Oyvind Lie, MD, PhD, MSc, is a senior consultant in interventional cardiology at Oslo University Hospital in Norway.

Anticoagulation therapy after transcatheter aortic valve implantation (TAVI) substantially reduced subclinical leaflet 

 and was noninferior for bleeding, thromboembolic events, and death compared with acetylsalicylic acid (ASA) monotherapy in the recent ACASA-TAVI trial.

Anticoagulant Monotherapy Reduces Thrombosis, Improves Bleeding After TAVI

European Society of Cardiology (ESC) Congress 2026

 in Munich, Germany, by Oyvind Lie, MD, PhD, MSc, a senior consultant in interventional cardiology at Oslo University Hospital in Norway, represent a step forward in challenging guideline recommendations for treatment and management post-TAVI. Currently, US guidelines strongly discourage anticoagulation in patients without an independent indication, based on results from 2 trials evaluating combinations of anticoagulants and antiplatelet therapies. The present trial contrasts this recommendation with evidence of the potential efficacy of anticoagulant monotherapy in this population.

“We have seen during observational studies and related trials that the prevalence of thrombotic processes on the leaflets of the TAVI valves is substantially lower in patients who have anticoagulation therapy, meaning patients with atrial fibrillation, venous thromboembolism, or other indications,” Lie told 

 in an exclusive interview. “This raised the question of whether or not there is merit to the anticoagulation domain of antithrombotic therapy, which led us into constructing this trial.”

ACASA-TAVI was a multicenter, randomized controlled trial that enrolled patients aged >65 and <80 years who had undergone successful TAVI. Patients with a strict indication or contraindication for anticoagulation or antiplatelet therapy, overt cognitive failure, or concomitant use of inducers or inhibitors of CYP3A4 or P-glycoprotein were excluded.

Participants were then randomly assigned in a 1:1 ratio to 12 months of treatment with either a factor Xa inhibitor non-vitamin K antagonist oral anticoagulant (NOAC) for the duration of the study and changed over to ASA indefinitely following the study (intervention) or to ASA monotherapy indefinitely (control). Patients assigned to receive NOAC began standard dosing of any commercially available anti-factor Xa NOAC within 72 hours of TAAVI, with standard dosing of 5 mg apixaban twice daily, 60 mg edoxaban once daily, or rivaroxaban 20 mg once daily. The ASA cohort received 75 mg ASA without dose adjustments.

The study’s co-primary endpoints were hypoattenuated leaflet thickening (HALT) and a safety composite of bleeding events, thromboembolic events, and all-cause death at 12 months. Secondary endpoints included a clinical efficacy composite of freedom from all-cause mortality, 

, hospitalization for procedure- or valve-related causes, and Kansas City Cardiomyopathy Questionnaire overall summary score of ≤45 or a decline from baseline of ≥10 points, among other criteria.

A total of 1983 patients were scanned, of whom 360 were enrolled – 180 patients were assigned to each group. In the NOAC group, 51% were given apixaban, 41% received edoxaban, and 8% received rivaroxaban. 11 patients in the ASA group received clopidogrel instead of ASA. A total of 47 patients had treatment deviations. 36 patients crossed over, 5 aborted therapy, and 6 had temporary treatment interruptions. All patients completing the trial with no deviations reported good adherence.

The co-primary efficacy endpoint occurred in 27 of 167 patients receiving NOAC (16.2%) and in 48 of 168 patients receiving ASA (28.6%) (risk ratio, 0.55; 95% CI, 0.37 to 0.82; 

 = .004). The number of patients with grade 1 HALT was similar between groups, but more severe HALT was more common in the ASA cohort. The primary safety endpoint occurred in 13 patients from the NOAC group (7.5%) and in 19 patients from the ASA group (10.6%) (absolute risk difference, -3.3%; 95% CI, -9.5% to 2.8%).

Ultimately, Lie and colleagues concluded that the present study serves as a demonstration for the efficacy of NOAC treatment following TAVI, contradicting widely accepted guideline recommendations. However, the team also notes a handful of limitations associated with the study, including its open-label design and the inability to extrapolate the results to older patients undergoing TAVI due to its focus on younger patients.

“I think the paradigm is challenged; how that will materialize into new practice guidelines, I am not the one to decide,” Lie said. “But this is absolutely not enough evidence to turn the guidelines around. For that, we need larger studies, longer-term follow-up, and convincing clinical outcomes.”

Editors’ Note: Lie reports disclosures with Edwards Lifesciences, Medtronic, and Abbott.

Dodgson CS, Herstad J, Kløve SF, et al. Anticoagulation monotherapy vs Antiplatelet Monotherapy after transcatheter aortic valve implant. JAMA. Published online August 30, 2026. 

Oslo University Hospital. AntiCoagulation Versus AcetylSalicylic Acid After Transcatheter Aortic Valve Implantation (ACASA-TAVI). ClinicalTrials.gov Identifier: NCT05035277. Updated June 9, 2026. Accessed September 10, 2026. 

https://clinicaltrials.gov/study/NCT05035277

Videos

Oyvind Lie, MD, PhD, MSc, discusses the results from the ACASA-TAVI trial, which sought to evaluate the efficacy of anticoagulant monotherapy in this population.

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 conference coverage page features articles, videos, and expert-led live coverage from major medical meetings throughout the year.

Credit: Northwestern Feinberg School of Medicine

 treatment continues to expand beyond injectable biologics, even as clinicians still lack tools to match patients with the right therapy up front. Response rates with current interleukin (IL)-4 and IL-13 blockade remain good but not complete, leaving a meaningful share of patients under-treated despite an increasingly crowded pipeline.

A prospective validation study of the AdvanceAD-Tx 487-gene expression profile test examined patients starting or switching systemic therapy for moderate to severe disease.¹ Among those identified with a Janus kinase (JAK) inhibitor responder profile, 45.5% achieved EASI 90 by 3 months on JAK therapy versus 8.3% on Th2-targeted treatment (

Separately, the oral STAT6 degrader KT-621 produced median STAT6 reductions of 94% in skin and 98% in blood after 4 weeks in the Phase 1b BroADen trial.² Blood IL-31 fell 54% on average, the first reported IL-31 reduction from a drug targeting the IL-4/IL-13 pathway. These findings point toward a future where clinicians choose between JAK inhibitors, biologics, and oral options based on molecular profile rather than trial and error.

For now, testing logistics and limited practice experience keep gene expression profiling from routine use, and most clinicians still personalize care empirically, starting with a biologic and layering on topical therapy as needed. Peter Lio, MD, clinical assistant professor of dermatology and pediatrics at Northwestern University Feinberg School of Medicine and founding director of the Chicago Integrative Eczema Center, tracks this pipeline closely in his atopic dermatitis practice.

In the following interview, Lio spoke with 

 at LEADderm 2026 in Newport Beach, California, about where precision medicine in atopic dermatitis stands today:

: What drugs or disease states with new data or PDUFA dates excite you?

There's a tremendous amount happening in dermatology. My focus is generally on atopic dermatitis, and there are several exciting drugs and new developments happening. We've seen some programs shift. A couple of drugs, particularly in the OX40 pathway for atopic dermatitis, have been dropped, which is interesting in itself, to see pathways that maybe aren't positive. But the one I'm excited about is an oral agent coming for atopic dermatitis. It's still fairly early on, but what's exciting is it's an oral pathway similar to the IL-4 and IL-13 blockades, but taken orally, and it seems to be highly effective.

There are also some new topicals in early phases, including a topical botanical agent for atopic dermatitis that I'm particularly excited about, because a lot of my patients want something more natural. It has antimicrobial effects as well as anti-inflammatory effects. I think we're finally beginning to see enough choices to start having precision medicine discussions. We also have a new lab test that can help decide between a JAK inhibitor and a more Th2-focused biologic, whether a patient is a better candidate for one or the other. I'd argue it's not quite ready for primetime, at least in my practice. I don't know how to use it yet, but it's an amazing first step.

This is exactly the kind of groundwork where, instead of just guessing, we're able to get a sense of somebody from a skin scraping or a swab and say this pathway is going to be good for you, or this pathway might not be good for you, you're more likely to have a side effect or an issue and it's not going to work. All of those pieces we're hopefully going to be able to predict and have that precision and personalized medicine, which has always been the goal, but we just haven't had the tools until now.

: Can you describe the test, and how close are we to true precision medicine?

 I think the precision medicine journey is something that will probably never hit an end point. It's going to be a continuous journey of refinement and improvement, much like the virtuous cycle of drug development: we get a new medicine, it teaches us more about the underlying disease state, and that in turn allows us to refine and get better medicines. It's a building process. Rarely do we have a breakthrough that solves the whole thing; most of what I'm involved in never works that way, it's a slow process of iteration. We're seeing that with psoriasis now. We've moved so far with psoriasis and refined it so much, though we still don't really have personalization yet.

What we've found is we have agents so good for so many people that you don't really have to personalize; you can say one of these newer agents gives a really good chance you'll be clear or almost clear very quickly. With atopic dermatitis, the numbers are good, but they're not that good, so there's still a lot of unmet need, and more testing would help. That first test is very specific and looks at one pathway. It would be nice to understand more: is this patient primarily a skin barrier problem, an inflammatory pathway issue and if so where, or somebody who might benefit from microbiome manipulation, or all of the above? The other possibility, especially with diseases like atopic dermatitis, is they're somewhat messy, so maybe we'll never fully personalize it because it's multiple components, and we'll always have to think more holistically.

Maybe great drugs will come to market, like with psoriasis, that obviate a lot of this. In other fields of medicine, particularly oncology, we've seen the biggest leaps in precision medicine, being able to understand tumor characteristics and say, you have this mutation, so this pathway is exactly what you need. That's really been the gold standard, and oncology is setting the tone for everybody else, but I don't think we're anywhere close to that yet with inflammatory conditions, which tend to be messier and, frankly, more interesting to me because of that.

We also have this whole world of over-the-counter products, which in Europe they might call dermo-cosmetics: cleansers, moisturizers, and skincare products we use often without as much data, though the science is rapidly progressing. I love being at conferences that showcase the science behind our OTCs, and I often feel we don't give them the same spotlight as drugs. Everybody focuses on a drug, but OTCs are undergoing their own renaissance, and it's been incredibly exciting to be part of that too.

: When did you first hear about precision medicine, and how has it evolved?

 We've always talked about and dreamed about precision medicine. In science fiction, somebody gets a body scan and knows exactly what's wrong. That's really the goal: personalizing to you what would be safe and effective, the right solution to your specific problem. We've always wanted that. We haven't had the tools, but now we're beginning to understand more of the genetics, and that's where the early work came with genetic diseases, where there was one gene, one protein, one mistake.

That opened the door, and for a minute everybody thought this is how all of medicine is going to be, we're going to solve it all. Then we quickly hit a wall: this isn't one gene, one protein, one disease. It's way more complicated, we can't find a gene mutation that's reliable, and it's different across populations and individuals. We've kind of understood some of those simpler diseases, for better or worse, and things like gene therapy are happening. But for these more complex diseases, we still have a ways to go. I hold out hope we're going to get there and understand them, even if they're multifactorial, and that's going to make it that much more satisfying when we do.

: Is the Castle test Dr. Swanson mentioned the one you meant?

Yes, that Castle [Biosciences] test is the one that helps us decide between a JAK inhibitor, which is broader, and a more targeted IL-4/IL-13 biologic. It's pretty good; it gives us a sense of which patient might do better with one or the other. Ultimately, the question it answers is whether a biologic would be enough for this patient, at least as a clinician how I interpret it. Smarter people might interpret it a little differently, but when I look at it as a clinician, it's: do I think I could get by with a biologic, which has a smaller safety profile and is a little easier to use?

The answer could sometimes be no, they're unlikely to do well with a biologic, so you have to use the bigger, more encompassing medicine, the JAK inhibitor, with the safety and tolerability issues it carries as well. We have to do lab monitoring and counsel a bit more about things like blood clots. So there's a potential bonus there. For me at this point, and it may change, and I'm excited for it to change and refine, I feel the logistics of the test and its potential to help me are fairly limited in usefulness right now. So I've often said, why not start with the biologic, and we can empirically know the answer pretty quickly?

Even if it doesn't fully help, sometimes the biologic will help a bit, and then I can add other things like topicals. I'm personalizing it a little more on what we might call a diagnosis ex juvantibus: what's helping them? I customize to the patient by trial and error, on an individual basis, to see if it's going to work. But I foresee a future when I'll be able to do a simple test and say you're not a good candidate for this, let's skip right to the good stuff.

Editor's Note: This transcript has been edited for grammar and clarity using artificial intelligence tools.

Silverberg JI, Eichenfield LF, Armstrong AW, et al. The 487-gene expression profile test guides systemic therapy selection to improve outcomes for patients with atopic dermatitis: results from a prospective trial. J Am Acad Dermatol. Published online February 16, 2026. doi:10.1016/j.jaad.2026.02.034.

Kymera Therapeutics. Kymera Therapeutics announces positive results from BroADen phase 1b clinical trial of KT-621, a first-in-class, oral STAT6 degrader, in patients with moderate to severe atopic dermatitis. Published December 8, 2025. Accessed September 10, 2026. 

https://investors.kymeratx.com/news-releases/news-release-details/kymera-therapeutics-announces-positive-results-broaden-phase-1b

Articles

Systemic therapy for moderate-to-severe atopic dermatitis is broadening beyond injectable IL-4/IL-13 biologics, yet upfront treatment selection remains largely empirical. A prospective validation of the AdvanceAD-Tx 487-gene expression profile identified a JAK-responder signature associated with higher and faster EASI 90 rates on JAK inhibition versus Th2-targeted therapy. In parallel, the oral STAT6 degrader KT-621 demonstrated deep STAT6 knockdown in skin and blood with concomitant IL-31 reduction. Practical barriers and limited clinical experience still constrain routine profiling adoption.

Peter Lio, MD, breaks down AdvanceAD-Tx testing and oral STAT6 degrader KT-621 in the atopic dermatitis pipeline.

Atopic Dermatitis

Atopic Dermatitis condition center page, audiences can find a variety of coverage mediums for medical news and updates, including articles, video interviews, podcasts, and breaking news on dermatitis research, treatment, and drug development.

Q&A: Precision Medicine's Next Steps in Atopic Dermatitis, With Peter Lio, MD

Jose Nicolau, MD, PhD, is a professor at the University of São Paulo Medical School and senior investigator at the Heart Institute InCor.

 who received evolocumab on top of statin therapy saw major reductions in the rate of total major adverse cardiovascular events (MACEs), based on a new subanalysis of the VESALIUS-CV trial.

Evolocumab Prevents Recurrent Cardiovascular Events Following MI or Stroke

 in Munich, Germany, by Jose Nicolau, MD, PhD, professor at the University of São Paulo Medical School and senior investigator at Heart Institute InCor, this subanalysis addressed a gap in existing VESALIUS data. While the original trial only analyzed patients without prior MI or stroke, Nicolau and colleagues aimed to determine whether evolocumab exhibited a similar cardioprotective effect on patients who had already experienced an event.

“The results of VESALIUS, the first results published in 

 at the end of last year, showed wonderful results with a very important benefit with evolocumab versus placebo,” Nicolau told 

 in an exclusive interview. “But the patient, if they don’t die, very often has more than 1 event. That’s what we analyzed in this prespecified subanalysis of VESALIUS – we analyzed both first and subsequent events.”

VESALIUS-CV was a double-blind, randomized, placebo-controlled clinical trial conducted at 774 sites internationally. Patients were eligible if they had LDL-C ≥90 mg/dL, non-HDL-C ≥120 mg/dL, or apolipoprotein B ≥80 mg/dL. Additionally, patients needed to have significant coronary artery disease, atherosclerotic cerebrovascular disease, peripheral artery disease, or diabetes mellitus.

Patients were randomly assigned in a 1:1 ratio to either 140 mg of evolocumab subcutaneously every 2 weeks or matching placebo. Primary endpoints included a composite of death from coronary heart disease, MI, or ischemic stroke (3-point MACE) and a composite of 3-point MACE and ischemia-driven arterial revascularization (4-point MACE).

A total of 12,257 patients were enrolled, with 6129 assigned to evolocumab and 6128 to placebo. Over a median follow-up of 4.6 years, 3-point MACE events occurred in 336 patients in the evolocumab group versus 443 in the placebo group. A 4-point MACE event occurred in 747 patients receiving evolocumab versus 907 receiving placebo. The trial concluded with no evidence of a between-group difference for safety events.

In the present analysis, Nicolau and colleagues analyzed total 3-P and 4-P MACE events, both first and subsequent, using a negative binomial regression model. All 12,257 patients from the original trial were included. By the end of the trial, 779 first 3-P MACE events and 146 subsequent events had occurred, for a total of 925 total events. For 4-P MACE, the team logged 1654 first events and 1107 subsequent events for 2761 total.

Evolocumab reduced 3-P MACE risk by 25% (HR, 0.75; 95% CI, 0.65-0.86), recurrent events by 37% (incidence-ratio rate [IRR], 0.63; 95% CI, 0.42-0.94), and total events by 27% (IRR, 0.73; 95% CI, 0.63-0.86). Similarly, evolocumab reduced 4-P MACE first event risk by 19% (HR, 0.81; 95% CI, 0.73-0.89), recurrent events by 25% (IRR, 0.75; 95% CI, 0.61-0.91), and total events by 20% (IRR, 0.8; 95% CI, 0.71-0.9; 

Based on these data, Nicolau and colleagues noted that, for every 1000 patients treated for 5 years, evolocumab prevented 20 first 3-P MACE events, 5 subsequent events, and 25 total events. For 4-P MACE, treatment with evolocumab prevented 31 initial events, 24 subsequent events, and 55 total events. These results were consistent across all subgroups, including by qualifying atherosclerosis and high-risk diabetes without atherosclerosis.

Ultimately, the team concluded that evolocumab is not only efficacious in preventing recurrent MACEs but also saw nearly double the number of recurrent events prevented versus placebo compared to the analysis of only first events. Nicolau and colleagues presented these data as further support for the key role of LDL-C lowering in patients with atherosclerosis or high-risk diabetes, regardless of whether these patients have experienced a prior MI or stroke.

“The fact is that, when you decrease the LDL-C in such a case with evolocumab, you are adding benefit. This is true for high-risk patients, people with previous MI or previous stroke,” Nicolau said. “But now, we are showing that this is also true for patients without previous MI or stroke. They are high risk, but not 

 high risk. This is a continuum, and we will continue to analyze and to study this population in the future.”

Editors’ Note: Nicolau reports disclosures with Amgen, AstraZeneca, Bayer, Novo Nordisk, Novartis, Janssen, and others.

Nicolau JS, Murphy S, Giugliano RP, et al. Reduction in total cardiovascular events with evolocumab in patients with no prior myocardial infarction or stroke: a pre-specified analysis of VESALIUS-CV. Presented at the European Society of Cardiology (ESC) Congress 2026, Munich, Germany. August 28-31, 2026.

Bohula EA, Marston NA, Bhatia AK, et al. Evolocumab in patients without a previous myocardial infarction or stroke. New England Journal of Medicine. 2026;394(2):117-127. 

Jose Nicolau, MD, PhD, discusses the results of his subanalysis of the VESALIUS-CV trial, examining secondary rather than first MACE.

Stroke

On the HCPLive stroke page, resources on the topics of medical news and expert insight into CVA can be found. Content includes articles, interviews, videos, podcasts, and breaking news on stroke medicine, and more.

Diana Isaacs, PharmD, is an endocrine clinical pharmacist, director of Education and Training in Diabetes Technology, and codirector of Endocrine Disorders in Pregnancy at the Cleveland Clinic.

Diabetes Dialogue: Technology, Therapeutics, & Real-World Perspectives

Insulin resistance and cardiovascular risk sit at the center of nearly every conversation in modern diabetes care, and 2 recent developments push this conversation forward. Co-hosts Diana Isaacs, PharmD, and Natalie Bellini, DNP, open this episode with the newly approved cardiovascular indication for tirzepatide, then turn to fresh data on statin therapy in adults over 70. Both topics carry immediate implications for how clinicians counsel patients on risk reduction across the lifespan.

Diabetes Dialogue: Tirzepatide's New CV Indication and the STAREE Statin Trial 

Tirzepatide Gains FDA Approval for Cardiovascular Risk Reduction

On August 28, 2026, the US Food and Drug Administration approved tirzepatide, marketed as Mounjaro, to lower the risk of major adverse cardiovascular events in adults with type 2 diabetes at high risk for these events.¹ The approval covers cardiovascular death, nonfatal heart attack, and nonfatal stroke.

Isaacs notes some clinicians expected this approval to be uncertain because the pivotal SURPASS-CVOT trial compared tirzepatide with dulaglutide rather than placebo and found noninferiority rather than superiority. Bellini points out dulaglutide already carries its own cardiovascular indication, so a noninferior result still places tirzepatide on equal footing with an agent already proven to reduce cardiovascular risk. The trial enrolled > 13,000 participants across 30 countries, giving the finding a broad and diverse evidence base.

Isaacs walks through a pair of additional analyses strengthening the case for approval. An imputed placebo comparison, built through statistical modeling rather than a true placebo arm, suggested tirzepatide would have shown superiority had an ethical placebo-controlled design been possible given the established benefit of comparator agents. A separate 5-point MACE analysis presented by cardiologist Steve Nissen, MD, of Cleveland Clinic, also favored tirzepatide once additional cardiovascular outcomes were incorporated beyond the original 3-point composite.

Isaacs highlights the approval covers patients at high risk for cardiovascular events rather than requiring established cardiovascular disease, a distinction she expects will broaden access. Bellini adds this framing captures a wide swath of everyday patients, since diabetes, hypertension, elevated cholesterol, and obesity all confer elevated risk on their own.

The hosts also raise an open mechanistic question: whether the cardiovascular benefit stems from tirzepatide's GLP-1 activity, its GIP activity, or both. Isaacs notes dulaglutide achieves cardiovascular benefit with considerably less glucose-lowering and weight-loss potency, raising questions about how much of tirzepatide's effect traces to the GIP component as dual and triple agonists enter development.

Bellini emphasizes patient selection remains individualized regardless of the new indication, since tolerability and prior response still guide the choice between agents. The discussion closes by noting semaglutide and tirzepatide carry distinct indications beyond cardiovascular risk, including kidney disease and MASH for semaglutide and sleep apnea for tirzepatide, keeping regimen selection a multifactorial decision.

STAREE Trial Supports Statin Use for Primary Prevention After Age 70

Statin therapy in older adults has long lacked robust trial evidence, since patients older than 70 have historically been excluded or underrepresented in pivotal statin studies. The STAREE trial, published in the

, randomly assigned nearly 10,000 adults with a mean age of 74.7 years to atorvastatin 40 mg or placebo.²

Bellini highlights the balanced enrollment of 52% women, addressing a long-standing gap in sex representation within statin research. Over a median follow-up of 5.9 years, atorvastatin reduced major cardiovascular events by 30% compared with placebo, a finding both hosts describe as clinically meaningful for a low-cost, generic medication.

Isaacs points out disability-free survival did not differ significantly between groups, suggesting age alone should not automatically dictate statin initiation. She reinforces the value of individualized, shared decision-making for patients with limited life expectancy or significant comorbidity burden.

Bellini adds serious adverse events occurred at similar rates in both arms, at 2.7%, countering the common perception statins routinely cause significant side effects in older patients. She encourages clinicians to try alternative statins before concluding a patient cannot tolerate the drug class. The hosts close by addressing dementia risk directly: daily statin therapy did not significantly change dementia rates over nearly 6 years, a neutral finding they frame as reassuring given ongoing patient concerns.

Editors’ Note: Disclosures for Isaacs include Dexcom, Abbott, Lilly, Novo Nordisk, Medtronic, Insulet, and others. Disclosures for Bellini include Abbott Diabetes Care, MannKind, Provention Bio, and others.

Eli Lilly and Company. FDA approves Lilly's Mounjaro (tirzepatide) to reduce cardiovascular risk in adults with type 2 diabetes. Press release. August 28, 2026. 

https://investor.lilly.com/news-releases/news-release-details/fda-approves-lillys-mounjaro-tirzepatide-reduce-cardiovascular

Zoungas S, Wolfe R, Moran C, et al. Atorvastatin, cardiovascular events, and disability-free survival in older adults. 

. Published online August 28, 2026. doi:10.1056/NEJMoa2607314

Podcasts

Diana Isaacs, PharmD, and Natalie Bellini, DNP, unpack tirzepatide's new CV indication and the STAREE statin trial in older adults.

Endocrinology

The HCPLive endocrinology page is a comprehensive resource for clinical news and insights on endocrine system conditions. This page consists of interviews, articles, podcasts, and videos on the research, treatment and development of therapies for diabetes, hormonal disease, and more.

This page also hosts content previously published by EndocrinologyNetwork. 


podcasts page features a feed of medical news and interview podcast series, including DocTalk, Lungcast, Derm Discussions, and Heart Trials.

Diabetes Dialogue

Diabetes Dialogue: Technology, Therapeutics, & Real-World Perspectives is a podcast hosted by Diana Isaacs, PharmD, and Natalie Bellini, DNP, aimed at providing a regular roundup of the latest clinically applicable insights across diabetes and metabolic diseases, with a focus on leveraging technology to improve care.

Strategic Alliance Partnership

"Byron Wade is a principal consultant at American Healthcare Strategies and co-founder of the Wade Family Foundation. He has more than 20 years of clinical and administrative healthcare experience, including leading physician recruitment strategy for UPMC.

Patient experience remains an underused data point in 

 (IgAN) research, even as the treatment landscape shifts from broad supportive care toward targeted, disease-modifying therapies. 

Byron Wade, a co-author on a new mixed-methods study examining the IgAN patient experience and a principal consultant at American Healthcare Strategies, brings both a professional healthcare background and firsthand knowledge of the disease to the work.¹ 

The study, presented at GlomCon 2026 in Maui, Hawaii, combined qualitative and quantitative methods to capture how patients navigate diagnosis, treatment access, and disease management, aiming to give clinicians a clearer view of the patient perspective.¹

Wade's decade-long wait for a diagnosis is not unusual, according to the study he co-authored. The mixed-methods GlomCon 2026 poster, combining 20 qualitative patient interviews with a 106-patient survey, found patients typically waited 1 to 2 years to reach a nephrologist after symptoms began, with hematuria and fatigue as the most commonly missed early signs.¹ It also found a gap between what patients want from treatment and what they feel they're getting: 80% ranked symptom control and preserved kidney function as top priorities, but only about 50% felt those goals were being met.¹

The same data set is the basis for two related HCPLive interviews with Gaia Coppock, MD, associate professor of clinical medicine and director of the Glomerular Disease Clinical Research Program at the Hospital of the University of Pennsylvania:

Mistaken for a UTI: Diagnosing IgA Nephropathy, With Gaia Coppock, MD

Personalizing IgA Nephropathy Care Conversations, With Gaia Coppock, MD

Diagnostic delay is common in IgAN, particularly when early symptoms are mild or intermittent, and family history can prompt closer monitoring without necessarily accelerating diagnosis. A separate report from University of Pennsylvania nephrologist Abdallah Geara, MD, and colleagues similarly outlines patient and provider perspectives across the diagnostic journey, reinforcing persistent gaps in how patient-reported experience informs everyday clinical care.² Eligibility criteria tied to kidney function have also limited access to newer IgAN therapies for patients diagnosed later in the disease course, leaving a treatment gap for a meaningful share of the IgAN population.

Wade was followed by a nephrologist for over a decade before a kidney biopsy confirmed his own IgAN diagnosis, following years of family history-driven surveillance tied to his sister's disease. He underwent a kidney transplant in 2023, with his wife, Melissa, serving as his living donor, and the two now co-lead the Wade Family Foundation, supporting living donation and IgAN research. Below, Wade shares his perspective on his diagnostic journey, his experience navigating treatment eligibility as a transplant recipient, and his advice for patients newly diagnosed with IgAN.

Q&A: Byron Wade on diagnosis, transplant, and patient advocacy

HCPLive: Can you walk us through your journey of recognizing you had IgA nephropathy, from first noticing something wrong to diagnosis?

Wade: I was followed by a nephrologist for years before I realized I had IgA nephropathy, for about 10 to 11 years. My sister had kidney disease, IgA nephropathy, so I was being tracked, but I never thought much of it. I went to my annual appointments and moved on with my life. It wasn't until fall of 2019 that I noticed blood in my urine, and that was my first real sign I had bigger problems than an annual nephrologist visit. I always tell people my experience is my experience, not necessarily that of everyone with IgA nephropathy. After that episode I was hospitalized for 5 days, but I still didn't follow up with a kidney biopsy. It felt like a single point in time, not enough data to justify an invasive procedure, so I decided to wait and see if anything happened again. Unfortunately, 3 to 4 months later I had the same thing happen again, was hospitalized, and that's when I was diagnosed with IgA nephropathy on biopsy.

HCPLive: Did having a family history change how quickly you were diagnosed or how seriously you took your symptoms, compared with other patients?

Wade: For me personally, the big thing is I work in healthcare, so I always try to take my health seriously. My background started in pre-hospital medicine as an EMT and progressed into administration. I think we all go through phases of life where we view our health differently. In your 20s, you feel invincible, and I think you start taking it more seriously as you get older. I'd say I took it more seriously than most of my peers and most other men my age, but this definitely made me look at it differently. Being followed by a nephrologist isn't normal for a 20- or 30-year-old with no issues at the time, but it was eye-opening when I started seeing signs and symptoms myself. That's when I realized this was real.

HCPLive: What has stood out throughout your treatment and appointments that has contributed to your confidence or preparedness?

Wade: I'm very fortunate to be embedded in the healthcare system, which gave me more inherent trust and the ability to seek out specific providers than maybe some of my peers who aren't in healthcare. When I was diagnosed with IgA nephropathy, there were more questions than answers, even from the medical team. I hope my peers with IgA nephropathy now find a little more hope in the system. That's the reason I got involved in this work, to help other people know there are options now that there are treatments for IgA nephropathy. It's not something you just have to live with anymore. When I was diagnosed, it was just controlling blood pressure with ACE inhibitors and ARBs and sometimes steroids, and now there are actual IgAN treatments.

HCPLive: Since the treatment landscape has evolved so significantly, does your current treatment address what matters most to you and other patients?

Wade: Unfortunately, I was diagnosed on biopsy in 2020, and there were no treatment options available then. When the first treatments came out, whether through trials or approved therapies, I didn't qualify because my GFR, my kidney function, was too low. So I haven't had any treatments. In 2023 I had a kidney transplant, and now I'm not eligible for treatment again. I'm currently in what some people call remission, though not everyone uses that term. IgA nephropathy is still in my other two kidneys, and there's a concern it could attack the donor kidney, which does happen to some patients. Fortunately, that hasn't happened to me so far. I look forward to these drugs being tested not just in IgAN patients now that they're approved, but eventually in transplant recipients too, so we have more options in the future. The hope for me is that we now actually have therapies for people to pursue, and more than one option, because what's right for one person isn't right for another. Unfortunately, I wasn't able to take part in any of these treatments or trials because my IgAN had progressed too far.

HCPLive: What would you tell someone who just got diagnosed with IgA nephropathy?

Wade: The great news is there are options and treatments available to pursue. You're your own biggest advocate, so arm yourself with knowledge. Find a good support system, a family member or friend who can help you navigate the process, because it's a lot to take in. Find providers you feel confident in. If you don't like your primary care doctor or nephrologist, seek out alternative options, and then seek out the right treatment for you. If you don't feel comfortable, ask questions, because I truly believe healthcare outcomes are shaped as much by mindset as by the actual treatment. My wife attends most of my appointments with me, and what she takes away from an appointment with a nephrologist, or in my case also a transplant nephrologist, is sometimes different from what I take away. We put that information together to get a better picture by the end of the appointment. I'll add one more thing: early intervention is key to success. For me, success means keeping people away from unnecessary transplants. Some people will progress too far and need a transplant, or face trauma or untreatable disease, but the best thing you can do for yourself is take care of yourself and try to stay in the stage of kidney disease you're in now. Kidney tissue doesn't repair itself, so you can't go back up the chain, but if you can maintain your current status, that's probably the best outcome versus assuming a transplant is your best option. If you do reach the point where you need it, that's great, but try to preserve the kidney function you currently have.

HCPLive: Was there anything else you felt was important to highlight?

Wade: At the end of the day, it comes down to taking good care of yourself, being diligent, and seeking out treatment and annual exams. A lot of people just forgo going to the doctor annually, and a lot of these symptoms aren't visible until it's too late. Blood work is your best friend.

Bensouda M, Wade B, Burns J, et al. IgA Nephropathy Patient Experience: A Qualitative and Quantitative Mixed-Methodology Study. Poster presented at: GlomCon 2026; August 3-7, 2026; Maui, HI.

Geara AS, Chen KB, Simmons W. Patient and Provider Perspectives on the Patient Journey in Immunoglobulin A Nephropathy. Kidney Med. 2026;8(3):101242. doi:10.1016/j.xkme.2026.101242.

Patient-reported experience remains underleveraged in IgA nephropathy despite a shift from supportive care toward disease-modifying therapies. Mixed-methods data presented at GlomCon 2026 characterizes diagnostic delays, fragmented journeys from mild/intermittent symptoms to biopsy confirmation, and access barriers driven by eGFR-based eligibility. Lived experience highlights how family-history surveillance may increase monitoring without expediting diagnosis. Advanced disease can exclude patients from trials and approved options, and transplant recipients remain largely unstudied for emerging IgAN agents. Emphasis is placed on advocacy, early intervention, and routine labs.

A principal healthcare consultant and study co-author shares his own decade-long path to an IgA nephropathy diagnosis and transplant.

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Patrick Campbell is the editorial director of HCPLive. Patrick has spent years spearheading coverage surrounding cardiometabolic health and rheumatic disease for MJH Life Sciences. Before joining MJH Life Sciences in 2019, he spent time as a beat reporter and/or multimedia specialist with the Pocono Record, Star News Group, and NJ Advance Media. He is the executive producer for multiple HCPLive podcasts, including Diabetes Dialogue, Don't Miss a Beat, Kidney Compass, Medical Ethics Unpacked, The Medical Sisterhood, and Skin of Color Savvy. 


Follow him on Twitter @RealPatCampbell or reach him via email at PCampbell@mjhlifesciences.com.

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