Edgar Lerma, MD

On IgA Nephropathy (IgAN) Awareness Day, HCPLive spoke with Edgar Lerma, MD, Clinical Professor of Medicine with the Section of Nephrology at the University of Illinois at Chicago, about the rapidly evolving treatment landscape, including the rise of targeted therapies, the emerging role of APRIL inhibition, and ongoing debates surrounding proteinuria as a surrogate endpoint in clinical trials.

Once considered a disease with limited therapeutic options beyond supportive care and immunosuppression, IgA nephropathy treatment has entered what Lerma described as a “mechanism-first era,” with multiple newly approved and investigational agents now targeting distinct pathways across the pathogenic cascade. From sparsentan and targeted-release budesonide to complement inhibitors and APRIL-targeting biologics, clinicians are increasingly tasked with determining how to sequence therapy, identify high-risk patients, and communicate prognosis in a more individualized way.

Despite these advances, real-world uptake of newly approved IgAN therapies has remained relatively low through 2025, with barriers including REMS requirements, safety monitoring burdens, prior authorization hurdles, and continued uncertainty surrounding long-term renal outcomes. At the same time, ongoing development of APRIL and dual APRIL-BAFF inhibitors has intensified discussion around upstream immune modulation and whether newer biologics may eventually become foundational therapies in IgAN management.

HCPLive sat down with Lerma for a Q&A on treatment sequencing, proteinuria endpoints, APRIL inhibition, and how clinicians should approach prognosis discussions in the modern IgAN era.

HCPLive: With 5 approved agents now targeting distinct points on the pathogenic cascade, how do you approach treatment selection and sequencing in patients with IgAN?

Lerma: Even though we now have 5 or more targeted options emerging, most guideline-consistent practice still begins with risk stratification. Clinicians are not routinely “stacking” disease-modifying agents at this point. More commonly, treatment involves substituting agents or intensifying therapy within a pathway based on patient response and tolerability. Combination approaches, such as endothelin receptor antagonists plus complement inhibitors, remain more in the trial territory than standard practice.

In my own practice, I still take a stepwise approach. First, patients are started on optimized supportive therapy. That includes maximizing renin-angiotensin system (RAS) blockade as tolerated, adding an SGLT2 inhibitor—which is now essentially standard across CKD, including IgAN—and targeting blood pressure below 130/80 mmHg. We also aim for proteinuria reduction, ideally below .5 g/day if feasible, although older guidelines used <1 g/day as the benchmark.

Once supportive care is optimized, the next step is defining the patient’s risk trajectory. If proteinuria persists above .5 g/day despite optimal care, if eGFR is declining, or if histopathology suggests higher-risk disease—such as crescents or concerning MEST-C scores—then we begin considering the newer pathway-targeted therapies. These include agents targeting IgA production, endothelin pathway therapies with hemodynamic and antifibrotic effects, and complement inhibitors targeting downstream injury modulation.

Recent real-world data suggest fewer than 5% of eligible IgAN patients received newly approved therapies through 2025, with REMS requirements and black box warnings cited as barriers. What do you think is driving that gap?

Lerma: The gap is real, but it’s also not unexpected when new therapies enter practice. The reasons tend to fall into about 5 major categories.

First is regulatory and safety friction. Some agents require REMS programs, frequent laboratory monitoring, or carry black box warnings, all of which create administrative burdens. Those challenges can be particularly difficult in community nephrology settings.

Second is skepticism surrounding proteinuria as a surrogate endpoint. Most clinicians view proteinuria reduction positively, but many still question whether it truly translates into long-term prevention of end-stage kidney disease. As a result, uptake of therapies approved on surrogate endpoints tends to lag behind approvals themselves.

Third are infrastructure barriers, including specialty pharmacy routing, prior authorizations, and documentation requirements proving failure of optimized supportive care. Monitoring demands can also exceed what some practices can realistically support.

Fourth is the inherent heterogeneity of IgAN. The disease is often slowly progressive and highly variable at the individual level, so clinicians may defer immunomodulatory or pathway-targeted therapies unless the patient appears clearly high risk.

Finally, there is the physician familiarity curve. Many nephrologists trained before the era of targeted therapies in IgAN. Historically, adoption of new CKD therapies can lag evidence by several years, so some delay is expected.

HCPLive: For patients who have been on sparsentan or budesonide for a year or more, what role do APRIL inhibitors play? Are you using them as add-on therapy, replacement therapy, or something else entirely?

Lerma: When we talk about APRIL inhibitors—such as sibeprenlimab and other APRIL biologics currently in development—we’re discussing agents that target a different, upstream mechanism. These therapies decrease mucosal B-cell activation and reduce production of galactose-deficient IgA1, which is central to IgAN pathogenesis.

Mechanistically, APRIL inhibitors act earlier in the disease cascade than either budesonide or sparsentan. In practice, there are currently 3 conceptual roles being explored.

One is replacement therapy. If APRIL inhibition demonstrates strong and durable proteinuria reduction with a favorable safety profile, it could potentially replace steroid-based approaches.

The second is sequential escalation. In that model, clinicians would begin with optimized supportive care and hemodynamic modulation, then escalate to APRIL inhibition if progression persists despite treatment.

The third possibility is combination therapy. Biologically, combining upstream and downstream approaches makes sense, but concerns remain regarding overlapping immunosuppression and whether combination therapy provides meaningful additional benefit.

At this point in 2026, APRIL inhibition is not yet standard add-on therapy in routine practice. It’s better viewed as a potentially foundational future therapy whose role is still being defined.

HCPLive: Several pipeline agents target both APRIL and BAFF simultaneously. How do you assess the rationale for dual blockade compared with the more selective approaches already approved?

Lerma: Dual APRIL-BAFF blockade is mechanistically appealing, but it also represents a more aggressive immunosuppressive strategy. Some would argue that selective APRIL inhibition may ultimately fit better within a precision nephrology framework unless dual blockade clearly demonstrates superior efficacy.

The rationale behind dual inhibition is broader suppression of the pathogenic B-cell axis. BAFF inhibition suppresses B-cell survival, while APRIL inhibition reduces plasma cell differentiation and IgA production. In theory, this could produce greater reductions in pathogenic IgA.

However, there are trade-offs. BAFF plays an important role in long-term B-cell homeostasis, so suppressing it may increase infection risk, contribute to hypogammaglobulinemia, or blunt vaccine responses.

Because of that, some clinicians favor APRIL-only inhibition, which may more selectively target pathogenic IgA production while preserving broader immune competence. That creates a potentially cleaner safety profile in patients with CKD.

Right now, the jury is still out, and many practicing clinicians are closely watching how those risk-benefit questions evolve.

HCPLive: Proteinuria as a surrogate endpoint continues to generate debate in IgAN drug development. What are your thoughts on that discussion?

Lerma: Proteinuria remains the central methodological tension in IgAN drug development. For FDA approval, the earliest signal therapies can realistically demonstrate is proteinuria reduction, which is why so many trials use it as a surrogate endpoint.

The challenge is that reducing proteinuria does not automatically prove preservation of long-term kidney outcomes. What clinicians ultimately want to see is stabilization of eGFR over time.

The difficulty is that meaningful eGFR preservation takes years to demonstrate. You may not see those differences within 6 months or even the first year of treatment. Sometimes even 2 years may still be too short.

Ultimately, the field will likely judge these therapies based on whether they meaningfully preserve kidney function long term.

HCPLive: As the treatment landscape expands, what is the most important shift in how clinicians should communicate prognosis to patients?

Lerma: This is probably where practice is changing the most. The older model was largely passive monitoring of kidney function over time. The newer model is much more evidence-driven and trajectory-based.

Risk is no longer viewed as binary. Instead, clinicians are increasingly focusing on proteinuria trajectory, eGFR slope, histologic risk—including MEST-C scoring—and response to therapy within the first 6 to 12 months.

Treatment response itself is now becoming part of prognosis. We know CKD progression is modifiable, even if the disease is not universally curable. The goal is increasingly about altering the slope of progression rather than promising cure.

At the same time, clinicians need to communicate uncertainty carefully. We should avoid overpromising kidney preservation based solely on surrogate endpoints while also acknowledging that individual responses can vary considerably.

Compared with several years ago, our understanding of IgAN pathogenesis has improved substantially, particularly with the development of the 4-hit hypothesis framework. There is still uncertainty, but it is narrower than it once was.

HCPLive: Is there anything else you’d like to highlight?

Lerma: I think the key point is that we are now in a mechanism-first era of IgAN, but not yet in a sequencing-consensus era. Uptake of therapies is being shaped not only by efficacy, but also by system-level barriers, monitoring requirements, and lingering skepticism around surrogate endpoints.

APRIL inhibition may ultimately become a foundational upstream therapy rather than simply an add-on option, while dual APRIL-BAFF blockade raises important questions about balancing broader efficacy with potential safety risks.

Proteinuria remains a necessary—but insufficient—surrogate for long-term renal survival. And importantly, communication with patients is shifting toward dynamic, response-based risk modeling rather than static CKD staging alone.

Articles

IgA nephropathy management is shifting from predominantly supportive care and nonspecific immunosuppression to mechanism-guided intervention across the pathogenic cascade. Current practice remains stepwise, anchored by optimized RAS blockade, SGLT2 inhibition, blood pressure control, and proteinuria targets, with targeted agents introduced for persistent proteinuria, eGFR decline, or high-risk histology. Adoption of newer therapies remains low due to REMS/monitoring burden, payer friction, and skepticism about proteinuria-based approvals. APRIL inhibition is positioned as an upstream, potentially foundational strategy, while dual APRIL-BAFF blockade raises safety trade-offs.

 An expert describes his perspective on sequencing, APRIL inhibition, proteinuria endpoints, and long-term kidney preservation in IgA nephropathy.



APRIL Inhibition, Dual Blockade, and Proteinuria Endpoints in IgAN, With Edward Lerma, MD

is rapidly transitioning into what clinicians described as a “mechanism-first era,” as emerging targeted therapies reshape how nephrologists approach diagnosis, risk stratification, and long-term disease management.

To commemorate IgAN Awareness Day on May 14, 2026, 

 spoke with nephrologists about key evolving concepts in IgAN, including earlier diagnosis, dynamic treatment sequencing, and unresolved questions around biomarkers and remission.

Corey Cavanaugh, DO — Cleveland Clinic nephrologist

Abdallah Geara, MD — Associate Professor of Clinical Medicine, University of Pennsylvania

Edgar Lerma, MD — Clinical Professor of Medicine, University of Illinois Chicago

“We now are in what we call a mechanism-first era,” said Edgar Lerma, MD. “We’re not in a sequencing-consensus era anymore in IgAN.”

Earlier Diagnosis Remains a Major Missed Opportunity

Despite therapeutic advances, clinicians emphasized that earlier recognition of IgAN remains one of the most important unmet needs in practice.

“The early diagnosis is, I think, the most critical,” said Corey Cavanaugh, DO. “That does not necessarily involve a new drug. It doesn’t even involve necessarily a new lab test.”

Instead, clinicians pointed to missed opportunities in routine care, particularly among younger patients presenting with microscopic hematuria, hypertension, or subtle urinary abnormalities.

“We know that 75% of patients with IgA nephropathy, when they’re biopsied, already have established CKD stage 3,” Geara said. “So early diagnosis is something we still need to work on.”

Experts also highlighted the lack of standardized screening approaches, including limited use of urinalysis in routine preventive care.

“If we can get sooner access and just basic things like urinalysis, blood pressure checks, creatinine checks in young people, we can identify a lot of this very early,” Cavanaugh added.

Risk Stratification Becomes More Dynamic and Prognostic

Clinicians described a shift away from static staging toward trajectory-based risk assessment incorporating proteinuria, eGFR slope, histology, and treatment response.

“The old model is that you have IgAN and will monitor kidney function over time,” Lerma said. “The new model is what we call an evidence-driven stratification era.”

He added that treatment response itself is now increasingly prognostic.

“How the patient responds to therapy within 12 months is becoming part of their prognosis,” Lerma said.

Proteinuria remains a central marker in clinical decision-making, despite limitations.

“The most powerful prognostic clinical indicator is proteinuria,” Cavanaugh said. “Unfortunately, it’s not a true biomarker in the sense that it tells us exactly what IgA is doing.”

A key challenge, clinicians added, is disease heterogeneity.

Expanding Treatment Options Complicate Sequencing Decisions

The IgAN treatment landscape now includes RAAS blockade, SGLT2 inhibitors, endothelin receptor antagonists, corticosteroids, targeted-release budesonide, complement inhibitors, and APRIL-directed therapies.

“The cornerstone remains ACE or ARB RAAS inhibition,” Cavanaugh said. “But endothelin receptor antagonists are the new nephron-sparing therapy that is not immunosuppression.”

He noted these agents can reduce proteinuria by approximately 50%, describing this as clinically meaningful for long-term prognosis.

Still, clinicians acknowledged there is no consensus on sequencing.

“The major question is who gets what and when,” Cavanaugh said.

“My core belief right now is nobody knows the right answer,” another clinician added. “The tools we have are inadequate to tell us exactly what to choose and when.”

Most clinicians, experts said, are still using a stepwise escalation approach rather than combination “stacking” of therapies.

Despite rapid innovation, adoption of newer therapies has been slower than expected.

Lerma outlined “five buckets” driving delayed uptake: regulatory burden, skepticism about surrogate endpoints like proteinuria, infrastructure challenges, disease heterogeneity, and physician familiarity.

“Most clinicians view reduction in proteinuria as positive,” Lerma said. “But whether it translates to preventing end-stage kidney disease still has some gray area.”

Additional barriers include prior authorization requirements, REMS programs, and monitoring demands.

“Adoption usually lags evidence by around 3 to 7 years in chronic kidney disease,” Lerma said.

APRIL Inhibition and the Future of Precision Nephrology

APRIL-targeted therapies are among the most closely watched emerging treatments, designed to reduce production of galactose-deficient IgA1 earlier in the disease pathway.

“These agents target upstream B-cell activation and reduce production of galactose-deficient IgA1,” Cavanaugh said.

Lerma added that APRIL inhibition may ultimately become a foundational therapy.

“In this moment, 2026, APRIL inhibition is not an add-on yet in standard practice, but it is a future backbone candidate,” he said.

Questions remain around dual APRIL–BAFF blockade and whether broader immunologic suppression improves outcomes or increases risk.

Despite therapeutic progress, clinicians emphasized that IgAN still lacks validated biomarkers for remission or precise response prediction.

“There’s still no definition of remission that we all agree on,” Cavanaugh said.

He added that improved therapies may ultimately force the field to define these endpoints more clearly.

“That’s the beauty of these therapies,” he said. “They force the issue of defining remission because we can actually achieve it.”

While IgAN remains incurable, clinicians expressed cautious optimism.

“There’s no cure,” Cavanaugh said. “But maybe we’re approaching that.”

Editor’s Note: Cavanaugh reports relevant disclosures with Otsuka Pharmaceutical Co, Novartis Pharmaceutical Corporation, Travere Therapeutics, and Vera Therapeutics. Abdallah reports relevant disclosures with Amgen, GlaxoSmithKline, Novartis, and others. Lerma reports disclosures with Amgen, Astra Zeneca, Calliditas, Novo Nordisk, Travere, Opko, and Otsuka

Cavanaugh C. Routine urinalysis in IgA nephropathy and young adults. 

 https://www.hcplive.com/view/routine-urinalysis-iga-nephropathy-young-adults-corey-cavanaugh

Geara A. Stratifying risk and optimizing therapy in IgA nephropathy. 

 https://www.hcplive.com/view/stratifying-risk-optimizing-therapy-iga-nephropathy-abdallah-geara-md

IgA nephropathy management is shifting to a mechanism-first paradigm as pathway-targeted agents expand beyond supportive care. Earlier recognition through urinalysis, blood pressure, and creatinine screening—particularly in young adults with microscopic hematuria—remains a major gap, with many first biopsied at CKD stage 3. Risk assessment is moving from static staging to trajectory-based prognostication using proteinuria, eGFR slope, histology, and 12‑month treatment response. Sequencing is unsettled amid more options and delayed adoption driven by regulatory, endpoint, infrastructure, and familiarity barriers. APRIL inhibition is a leading future backbone candidate.

On IgAN Awareness Day, clinicians highlight earlier diagnosis, dynamic risk stratification, and emerging targeted therapies reshaping care.

IgAN Enters “Mechanism-First Era” Reframing Diagnosis, Treatment, and Remission

Despite being the most common primary glomerulonephritis worldwide, 

 and end-stage kidney disease. Despite advances in understanding its pathophysiology, treatment options have historically been limited to supportive care, including renin-angiotensin system inhibitors, blood pressure control, and corticosteroids for high-risk patients.

Recently, a growing understanding of the immunopathogenesis of IgAN has led to the emergence of novel therapeutic strategies, including the inhibition of A proliferation-inducing ligand (APRIL), a key driver of IgA production. By reducing pathogenic IgA1 production at its source, APRIL inhibition has the potential to alter the course of the disease. Accordingly, several anti-APRIL drug candidates, including sibeprenlimab, atacicept, telitacicept, and zigakibart, are in clinical development for IgAN.

For more on APRIL inhibition and the current IgAN treatment landscape, the editorial team of 

 spoke with Edgar Lerma, MD, a clinical associate professor of medicine in the section of nephrology at the University of Illinois at Chicago.

: Can you provide an overview of the current treatment landscape for IgA nephropathy and what unmet needs exist for patients?

: One of the things that's interesting [about IgAN] is that this is considered a rare kidney disease, but it is the most common primary glomerulonephritis worldwide. In fact, there's an annual global incidence of 2.5 cases per 100,000 persons.

The disease manifests in several ways. Patients can present with asymptomatic hematuria, which means blood in the urine, or proteinuria, and that is protein in the urine, or they can present with advanced stages of kidney disease.

If you think about it, any patient who is diagnosed with what is called a rare kidney disease, it's a little bit disconcerting, right? So there's uncertainty about it, and this obviously impacts the patient's physical, mental, and emotional health. A lot of patients become anxious, and this can affect their daily activities, as well as even their daily work lives.

One of the things that's important about IgA nephropathy is that when patients are diagnosed, usually they are between 20 and 40 years of age. That's a very young population, right? So if these patients are 20 to 40 years of age, if you think about them and you think they eventually progress to kidney failure or what we call end-stage kidney disease, that means requirement of dialysis or kidney transplantation, this happens in their lifetimes.

So if they get to that point of reaching kidney failure, it's really a lifestyle change. They have to adjust to this new condition in their lives and it affects not only their personal lives, but also the lives of their families and their relatives.

: What challenges exist for developing effective pharmacologic therapies for IgA nephropathy?

: Let me put this in perspective. For many years, for many decades, whenever we diagnosed a patient with IgA nephropathy, and by the way, the only way to diagnose a patient with IgAN is through a kidney biopsy. Whenever a patient is diagnosed with IgAN, we explain to them that this is how the disease happens, this is what to expect, and so on and so forth.

For many years, the only thing we had to offer patients was treatment and medications to manage their symptoms and maybe slow down the progression of the kidney disease.

For blood pressure control, we use certain antihypertensive agents called renin-angiotensin system blockers. And of course, along with that, it's lifestyle – dietary salt restriction, aerobic exercise on most days, weight loss if necessary, cessation of smoking, so on and so forth.

And then the only other treatment that we offer is, whenever they don't respond to the ones I mentioned earlier, the next step would be to consider immunosuppressive therapies.However, the therapies that we had available back then had significant side effects and long-term toxicity.

So when you mention novel agents, over the past few years, we have had a deluge of novel therapeutic agents for IgAN. We now have a better understanding of the pathophysiology of how it can develop, and by understanding this mechanism, several phase 2 and phase 3 clinical trials have been published and have influenced the way we manage the disease. There are now different options for treatment that target the different pathophysiologic steps that lead to eventual kidney failure.

: There has recently been an increased focus on targeting APRIL. Can you tell me a little bit about that?

: So when we say APRIL, it stands for A proliferation-inducing ligand. This is actually a cytokine in the tumor necrosis factor family, and APRIL is integral to the development and progression of IgAN.

When we say cytokine, it is a substance secreted by certain cells of the immune system, and these cytokines have an effect on the other cells.

APRIL actually promotes the survival and the class switch, switching up B cells to produce IgA, particularly what we call the pathogenic galactose deficient IgA1. The abbreviation is Gd-IgA1, which actually forms immune complexes in the kidneys.

So these complexes are deposited in the glomeruli, which later on triggers inflammation, and as you trigger this inflammation, it leads to kidney damage. One way of thinking about this is you think of APRIL as a toggle within the immune system. So if you think of an electrical grid, APRIL powers specific circuits, and when you activate it, you turn it on, it helps promote the production of these pathogenic Gd-IgA1 and immune complexes formation and this leads to kidney damage and injury.

If you target APRIL, you turn it off, it is like pushing the toggle, turning it off and then this reduces the production of those harmful molecules that I mentioned. If you reduce the production of those molecules, then you prevent that damage and the injury that follows.

So, targeting APRIL represents a potential therapeutic strategy that disrupts this pathogenic sequence. If you inhibit APRIL, you can decrease the production of those harmful molecules, those Gd-IgA1, and eventual immune complex formation deposition into the kidneys, which eventually leads to end-stage kidney disease and the need for dialysis or transplantation.

: There are some promising agents in clinical development progressing through phase 2 and phase 3 trials. Is there anything that you think holds the most therapeutic potential for improving IgAN care?

: Right now we are actually looking at the guidelines for sort of directing how these agents will be used in the future, so it's exciting for us as nephrologists because now we have so many options. Before, we only had symptom management and blood pressure control.

For more information about IgAN and the role of APRIL, there's actually a website, 

, that has a lot of new insights and news about IgAN.

Editors’ note: Lerma has relevant disclosures with Travere Therapeutics, Akebia/Otsuka, Astra Zeneca, Bayer, Glaxo Smith Kline, Otsuka, Vifor, and Bayer.

Mathur M, Chan TM, Oh KH, et al. A PRoliferation-Inducing Ligand (APRIL) in the Pathogenesis of Immunoglobulin A Nephropathy: A Review of the Evidence. 

IgA nephropathy (IgAN) is a prevalent primary glomerulonephritis and a significant cause of chronic and end-stage kidney disease. Traditional treatments have been limited to supportive care, but recent insights into IgAN's immunopathogenesis have led to novel therapies targeting APRIL, a cytokine involved in IgA production. Inhibiting APRIL could alter disease progression by reducing pathogenic IgA1 production. Several anti-APRIL drugs, such as sibeprenlimab and atacicept, are in clinical trials, offering hope for improved management of IgAN and addressing unmet therapeutic needs.

Lerma discusses the current treatment landscape for IgA nephropathy and what role APRIL inhibition may play in treating IgAN.

The Therapeutic Potential of APRIL Inhibition in IgAN, with Edgar Lerma, MD

Exploring the Cardiovascular Benefits, Potential of Finerenone

Management of chronic kidney disease among patients with type 2 diabetes has undergone significant change in the last decade. Once handcuffed by a lack of safe and efficacious options, changing standards of care coming as the result of pharmacotherapeutic advancement have ushered in a new era of management for this patient population.

This change has been spearheaded by 2 particular classes—a familiar face in the form of SGLT2 inhibitors and the novel nonsteroidal mineralocorticoid receptor antagonist (nsMRA) finerenone (Kerendia), which received approval in July 2021 for reducing the risk of sustained eGFR decline, kidney failure, cardiovascular death, non-fatal myocardial infarction, and hospitalization for heart failure in adult patients with chronic kidney disease associated with type 2 diabetes.

Finerenone first captivated the attention of nephrologists, endocrinologists, and other providers managing patients with type 2 diabetes with the release of data from the FIDELIO-DKD and FIGARO-DKD trials. The number of specialists captivated by the agent and its potential benefit grew with the release of data surrounding the cardiovascular benefits among patients with heart failure observed within the FINEARTS-HF trial at the European Society of Cardiology Congress 2024.

In this segment, which is part 5 of a 5-part series, discussants Edgar Lerma, MD, a nephrologist, and Anuradha Lala-Trindade, MD, a cardiologist, dive into the cardiovascular benefits highlighted in the FINEARTS-HF trial with finerenone, specifically its impact on heart failure with preserved ejection fraction (HFpEF). Lala-Trindade elaborates on the historical challenges of treating HFpEF, noting that earlier trials with steroidal MRAs like spironolactone showed mixed results. However, finerenone demonstrated a significant reduction in cardiovascular death and heart failure hospitalizations, marking a substantial advancement for both heart and kidney health in HFpEF patients.

They discuss the paradigm shift in treatment approaches—favoring simultaneous, low-dose initiation of all four heart failure “pillars” rather than sequential dosing. Lala-Trindade points to finerenone’s unique, manageable side-effect profile, particularly its lower risk of hyperkalemia, as promising for broader applicability. They conclude with a look at the practical questions surrounding accessibility and cost, noting the need for more data on the value finerenone may add compared to traditional MRAs.

 a clinical professor of Medicine in the Section of Nephrology at the University of Illinois at Chicago and a nephrologist with Associates In Nephrology based in Chicago.

 the director of Heart Failure Research, program director of the Advanced Heart Failure and Transplant Fellowship, and associate professor of Medicine at The Mount Sinai Fuster Heart Hospital & Department of Population Health Science and Policy.

Relevant disclosures for Lerma include Akebia, Astra Zeneca, Bayer, Boehringer Ingelheim, Glaxo Smith Kline, Otsuka, Travere, Vifor, and Fresenius. Relevant disclosures for Lala-Trindade include Merck, AstraZeneca, Cytokinetics, and Novartis.

Campbell P. Finerenone (Kerendia) approved for chronic kidney disease associated with type 2 diabetes. HCP Live. July 9, 2021. Accessed October 23, 2024. https://www.hcplive.com/view/finerenone-kerendia-approved-chronic-kidney-disease-associated-with-type-2-diabetes.

Campbell P. FDA updates Finerenone label to reflect Cardiovascular Outcomes Data. HCP Live. September 8, 2022. Accessed October 23, 2024. https://www.hcplive.com/view/fda-updates-finerenone-label-to-reflect-cardiovascular-outcomes-data.

Solomon SD, McMurray JJV, Vaduganathan M, et al. Finerenone in Heart Failure with Mildly Reduced or Preserved Ejection Fraction. 

. Published online September 1, 2024. doi:10.1056/NEJMoa2407107

Videos

In the final part of this 5-part series, Lala-Trindade discusses the findings of the FINEARTS-HF trial and how it might inform use of finerenone. 