralocorticoid receptor antagonist (MRA), doesn't target the immune mechanisms driving 

 and according to Brendan Neuen, MBBS, PhD, that's exactly the point. The FIND-CKD trial excluded patients treated with immunosuppression in the 6 months prior to enrollment, a design choice Neuen said reflected the conservatism of the trial's 2020 design rather than a signal against combining the two treatment approaches.

"We're not reducing Gd-IgA1 with finerenone," Brendan Neuen, MBBS, PhD, told HCPLive. "That's not the point of the drug."

Why FIND-CKD Excluded Recent Immunosuppression

"We weren't necessarily surprised that the treatment effect was consistent across, regardless of the type of kidney disease," Neuen said. "We know that mineralocorticoid receptor antagonism is a final common pathway across many forms of kidney disease, and so if you think about it that way, it's not surprising that the benefits are there across different forms of kidney disease, including GN."

Neuen said the immunosuppression exclusion criterion was a product of its era. "This was back in 2020, as I like to remind people, before DAPA-CKD," he said. "If we'd done it again, perhaps I would. I mean, we would have liked to, and I think we're being much more inclusive with kidney outcome trials now."

A More Inclusive Approach in Current Trial Design

Neuen described how his approach to eligibility criteria has shifted in trials he has since been involved in. "If people have a kidney disease requiring immunological therapy, so long as that treatment is stable, and investigators don't anticipate a relapse or something else, then it's worth including those patients in, because it allows us to be more inclusive and our results are more generalizable," he said.

He noted the tradeoff cuts both ways. "If you do include a group like that in whom the treatment might not work and that muddies the overall result, then we're not really advancing care for anyone. So it's a fine balance to walk," Neuen said.

The Case for Combining Finerenone With Immunosuppressive Therapy

From a mechanistic standpoint, Neuen sees no barrier to using finerenone alongside immunological treatment. "If you just think about the way that our drugs work, and what guidelines say, you know, KDIGO for IgA nephropathy: target the underlying immunological problem and the downstream consequences of IgA-mediated nephron loss," he said. "I see no reason why we shouldn't be doing these together simultaneously with a SGLT2 inhibitor and an MRA, because they're targeting completely different pathways and complementary pathways."

Neuen's framing aligns with the 2025 Kidney Disease: Improving Global Outcomes (KDIGO) Clinical Practice Guideline for the Management of IgA Nephropathy (IgAN), which explicitly recommends combining anti-inflammatory and antifibrotic agents with therapies that target IgA immune-complex formation. The guideline notes that the optimal sequencing of these combinations still needs to be established through trials, a gap Neuen's comments suggest FIND-CKD and future analyses are beginning to address.

Neuen said forthcoming data will help clarify how finerenone exerts its protective effect in IgA nephropathy specifically. "Later this year, at another meeting, I'll be presenting some of the data specifically in the IgAN cohort, helping us to understand how finerenone is exerting its kidney disease protective effects," he said. "No surprises: it's probably not targeting the immunological aspect of the disease."

Layering and Sequencing as the Next Frontier

Neuen framed the immunological and non-immunological pathways as complementary rather than competing. "The point of the drug is to address the common final pathways that are not unique to IgAN, but all forms of kidney disease, and we can do that in parallel with disease-modifying therapies now," he said.

He pointed to layering and sequencing as an emerging area of focus. "I think that is the really exciting part of this whole conversation, which is how do we layer these therapies, how do we sequence them," Neuen said, adding that the topic warrants further discussion beyond this conversation.

Editors' Note: Disclosures for Wadhwani include Boehringer Ingelheim, Calliditas Therapeutics, GSK, Otsuka Pharmaceutical Co., Travere Therapeutics, and others. Disclosures for Neuen include AstraZeneca, Bayer, Boehringer Ingelheim, Janssen, and others.

Heerspink HJL, Neuen BL, Agarwal R, et al. Finerenone in persons with chronic kidney disease without diabetes. 

Floege J, Barratt J, Cook HT, et al. Executive summary of the KDIGO 2025 Clinical Practice Guideline for the Management of Immunoglobulin A Nephropathy (IgAN) and Immunoglobulin A Vasculitis (IgAV). 

Videos

Brendon Neuen explains why finerenone's mechanism supports combining it with immunosuppressive therapy in glomerulonephritis.

, HCPLive's podcast co-hosted by Shikha Wadhwani, MD, and Brendan Neuen, MBBS, PhD. In this episode, Neuen steps out of his usual co-host role to join as a guest, discussing the FIND-CKD trial results he presented at ERA. The full episode also covers the glomerulonephritis subgroup analysis and pooled safety data.

Inside FIND-CKD: The Data Behind the Trial's 23% Risk Reduction

Finerenone reduced the risk of kidney and cardiovascular events by 23% in patients with non-diabetic 

, according to results from the phase 3 FIND-CKD trial. The effect was driven by a 0.7 mL/min/1.73m² per year improvement in total glomerular filtration rate (GFR) slope that held consistent across every prespecified subgroup investigators examined.

"So, really clear, clear-cut effects on slope, the clinical outcome, as well as a safety profile that was entirely in keeping with what we expected about the drug," Brendan Neuen, MBBS, PhD, told 

Primary Endpoint: Total GFR Slope Improvement Matched the Trial's Own Power Calculation

FIND-CKD was powered to detect a 0.7 mL/min/1.73m² per year improvement in total GFR slope with finerenone versus placebo, a figure derived from the treatment effect observed in the earlier FIDELIO-DKD trial. Over 32 months of follow-up, the trial hit that number.

"For the primary outcome of total GFR slope, we saw exactly as we anticipated and powered for, a 0.7 mL per minute per year improvement with finerenone versus placebo over a 32 month follow-up period," Neuen said.

Excluding the acute, treatment-related dip in GFR that occurs shortly after MRA initiation, the effect on chronic slope alone was larger, at 1.2 mL/min/1.73m² per year. Investigators noted this pattern is expected with kidney-protective therapies, where an early hemodynamic drop is followed by a slower rate of long-term decline.

Effect Was Consistent Across Every Prespecified Subgroup

Neuen emphasized that the slope benefit did not vary meaningfully by underlying kidney disease etiology or baseline patient characteristics.

"That effect was entirely consistent regardless of cause of kidney disease, hypertensive, ischemic nephrosclerosis, glomerular diseases, and others," Neuen said. "It was consistent across different levels of kidney function, different levels of albuminuria, and regardless of SGLT2 inhibitor use."

This consistency extended to the trial's glomerulonephritis (GN) subgroup, which made up roughly 60% of the overall cohort, as well as to patients already on background sodium-glucose cotransporter 2 (SGLT2) inhibitor therapy, a group whose representation grew over the course of the trial as standard of care shifted.

Key Secondary Endpoint: 23% Reduction in Kidney-Cardiovascular Composite

Because slope is a surrogate measure, investigators built the trial's key secondary endpoint around outcomes with more direct clinical meaning to patients and clinicians: a composite of a 57% decline in GFR (equivalent to a doubling of serum creatinine), kidney failure, heart failure hospitalization, or cardiovascular death.

"We knew that while slope is important, clinicians, payers, and patients really want to know what is the effect on clinical outcomes and how people feel, function, and survive," Neuen said.

The composite endpoint was reduced by 23% with finerenone versus placebo, a statistically significant result that tracked closely with what the observed slope effect would predict. Investigators also reported an approximately 40% reduction in albuminuria over 12 months and a modest reduction in blood pressure.

Safety: Hyperkalemia More Common, but Discontinuations Remained Rare

As with other agents in the MRA class, hyperkalemia emerged as the primary safety signal. Mean serum potassium increased by approximately 0.12 mmol/L over the course of the trial, and hyperkalemia occurred more frequently with finerenone than placebo (17% vs 13%).

"Hyperkalemia events that led to discontinuation of study treatment were very uncommon overall, at about 1%," Neuen said.

Contextualizing the Effect Size: How Finerenone Compares to SGLT2 Inhibitors

For clinicians unfamiliar with GFR slope as a trial endpoint, Neuen offered a direct comparison to a more familiar drug class. The 0.7 mL/min/1.73m² per year effect observed with finerenone compares to a roughly 0.5 to 0.6 mL/min/1.73m² per year effect on total slope observed with SGLT2 inhibitors in the 

 and EMPA-KIDNEY trials, both of which also enrolled patients with non-diabetic CKD.

"These effects are at least comparable to the SGLT2 inhibitor class, and suggest a role for combination treatment in non-diabetic kidney disease in the future," Neuen said.

Until now, patients with non-diabetic CKD have had access to only SGLT2 inhibitors on top of renin-angiotensin system (RAS) inhibition, a narrower toolkit than the four-pillar regimen (RAS inhibitors, SGLT2 inhibitors, nonsteroidal MRAs, and GLP-1 receptor agonists) established for diabetic kidney disease. The consistency of benefit across kidney function levels, albuminuria levels, and SGLT2 inhibitor exposure suggests finerenone could be layered onto existing background therapy rather than positioned as a replacement for it, an approach Neuen and colleagues plan to characterize further in subgroup-specific analyses, including in the trial's GN population.

Finerenone slows kidney function decline and reduces cardiovascular-kidney risk in non-diabetic chronic kidney disease, major trial shows [press release]. European Renal Association. Published June 4, 2026.

Heerspink HJL, Tuttle KR, Perkovic V. Finerenone in patients with chronic kidney disease. Presented at: 63rd ERA Congress; June 3-6, 2026; Glasgow, Scotland. Abstract 186.

Brendan Neuen breaks down the full FIND-CKD primary and secondary endpoint data, subgroup consistency, and safety signals.

In a special episode of Kidney Compass, Shikha Wadhwani, MD, MS, puts her regular co-host, Brendan Neuen, MBBS, PhD, in the "hot seat," asking him about results from FIND-CKD, the phase 3 trial showing finerenone slows eGFR decline and cuts cardiorenal risk by 23% in non-diabetic 

 over 32 months of follow-up, including the prespecified glomerulonephritis (GN) subgroup analysis he presented at the European Renal Association (ERA) Congress in June. 

Kidney Compass: Finerenone Cuts Cardiorenal Risk 23% in FIND-CKD

FIND-CKD was published simultaneously in the New England Journal of Medicine, JAMA, and The Lancet. The conversation covers why the trial was needed, its design and population, the primary GFR slope findings, the GN-specific results, safety, and where finerenone fits alongside other guideline-directed therapies going forward.

Filling a Treatment Gap in Non-Diabetic Kidney Disease

Wadhwani opens by asking Neuen to frame how far kidney disease management has come. Neuen notes diabetic kidney disease now has 4 proven therapies, the "4 pillars": renin-angiotensin system (RAS) inhibition, sodium-glucose cotransporter 2 (SGLT2) inhibitors, nonsteroidal mineralocorticoid receptor antagonists (MRAs), and glucagon-like peptide-1 (GLP-1) receptor agonists. Non-diabetic kidney disease, by contrast, has had only SGLT2 inhibitors added on top of RAS inhibitors, despite non-diabetic causes accounting for most CKD worldwide.

Neuen points to FIDELIO and FIGARO, which established finerenone's benefit in diabetic kidney disease. As he describes it, mineralocorticoid receptor antagonism works "by blocking the impact of aldosterone excess" to reduce inflammation and fibrosis, a mechanism unrelated to glycemic control. That rationale is what led to testing whether the same mechanism could benefit non-diabetic kidney disease.

Neuen adds that FIND-CKD was designed in 2020, before DAPA-CKD had reported, when SGLT2 inhibitors were neither widely recommended nor broadly available. About 17% of participants were on an SGLT2 inhibitor at baseline, a proportion that rose considerably over the trial as standard of care shifted.

Inside the FIND-CKD Trial: Endpoints, Population, and Powering

Neuen describes FIND-CKD as a randomized, double-blind, placebo-controlled trial of 1,584 patients across 24 countries with non-diabetic CKD, an eGFR of 25 to 60 mL/min/1.73 m² and urine albumin-to-creatinine ratio (UACR) of 200 to 500 mg/g, or an eGFR ≥ 25 mL/min/1.73 m² with UACR > 500 mg/g. All participants were on maximum tolerated RAS inhibition, and SGLT2 inhibitor use was permitted. Diabetic kidney disease, heart failure with a guideline indication for an MRA, and glomerular disease treated with immunosuppression in the prior 6 months were excluded.

Neuen explains the trial used total GFR slope as its primary endpoint, powered to detect a 0.7 mL/min/1.73 m² per year improvement, the treatment effect observed in FIDELIO, which prior work from Lesley Inker and colleagues in the CKD-EPI consortium had linked to an expected 23% relative risk reduction in clinical events. Wadhwani asks Neuen to address the choice of total versus chronic slope; Neuen notes total slope, which includes both the acute and chronic treatment effect, is the more validated surrogate for kidney outcomes, though chronic slope remains clinically informative over longer time horizons.

Baseline characteristics: mean age was about 55 years, roughly two-thirds were men, and about half of participants were enrolled from Asia. Mean eGFR was 47 mL/min/1.73 m², and median UACR was 820 mg/g. Neuen describes this as a lower cardiovascular-risk population than prior kidney outcome trials, with a lower prevalence of atherosclerotic disease and heart failure than in FLOW or DAPA-CKD, and no participants with diabetes.

Finerenone Slows eGFR Decline and Cuts Cardiorenal Risk

Neuen reports a 0.7 mL/min/1.73 m² per year improvement in total GFR slope with finerenone versus placebo over 32 months of follow-up, consistent regardless of cause of kidney disease, eGFR, albuminuria level, or SGLT2 inhibitor use. Chronic slope, which excludes the acute effect, showed a larger 1.2 mL/min/1.73 m² per year improvement, also consistent across subgroups.

On the key secondary composite endpoint, a sustained 57% decline in eGFR (equivalent to a doubling of serum creatinine), kidney failure, heart failure hospitalization, or cardiovascular death, Neuen reports a statistically significant 23% relative risk reduction, matching the effect size the trial was powered to detect. Additional findings included a roughly 40% reduction in albuminuria at 12 months, a modest blood pressure reduction, and a mean potassium increase of approximately 0.12 mmol/L. Neuen contextualizes the 0.7 mL/min/1.73 m² per year slope effect against SGLT2 inhibitor data in non-diabetic CKD, where DAPA-CKD and EMPA-KIDNEY showed effects of about 0.5 to 0.6 mL/min/1.73 m² per year, suggesting finerenone's effect is at least comparable and supports a role for combination therapy.

Wadhwani points out that, unlike in some glomerular disease-specific trials, the placebo arm in FIND-CKD showed essentially no reduction in albuminuria, which she attributes to participants already being on maximized RAS inhibition at enrollment. That contrast, she says, makes finerenone's proteinuria-lowering effect more clinically meaningful, and notes the effect appeared quickly and was sustained through follow-up.

Benefit Holds Across Glomerulonephritis Subtypes

About 60% of FIND-CKD participants (903 of 1,584) had an investigator-reported GN diagnosis, including 416 with IgA nephropathy, 215 with focal segmental glomerulosclerosis (FSGS), and 90 with membranous nephropathy. Neuen notes these patients were younger, more often female, and had higher eGFR, higher proteinuria, and higher SGLT2 inhibitor use at baseline than the rest of the cohort.

In the GN subgroup, the total slope benefit was consistent with the overall trial at 0.7 mL/min/1.73 m² per year. For the exploratory outcome of a 40% eGFR decline or kidney failure, chosen because it occurred more frequently in this subgroup, Neuen reports a 26% relative risk reduction, alongside a 40% reduction in albuminuria. These effects held regardless of SGLT2 inhibitor use or specific GN diagnosis, with no evidence of interaction by disease type.

About 80% of the GN subgroup had an available, reported biopsy, with a median time from biopsy of about 3.5 years. Restricting the analysis to biopsy-confirmed cases produced consistent, and in some cases slightly larger and more precise, treatment effects. Neuen says the consistency wasn't surprising: mineralocorticoid receptor antagonism is "a final common pathway across many forms of kidney disease," so a treatment effect that holds regardless of the underlying diagnosis fits the mechanism.

Wadhwani raises the question of immunosuppression exclusion criteria, asking whether Neuen would design the trial differently today. Neuen says kidney outcome trials are now more inclusive of patients on stable immunological therapy, since MRA treatment and immunological therapy target different, complementary pathways with no mechanistic reason to conflict.

Hyperkalemia Risk Stays Manageable, Discontinuations Rare

Neuen reports the overall safety profile was consistent with finerenone's established data from FIDELIO and FIGARO, in which more than 13,000 patients were followed over a median of 3 years. Hyperkalemia occurred more often with finerenone than placebo (about 17% versus 13%), but discontinuation due to hyperkalemia was uncommon, at approximately 1%. Safety findings in the GN subgroup were consistent with the overall trial.

Pooled Data Point to a Broader Role for Finerenone

Neuen frames finerenone as addressing common downstream pathways of kidney injury rather than the immunological drivers specific to diseases like IgA nephropathy, positioning it as complementary to, rather than competitive with, disease-modifying immunological therapies, including emerging B-cell-directed treatments. He points to persistent residual proteinuria as a long-term risk even when immunological therapy controls disease activity, and to heart failure, rather than myocardial infarction or stroke, as the dominant modifiable cardiovascular risk in this population.

Neuen also describes a pooled analysis combining FIDELIO, FIGARO, and FIND-CKD across roughly 14,500 participants with diabetic and non-diabetic kidney disease. Pooled results showed a 24% reduction in kidney disease progression (doubling of serum creatinine or kidney failure) and a 23% reduction in need for dialysis or transplantation.

On cardiovascular and mortality outcomes, the pooled analysis showed a 20% reduction in heart failure hospitalization or cardiovascular death, an 18% reduction in cardiovascular death, and a 12% reduction in all-cause mortality, with consistent effects regardless of cause of kidney disease, kidney function, or SGLT2 inhibitor use. Neuen says the results support finerenone "as a foundational guideline-directed therapy in kidney disease alongside SGLT2 inhibitors."

Wadhwani notes that in glomerulonephritis, biopsy often comes years after disease onset, meaning many patients have already lost significant kidney function by the time they're diagnosed. Neuen agrees, adding that this reality argues for using finerenone alongside immunological therapy rather than waiting for earlier diagnosis to guide treatment. Both discuss combining finerenone with SGLT2 inhibitors and emerging immunological or endothelin receptor antagonist therapies as the likely path forward for high-risk patients. Neuen previews a deeper dive into FIND-CKD biomarker and subgroup data, including primary versus secondary FSGS, at the American Society of Nephrology (ASN) meeting later this year.

Heerspink HJL, Neuen BL, Agarwal R, et al. Finerenone in persons with chronic kidney disease without diabetes. N Engl J Med. Published online June 4, 2026. doi:10.1056/NEJMoa2604625

Neuen BL, Perkovic V, Agarwal R, et al. Finerenone in patients with chronic kidney disease due to glomerular diseases: a randomized clinical trial. JAMA. 2026;336(3):224-235. doi:10.1001/jama.2026.9923

Neuen BL, Heerspink HJL, Perkovic V, et al. Efficacy and safety of finerenone in patients with chronic kidney disease: an individual participant data pooled analysis (INFINITY). Lancet. 2026;407(10546):2375-2386. doi:10.1016/S0140-6736(26)01009-3

Bakris GL, Agarwal R, Anker SD, et al. Effect of finerenone on chronic kidney disease outcomes in type 2 diabetes. N Engl J Med. 2020;383:2219-2229. doi:10.1056/NEJMoa2025845

Bayer. Phase III FIND-CKD results show Bayer's Kerendia (finerenone) improved eGFR slope and reduced risk of a composite kidney-cardiovascular outcome in adults with non-diabetic chronic kidney disease. Press release. June 5, 2026. 

https://www.bayer.com/en/us/news-stories/kerendia-for-non-diabetic-chronic-kidney-disease

Podcasts

Brendan Neuen, MBBS, PhD, joins Shikha Wadhwani, MD, MS, to unpack FIND-CKD's GN subgroup data and 23% risk reduction.

Kidney Compass: FIND-CKD Extends Finerenone's Benefit to Non-Diabetic CKD

The Phase 3 VISIONARY trial enrolled 510 patients with biopsy-proven, high-risk IgA nephropathy (IgAN), making it the largest IgAN trial to date. The global, randomized, double-blind, placebo-controlled study was built to test whether selectively blocking APRIL, a cytokine central to the disease's underlying immune biology, could change the course of a condition typically defined by relentless kidney function decline.

“The VISIONARY trial was a phase three trial. It's a global study that enrolled patients with biopsy-proven IgA nephropathy, primary IgA nephropathy, really from all around the world, so very good representation,” Dana Rizk, MD, professor of medicine in the Division of Nephrology at the University of Alabama at Birmingham, said in an interview with HCPLive.

How VISIONARY's Design Targets APRIL in IgA Nephropathy, With Dana Rizk, MD

A High-Risk, Globally Representative IgAN Population

To enroll in VISIONARY, patients needed a biopsy confirming primary IgAN and an estimated glomerular filtration rate (eGFR) > 30 mL/min/1.73 m². Rizk noted the trial built in a timing requirement tied to how preserved a patient's kidney function was at screening.

“They had to have a GFR over 30, and it might be worth mentioning that if their GFR was between 30 and 44, they had to have a biopsy within three years. If it was over 45, so, you know, pretty good preserved GFR, they could have had a biopsy at any point in time,” Rizk said.

Patients also had to meet a proteinuria threshold to qualify as high-risk: > 1 g/day of protein, or a urine protein-to-creatinine ratio > 0.75 g/g, based on a 24-hour collection.

Before randomization, all participants were optimized on background therapy reflecting current standard of care. Patients were maintained on maximum tolerated renin-angiotensin system (RAS) inhibition, and those on sodium-glucose cotransporter-2 (SGLT2) inhibitors had to be on a stable dose for at least 3 months prior to enrollment. Concomitant immunosuppressive medications were not permitted leading up to the study.

Once patients cleared screening, they were randomized to receive sibeprenlimab, 400 mg subcutaneously every 4 weeks, or placebo.

How Anti-APRIL Therapy Targets IgA Nephropathy

Sibeprenlimab is an anti-APRIL therapy, and Rizk walked through why that mechanism was chosen to target IgAN at its immunologic root.

“APRIL is a cytokine that is important in allowing B cells to become IgA-secreting cells, and also is important for the survival of B cells,” Rizk said.

IgAN is an immune-mediated disease, and its pathogenesis has been summarized by the four-hit hypothesis: overproduction of galactose-deficient IgA1 (Gd-IgA1) triggers the formation of autoantibodies against it, which in turn form circulating immune complexes. Those complexes ultimately deposit in the kidneys, driving inflammation and, over time, fibrosis.

“Targeting B cells and this immune backbone to the disease is of course important, makes sense, and that was the premise for the anti-APRIL therapy design,” Rizk said.

Sibeprenlimab (marketed as VOYXACT) received accelerated approval from the U.S. Food and Drug Administration (FDA) in November 2025 for reduction of proteinuria in adults with IgAN at risk of disease progression, based on VISIONARY's primary endpoint results. The trial's key secondary endpoint, annualized eGFR slope over 24 months, offers a longer-term view of whether that upstream mechanism translates into preserved kidney function.

include AstraZeneca, Bayer, Boehringer Ingelheim, Janssen, and others. Disclosures for

include Boehringer Ingelheim, Calliditas Therapeutics, GSK, Otsuka Pharmaceutical Co., Travere Therapeutics, and others. Disclosures for

include Novartis Pharmaceuticals, Otsuka Pharmaceutical Inc., Vera Therapeutics, Biogen, Travere Therapeutics, and others.

Perkovic V, Trimarchi H, Tesar V, et al. Sibeprenlimab in IgA nephropathy: interim analysis of a phase 3 trial. 

. 2026;394(7):635-646. doi:10.1056/NEJMoa2512133

Otsuka. Otsuka unveils unprecedented phase 3 VISIONARY two-year eGFR results demonstrating VOYXACT (sibeprenlimab-szsi) stabilizes kidney function decline to baseline physiologic rate, fundamentally altering disease progression in IgA nephropathy (IgAN). News release. August 3, 2026. 

https://www.otsuka-us.com/news/otsuka-unveils-unprecedented-phase-3-visionary-two-year-egfr-results-demonstrating-voyxactr

Rizk DV, Perkovic V, Trimarchi H, et al. Two-year eGFR and safety results from the VISIONARY phase 3 trial of sibeprenlimab in IgA nephropathy. Presented at: GlomCon Hawaii; August 3-7, 2026; Maui, HI.

VISIONARY enrolled 510 high-risk IgAN patients globally. Learn how the trial's design and anti-APRIL mechanism were built to target disease at its root.


Shikha Wadhwani, MD, MS

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