Lebrikizumab led to significant itch reduction, with over 41% of patients achieving a 4-point Worst Itch Scale improvement.

More than 60% of lebrikizumab-treated patients saw clinically meaningful quality-of-life improvements.

Skin infections were less common with lebrikizumab than placebo, with no discontinuations due to adverse events.

In newly-released phase 3 findings, lebrikizumab therapy produced meaningful improvements in itch, quality of life, and overall disease burden among children and adolescents with 

These efficacy and safety findings were released from the ADorable-1 trial and presented at the Society of Pediatric Dermatology conference. Lawrence Eichenfield, MD, of the University of California San Diego and Rady Children's Hospital, served as an investigator on the study.

 interview, Eichenfield reported that itch outcomes varied by age group, with younger children assessed via the Worst Scratch/Itch Scale and older children evaluated using a 4-point improvement threshold.

What the ADorable-1 Trial Means for Pediatric Atopic Dermatitis Eczema Care

What the ADorable-1 Trial Means for Pediatric Eczema Care

How Much Did Lebrikizumab Improve Itch and Quality of Life?

Approximately 35% of lebrikizumab-treated patients achieved a 4-point drop in itch severity compared with 5% of those on placebo. The separation was even more pronounced on the Worst Itch Scale, where 41.6% of patients receiving lebrikizumab achieved a 4-point improvement, compared with no placebo-treated patients.

Quality-of-life measures also favored the active treatment arm. Eichenfield noted that a 6-point reduction from baseline is generally considered clinically meaningful; 61.6% of lebrikizumab-treated patients met that threshold, compared with 36% of the placebo group.

Is Lebrikizumab Safe for Children With Atopic Dermatitis?

Eichenfield described overall adverse event rates as not markedly different between arms, with no deaths and few serious adverse events reported. No patients discontinued treatment due to adverse effects, he noted. Skin infections occurred less frequently with lebrikizumab plus topical corticosteroids (2.4%) than with placebo plus topical corticosteroids (8.5%).

This was a finding Eichenfield attributed to the anti-inflammatory effect of IL-13 blockade on the skin microbiome. Conjunctivitis rates were described as 7.3% with lebrikizumab and 5.1% with placebo, and no cases of keratitis were observed.

What Unmet Needs Remain in Pediatric Atopic Dermatitis?

Looking ahead, Eichenfield emphasized unmet needs in young patients with moderate-to-severe atopic dermatitis, including questions about optimal biologic selection, treatment duration, and whether early intervention can modify long-term disease course.

He expressed particular interest in whether IL-13 blockade might also reduce the development of atopic comorbidities over time, an area he said warrants further long-term investigation.

Disclosures: Eichenfield previously reported receiving personal fees from Pfizer Inc; grant funding from AbbVie, Arcutis Biotherapeutics, Bausch + Lomb, Castle Biosciences, Dermavant Sciences Inc, Galderma SA, Pfizer Inc, Regeneron, and Sanofi SA and consulting for ASLAN Pharmaceuticals, AbbVie, Almirall, SA, Arcutis Biotherapeutics, Arena Pharmaceuticals Inc, Dermavant Sciences Inc, Galderma SA, Incyte Corporation, LEO Pharma A/S, Eli Lilly and Company, Ortho Dermatologics, Pfizer Inc, Regeneron Pharmaceuticals Inc, Sanofi SA, and UCB; and serving on the board of directors of Forté Pharma.

Eichenfield LF, Ornelas J, Prajapati VH, et al. Lebrikizumab for pediatric patients aged ≥6 months with moderate-to-severe atopic dermatitis: Phase 3 ADorable-1 Week 16 results. Poster presented at: Society for Pediatric Dermatology Annual Meeting; July 22-25, 2026; Minneapolis, MN.

Paller A. Significance of ADorable-1 Data on Lebrikizumab in Children with Atopic Dermatitis, With Amy Paller, MD. HCPLive. March 17, 2026. Accessed July 30, 2026. 

https://www.hcplive.com/view/significance-adorable-1-data-lebrikizumab-children-atopic-dermatitis-with-amy-paller-md

Videos

Lebrikizumab improved itch, quality of life, and infection rates in kids with moderate-to-severe atopic dermatitis, ADorable-1 results suggest.

ADorable-1 met key efficacy endpoints in pediatric moderate-to-severe atopic dermatitis.

Lebrikizumab demonstrated higher skin clearance rates than placebo plus topical corticosteroids.

The findings expand evidence supporting IL-13 inhibition in children with atopic dermatitis.

The growing armamentarium of treatments for 

 continues to generate new data available for clinicians managing moderate-to-severe cases of this 

 at the Society for Pediatric Dermatology (SPD) Annual Meeting, Lawrence Eichenfield, MD, discussed findings from the phase 3 ADorable-1 trial evaluating lebrikizumab in patients aged 6 months to younger than 18 years.

 He highlighted both the study's design and the efficacy outcomes, emphasizing the potential role of the therapy in younger patient populations.

ADorable-1 phase 3 study results: Key findings in pediatric atopic dermatitis for children with eczema

ADorable-1 Results: Key Findings in Pediatric Atopic Dermatitis

“Their initial approval was 12 years of age and older and [for] context, we know right now the only approved systemic biologic agent for atopic dermatitis under 12 is to is dupilumab,” Eichenfield explained.

New Phase 3 Data Highlight Pediatric Efficacy of Lebrikizumab

Eichenfield noted that the pediatric study builds on previous work evaluating lebrikizumab in adolescents, where the therapy was initially approved for patients aged 12 years and older. The ADorable-1 trial expanded the evaluation to include infants, children, and adolescents, enrolling patients from 6 months through 17 years of age.

Participants were divided into age-based cohorts, with one including children aged 6 months to younger than 2 years and another spanning older pediatric patients through adolescence.

According to Eichenfield, ADorable-1 was conducted as a randomized, placebo-controlled trial in which all participants received background topical corticosteroid therapy. He described this design as reflecting ethical considerations in pediatric research, ensuring that children in the placebo group still received active topical medications rather than remaining untreated.

Following a two-week run-in period with topical corticosteroids, participants were randomized to receive weight-based lebrikizumab plus topical corticosteroids or placebo plus topical corticosteroids for 16 weeks. Patients who achieved clear skin were permitted to taper topical corticosteroid use and transition to moisturizers alone.

Eichenfield emphasized that the trial enrolled a population with substantial atopic dermatitis burden. Approximately one-quarter of participants had severe disease at baseline, while the remainder met criteria for moderate disease.

Patients also presented with a mean Eczema Area and Severity Index (EASI) score of approximately 28 and nearly half of their body surface area affected, underscoring the severity of disease within the study population.

Lebrikizumab Results in Atopic Dermatitis at Week 16

By the 16-week mark, the study demonstrated clinically meaningful improvements across multiple efficacy endpoints. Among patients receiving lebrikizumab, 43.5% attained clear or almost clear skin compared with 15.0% of those receiving placebo plus topical corticosteroids. Similarly, 62.6% achieved EASI-75 versus 21.6% in the placebo arm of the trial.

Eichenfield also highlighted higher-threshold responses, including EASI-90 in 38.6% of treated patients and complete skin clearance (EASI-100) in 13.7%, describing the separation between treatment groups as encouraging for clinicians caring for pediatric patients with moderate-to-severe atopic dermatitis.

New phase 3 ADorable-1 data show lebrikizumab improved skin clearance in children with moderate-to-severe atopic dermatitis.

Michelle Kittleson, MD, PhD | Image Credit: American College of Cardiology

The American College of Cardiology (ACC) has published an updated 2026 Expert Consensus Decision Pathway (ECDP) for the management of 

heart failure with preserved ejection fraction (HFpEF)

The document, chaired by Michelle M. Kittleson, MD, PhD, reframes HFpEF as a multisystem syndrome driven by visceral adiposity, inflammatory adipokines, and metabolic dysfunction rather than a single cardiac condition. The update incorporates new trial data on sodium-glucose cotransporter 2 (SGLT2) inhibitors, nonsteroidal mineralocorticoid receptor antagonists (MRAs), and incretin-based therapies.

What does the 2026 ACC ECDP recommend as foundational pharmacotherapy for HFpEF?

An SGLT2 inhibitor plus a nonsteroidal MRA, with finerenone favored over spironolactone, unless contraindicated.

Which patients with HFpEF should receive incretin-based therapy?

Patients with a body mass index of 30 kg/m² or higher, per STEP-HFpEF and SUMMIT trial data.

How does the updated pathway approach HFpEF diagnosis?

It recommends sequential use of the H2FPEF and HFA-PEFF scoring systems, systematic exclusion of noncardiac and cardiac mimics, and attention to sex-specific presentation differences.

The revision responds to a rapidly evolving therapeutic landscape since 2023, when finerenone, semaglutide, and tirzepatide lacked HFpEF-specific outcomes data. According to the ACC, these agents now offer benefits extending beyond heart failure to broader cardiovascular, kidney, and metabolic health. The writing committee positions accurate diagnosis as a prerequisite for guideline-based therapy, given persistent underrecognition of HFpEF in practice.

The ECDP outlines three validated scoring systems for establishing diagnostic probability in patients presenting with dyspnea or edema: H2FPEF, HFA-PEFF, and HFpEF-ABA. The writing committee recommends H2FPEF as an initial screening tool followed by HFA-PEFF for confirmation, noting that discordance between the two can prompt further advanced testing. Each carries distinct tradeoffs: H2FPEF offers greater accuracy with fewer input variables and higher sensitivity, while HFA-PEFF is more specific but often requires diastolic stress testing or invasive hemodynamics rarely feasible in routine practice.

Beyond scoring, the pathway calls for systematic exclusion of noncardiac mimics, including pulmonary disease, kidney disease, high-output states, obesity, and frailty, along with cardiac mimics such as valvular disease, pericardial constriction, infiltrative cardiomyopathies, and ischemic heart disease, before confirming HFpEF as a diagnosis of exclusion. The document also details sex-specific differences in presentation. Women with HFpEF show lower natriuretic peptide levels, greater concentric left ventricular remodeling, and worse symptom burden compared with men.

Optimal medical therapy and comorbidity management in HFpEF

For pharmacotherapy, the ECDP designates an SGLT2 inhibitor plus a nonsteroidal MRA as foundational treatment for most patients, unless contraindicated, based on evidence from DELIVER, EMPEROR-Preserved, and FINEARTS-HF. Finerenone, which received US Food and Drug Administration approval in July 2025 for patients with left ventricular ejection fraction of 40% or higher, is now favored over spironolactone as the mineralocorticoid antagonist of choice, given its improved hyperkalemia profile. For patients with a body mass index of 30 kg/m² or higher, the pathway recommends incretin-based therapy with semaglutide or tirzepatide, citing STEP-HFpEF and SUMMIT.

Sacubitril-valsartan is positioned as a reasonable option in women and patients with an ejection fraction below 55% to 60%, based on subgroup findings from PARAGON-HF, while angiotensin receptor blockers serve as an alternative when angiotensin receptor-neprilysin inhibitors are unavailable or contraindicated. The committee advises against routine beta-blocker use absent angina or atrial fibrillation rate control, citing risk of chronotropic incompetence. Comorbidity management extends to coronary artery disease, atrial fibrillation, hypertension, chronic kidney disease, diabetes, and obesity, with a systolic blood pressure target of 120 to 129 mm Hg identified as optimal for HFpEF.

“In the interim, this ECDP addresses contemporary management of HFpEF,” Kittleson and colleagues wrote. The authors add the pathway provides structure for clinical decision-making as pharmacologic and nonpharmacologic evidence continues to accumulate.

The ECDP notes several device-based interventions, including atrial shunt devices, splanchnic nerve ablation, and permanent pacing, have not shown consistent benefit and remain under evaluation. The document operates within the framework of the 2022 AHA/ACC/HFSA heart failure guideline while incorporating trial evidence unavailable at that guideline's publication.

Kittleson MM, Panjrath GS, Bates K, et al. Management of heart failure with preserved ejection fraction: 2026 ACC expert consensus decision pathway: a report of the American College of Cardiology Solution Set Oversight Committee. J Am Coll Cardiol. Published online July 23, 2026. 

American College of Cardiology. Updated ACC expert consensus decision pathway addresses management of HFpEF. Published July 23, 2026. Accessed July 30, 2026. 

https://www.acc.org/latest-in-cardiology/journal-scans/2026/07/22/17/25/updated-acc-ecdp-addresses-management-of-hfpef

Articles

ACC’s 2026 HFpEF pathway recasts the condition as a multisystem, adiposity- and metabolism-driven syndrome and emphasizes rigorous diagnostic confirmation before therapy. It recommends staged use of H2FPEF then HFA-PEFF scoring, with advanced testing for discordance and systematic exclusion of cardiac and noncardiac mimics; sex-specific phenotypes are highlighted. Foundational pharmacotherapy is SGLT2 inhibition plus nonsteroidal MRA, favoring finerenone, with incretin-based agents for obesity. ARNI is selective; routine beta-blockade is discouraged; comorbidity targets include SBP 120–129 mm Hg. Several device strategies lack consistent benefit and remain investigational.

The ACC's new decision pathway incorporates SGLT2 inhibitor finerenone and data on incretin therapy into HFpEF diagnosis and management guidance.

ACC Updates Expert Consensus Pathway for HFpEF Management

A phase 3, randomized, double-blind, placebo-controlled trial found the sublingual mucosal vaccine MV130 significantly reduced the number of moderate and severe exacerbations in patients with frequent-exacerbator 

 (COPD) over an 18-month study period, according to results published in the 

Respiratory infections remain the primary trigger of COPD exacerbations, yet no approved vaccine directly targets the pathogens responsible, leaving prevention strategies limited beyond standard maintenance therapy.

 MV130 is formulated from heat-inactivated whole-cell bacteria administered sublingually, designed to induce trained immunity, a nonspecific innate immune memory offering broad-spectrum protection beyond its bacterial antigens.

 The trial enrolled patients with a frequent-exacerbator phenotype already receiving maintenance COPD therapy, a population with limited additional preventive options.

Luis Puente Maestú, MD, PhD, Chief of the Pneumology Department at the University Hospital General Gregorio Marañón, Madrid, and colleagues wrote that “As a trained immunity-based vaccine, MV130 induces long-lasting, nonspecific immunity to subsequent microbial challenges via epigenetic reprogramming of innate immune cells, thereby conferring broad-spectrum protection beyond its constituent antigens.”

Is MV130 Efficacious in Reducing COPD Exacerbations?

The phase 3, multicenter trial randomized 198 patients across 7 hospitals in Spain 1:1 to daily sublingual MV130 (300 FTU) or placebo for 12 months, followed by 6 months of observation (NCT01842360).

 Eligible patients had 3 or more moderate exacerbations, or 2 or more with at least 1 requiring hospitalization, in the prior year.

 The primary outcome was the total number of exacerbations over the full 18-month period, assessed in both intention-to-treat (ITT, n=198) and per-protocol (PP, n = 142) populations.

In the ITT population, MV130 reduced the median number of exacerbations to 2.0 (IQR, 1.0-3.0) versus 3.0 (IQR, 1.0-5.0) with placebo (

 =.001), with 216 total exacerbations recorded in the MV130 group versus 363 with placebo.

 The exacerbation rate was 1.87 events per patient-year with MV130 versus 2.68 with placebo, a difference of 0.81 events (95% CI, 0.44-1.18; 

 By severity, MV130 reduced moderate exacerbations (IRR, 0.70; 95% CI, 0.57-0.86) and severe exacerbations (IRR, 0.51; 95% CI, 0.34-0.76), with no significant effect on mild exacerbations (IRR, 1.10; 95% CI, 0.67-1.81).

MV130, a sublingual mucosal trained immunity-based vaccine, is being studied as an adjunct preventive therapy to reduce moderate and severe exacerbations in patients with frequent-exacerbator COPD; it is not an approved product.

MV130 contains heat-inactivated whole-cell bacteria administered sublingually, designed to induce trained immunity, a form of innate immune memory conferring broad, nonspecific protection against respiratory pathogens beyond its own bacterial antigens.

What did the phase 3 MV130 COPD trial show?

MV130 significantly reduced total, moderate, and severe COPD exacerbations versus placebo over 18 months and was associated with reduced hospitalizations, antibiotic use, and improved 12-month quality-of-life scores, with an adverse event rate similar to placebo.

How Could MV130 Affect Healthcare Use and Quality of Life?

Time to first exacerbation did not differ significantly between groups over the full 18-month study period (HR, 1.26; 95% CI, 0.92-1.72; P=.14).

 When the analysis was restricted to the 6-month post-treatment follow-up period alone, time to first exacerbation was significantly delayed with MV130 (HR, 2.15; 95% CI, 1.37-3.36; 

 = .001), a pattern the study authors attributed to a time-dependent treatment effect.

 MV130 was also associated with reductions in antibiotic use (IRR, 0.62; 95% CI, 0.59-0.65), systemic corticosteroid use (IRR, 0.81; 95% CI, 0.73-0.90), hospitalizations (IRR, 0.60; 95% CI, 0.37-0.96), and emergency room visits (IRR, 0.48; 95% CI, 0.32-0.71).

COPD Assessment Test (CAT) scores differed by 2.2 points favoring MV130 at 12 months (95% CI, -4.3 to -0.14; 

 = .037), exceeding the established minimum clinically important difference, though the difference was not significant at 18 months (1.5 points; 95% CI, -3.8 to 0.7).

 A total of 229 adverse events occurred in 103 participants (52%), with similar rates between MV130 (50.4%) and placebo (49.6%) groups.

 Two nonserious adverse events, urticaria in the placebo group and pruritus in the MV130 group, were assessed as possibly related to study medication; 3 deaths occurred during the trial, none considered treatment-related.

The study authors noted a prior phase 2b trial of a targeted Haemophilus influenzae/Moraxella catarrhalis vaccine failed to reduce moderate or severe COPD exacerbations, contrasting with the broader trained-immunity mechanism reported for MV130.

 Because its mechanism differs from other recently studied COPD exacerbation therapies, including the interleukin-4/13 inhibitor dupilumab, the study authors suggested MV130 could offer a complementary approach alongside existing treatments.

Maestu LP, Rubio MC, Benedetti P, et al. Prevention of COPD exacerbations with a mucosal trained immunity-based vaccine (MV130): a randomised phase 3 trial. Eur Respir J. 2026; in press. doi:10.1183/13993003.00027-2026

Andreas S, Testa M, Boyer L, et al. Non-typeable Haemophilus influenzae-Moraxella catarrhalis vaccine for the prevention of exacerbations in chronic obstructive pulmonary disease: a multicentre, randomised, placebo-controlled, observer-blinded, proof-of-concept, phase 2b trial. Lancet Respir Med. 2022;10(5):435-446.

A multicenter phase 3 trial in frequent-exacerbator COPD showed that 12 months of daily sublingual MV130, a heat-inactivated whole-cell bacterial mucosal vaccine intended to induce trained immunity, reduced moderate and severe exacerbations over 18 months versus placebo. Exacerbation burden decreased despite no overall difference in time to first event, with signals of delayed first exacerbation during post-treatment follow-up. MV130 also lowered antibiotic and systemic corticosteroid use, hospitalizations, and emergency visits, with similar overall adverse-event rates between groups.

MV130, a sublingual mucosal trained immunity vaccine, showed significant benefits vs placebo, with benefit sustained after treatment ended.

MV130 Mucosal Vaccine Reduces COPD Exacerbations in Phase 3 Trial

 is among the most common and frequent acute aortic diseases, much regarding this lethal disease is unknown. Additionally, despite a relatively easy method of identification via screening and genetic testing, the majority of aortic dissections go unreported due to a lack of autopsy data in much of the US. For this reason, the majority of patients at risk for aortic dissection are unaware of the condition.

Aortic Dissection: A Fatal Condition With an Underrepresented Genetic Risk

In an interview with Benjamin van Boxtel, MD, the surgical director at Atlantic Aortic Center and a cardiac surgeon with the Atlantic Health System, the 

 editorial team discussed proper treatment and diagnosis of this devastating disease, particularly in the face of its little-known genetic roots.

“I have many, many patients in my practice who have a heritable aortic condition where they have an aortic dissection, or they have elective surgery to prevent an aortic dissection,” van Boxtel told 

 in an exclusive interview. “If you go through their family history, it’s, ‘well, you know, my dad died of heart problems early and never got an autopsy. My grandpa died of heart problems early and never got an autopsy.’ Well, those are probably uncounted aortic dissections.”

Aortic dissection is a process in which a tear in the inner lining of the aorta leads to the separation of the intima-medial aortic laminas from the adventitia. This directly leads to the formation of an additional aortic lumen within the existing lumen. An aortic dissection in the ascending aorta is known as Type A dissection, regardless of the involvement of the aortic arch and descending aorta. Dissections involving the aortic arch but not the ascending aorta are known as non-A non-B aortic dissection, while those involving only the descending aorta are a Type B dissection.

Invasive treatment generally involves the elimination of the most proximal communication between both lumens, which is typically the primary entry. Clinicians use 3 strategies to accomplish this, including resecting the respective aortic segment and replacing it with a prosthesis, thoracic endovascular aortic repair (TEVAR) and stent-graft implantation, and implanting a hybrid prosthesis.

According to the American Heart Association (AHA)/American College of Cardiology (ACC) guidelines for the treatment of aortic disease, the primary goals of any aortic dissection treatment are to prevent aortic rupture, retrograde extension of the dissection into the aortic root, and antegrade propagation of the dissection into yet undissected distal segments. To this end, the majority of treatment strategies are guided by the patient’s signs and symptoms, the presence of complications and the specific features of the aortic and branch vessel anatomy.

Additionally, the guidelines suggest that choice of initial imaging modality should be determined by the patient’s history and clinical presentation. CT scans have become the preferred modality, due to their capacity for diagnosing the underlying AAS as well as showing the full extent of the dissection. However, patients with a history of iodinated contrast reaction, for whom CT may not be preferred or possible, echocardiography is a common alternative, due to its high sensitivity and anatomic resolution.

“The thing to remember with aortic dissections is that they’re highly lethal,” van Boxtel said. “These should be thought of like a myocardial infarction or a stroke. There’s a golden hour for these patients. If you look at the risk of death from a dissection, it’s several percentage points per hour. It’s at least 1% per hour. So, the time matters.”

Editors’ Note: van Boxtel reports no relevant disclosures.

Rylski B, Schilling O, Czerny M. Acute aortic dissection: Evidence, uncertainties, and future therapies. European Heart Journal. 2022;44(10):813-821. 

Isselbacher EM, Preventza O, Hamilton Black J, et al. 2022 ACC/AHA guideline for the diagnosis and management of Aortic Disease: A Report of the American Heart Association/American College of Cardiology Joint Committee on Clinical Practice Guidelines. Circulation. 2022;146(24). 

Benjamin van Boxtel, MD, discusses the importance of familial screening for aortic dissection and the danger of missing potential risk factors.

a nephrologist and the Director of Acute Dialysis Services and the Polycystic Kidney Disease (PKD) Center of Excellence at UC San Diego Health and Chief Medical Officer of the American Kidney Fund

a nephrologist at Florida Kidney Physicians and Director of the FKP Glomerulonephritis Center of Excellence in Boca Raton, Florida.

an assistant Professor in the Division of Nephrology at the University of California, San Francisco (UCSF) and the medical director of the nephrology-based kidney stone prevention center at UCSF.

 care has entered a new era, but what does this mean for nephrologists managing patients today?

After decades with few disease-modifying options beyond blood pressure control and renin-angiotensin system blockade, clinicians now have multiple therapies targeting different pathways involved in kidney disease progression. The challenge in 2026 is no longer simply whether effective treatments exist, but how best to identify patients who need them and implement them in practice.

“I think a lot of nephrologists have been sort of swayed to sleep by 20 to 25 years of really no groundbreaking developments in how we manage chronic kidney disease,” said Marc Richards, MD. “We've gone from that to now potentially 3 new classes of agents on the market, and potentially more, that can delay progression of kidney disease in our patients and prevent progression to end-stage kidney disease.”

Historically, CKD care focused largely on controlling blood pressure, managing diabetes, and slowing kidney damage with renin-angiotensin system (RAS) blockade. However, the treatment landscape has expanded with therapies targeting multiple pathways involved in kidney disease progression, proteinuria, cardiovascular risk, and metabolic dysfunction.

“The modern management of CKD relies on the integration of foundational and newer nephroprotective therapies,” Richards said.

From Supportive Care to Disease-Modifying Therapy

The expanding CKD treatment landscape reflects a shift toward evidence-based therapies that target specific mechanisms involved in disease progression.

CKD Treatment Toolbox: Key Kidney-Protective Therapies in 2026


Longstanding foundational therapy, particularly for patients with proteinuric CKD and hypertension.


Reduce kidney disease progression and cardiovascular risk and are now considered foundational therapy across broad CKD populations.

Nonsteroidal mineralocorticoid receptor antagonists (MRAs)


Target aldosterone-related pathways and are particularly used in patients with proteinuric CKD, with evidence expanding beyond diabetic kidney disease.

 semaglutide, liraglutide, tirzepatide (dual GIP/GLP-1 agonist)



Provide cardiovascular and metabolic benefits and are increasingly incorporated into cardio-kidney-metabolic risk reduction strategies.

“Now our data is exploding,” Richards said. “We have evidence with ACE inhibitors and ARBs for proteinuric kidney disease states. We have SGLT2 inhibitors becoming a standard of care. We now have the nonsteroidal MRAs that are on the market, both in diabetic and—now we're learning—non-diabetic kidney disease, that could benefit our patients. Data is emerging with GLP-1 agonists.”

RAS inhibitors, including angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs), remain foundational therapies for patients with CKD, particularly those with proteinuric disease.

“RAS inhibitors such as ACE inhibitors or angiotensin receptor blockers have a long and safe history of being the first-line therapy for treatment of diabetes and kidney disease, and even high blood pressure,” Richards said. “That remains unchanged.”

Over the past decade, sodium-glucose cotransporter-2 (SGLT2) inhibitors have become another cornerstone of CKD management, with evidence supporting kidney and cardiovascular benefits across broad patient populations.

“Over the last decade, we've now added SGLT2 inhibitors that have the added benefit of preventing heart failure and cardiovascular disease, and even progression of kidney disease,” Richards said. “They now form the cornerstone of treating all chronic kidney disease.”

Nonsteroidal mineralocorticoid receptor antagonists (MRAs), including finerenone, have further expanded treatment options, particularly among patients with proteinuric kidney disease.

“The nonsteroidal mineralocorticoid receptor antagonists are added on, especially in people who have proteinuric kidney disease,” Richards said.

The Cardio-Kidney-Metabolic Connection Expands CKD Care

Another major shift in CKD management has been the recognition that kidney disease cannot be treated independently from cardiovascular and metabolic health.

Glucagon-like peptide-1 (GLP-1) receptor agonists, once primarily viewed as glucose-lowering therapies, are increasingly being incorporated into CKD care because of their cardiovascular and metabolic benefits.

“Over the last few years, the biggest shift is that GLP-1 agonists have gone from being viewed as just glucose-lowering drugs to drugs that now treat the broader cardio, kidney, metabolic syndrome,” said Pranav Garimella, MD.

“That’s really critical because we’ve come to realize that we can’t treat these organs in silos anymore,” he continued. “The kidneys, the heart, and the metabolic system are intricately tied together.”

Garimella said GLP-1 receptor agonists should now be considered part of the broader CKD treatment toolkit.

“GLP-1s no longer belong just in the treatment of diabetes, but they are integral to preventing heart failure and kidney disease progression,” he said.

However, he emphasized that GLP-1 receptor agonists should be viewed as complementary to existing kidney-protective therapies rather than replacements for foundational treatments.

For example, a patient with CKD, hypertension, diabetes, and proteinuria may benefit from RAS blockade followed by an SGLT2 inhibitor and potentially a nonsteroidal MRA. In contrast, a patient with CKD, obesity, sleep apnea, and increased cardiovascular risk may derive additional benefit from GLP-1 receptor agonist therapy.

“The GLP-1s are seen now as complementary,” Garimella said.

Emerging Targets: The Role of Aldosterone in CKD

Beyond currently established therapies, researchers continue to investigate additional pathways involved in CKD progression, including aldosterone signaling.

Richards said aldosterone has become an increasingly important therapeutic target because of its effects on cardiovascular and kidney health.

“Now we have a focus on targeting aldosterone as a way of trying to help limit stress on the kidney or limit stress on the heart,” Richards said. “With older drugs like spironolactone and eplerenone, newer medicines like finerenone, and even looking into novel agents like aldosterone synthase inhibitors to even prevent aldosterone from being released in the first place.”

Aldosterone contributes to processes including hypertension, electrolyte abnormalities, and organ stress over time, making it an important pathway of interest for future CKD therapies.

Beyond eGFR: Moving Toward Personalized CKD Management

While the expansion of treatment options has changed CKD care, experts emphasized that effective management still depends on understanding the individual patient and their underlying disease drivers.

Matthew Breeggemann, MD, said evaluating CKD requires looking beyond a single kidney function measurement.

“I think for me it’s really helpful to get a really detailed history when you first meet them, and this would include the patient and the patient’s family, and just trying to fit those pieces of the puzzle together,” Breeggemann said.

A patient with diabetes may have straightforward diabetic kidney disease, he explained, while another patient may have diabetes along with hypertension, kidney stones, or other contributors that require a different management approach.

When assessing CKD severity, Breeggemann said clinicians should focus on trends over time rather than isolated values.

“I really want to see the trend,” he said.

He explained that one patient may have an eGFR of 50 mL/min/1.73 m² that remains stable for years, while another patient with the same baseline value may experience a rapid decline over a short period of time.

Beyond laboratory values, Breeggemann highlighted the growing role of precision approaches, including genetic testing and kidney biopsy.

“Our center also does perform a substantial amount of genetic testing for kidney disorders, and these findings have definitely led to a change in how we approach and manage some patients with CKD,” he said.

He also emphasized the importance of incorporating patient preferences into treatment decisions.

“We want to ensure that patients understand why we recommend what we recommend, and importantly, lastly, take into account the patient’s priorities for their own care to really make sure we’re working with them and honoring their treatment preferences,” Breeggemann said.

Recognizing AKI as a Driver of Long-Term Kidney Health

Another shift in kidney care has been the recognition that acute kidney injury (AKI) may have long-term consequences for kidney health.

Breeggemann said AKI should not be viewed simply as a temporary event that resolves once creatinine improves.

“An episode of acute kidney injury should not really be viewed as a simple transient condition, even when perhaps labs may improve and then thus suggest so,” he said.

AKI episodes can contribute to structural changes in the kidney, inflammation, cellular injury, and vascular damage, potentially increasing the risk of future CKD development or progression.

“It would be a mistake to just say, okay, great, nothing, no additional evaluation or monitoring is needed,” Breeggemann said.

He added that many patients who experience AKI may not receive consistent follow-up after discharge, despite their increased risk.

The Remaining Challenge: Translating Evidence Into Practice

Despite major advances in CKD treatment, experts said a significant challenge remains: ensuring that evidence-based therapies reach the patients who could benefit.

Breeggemann noted that implementation of new therapies often takes years.

“It takes approximately 17 years following a new medical intervention or therapy to be routinely used in clinical practice,” he said.

Barriers include delayed diagnosis, delayed referral to nephrology, insurance challenges, clinician familiarity, and coordination between specialties.

Garimella also highlighted clinician familiarity as an ongoing challenge as GLP-1 receptor agonists expand beyond diabetes care.

“Historically we viewed these medications as being exclusively diabetic medications,” he said. “However, now we know that these medications can prevent kidney disease progression; they can prevent heart disease progression.”

Looking ahead, Richards said continued research will be essential to further improve CKD care.

“Potentially the next great treatment is out there, but we just need to get patients into clinical trials to see if we can establish new standards of care to optimize management of our patients,” he said.

Editor’s Note: Richards reports no relevant disclosures; Garimella has relevant disclosures with Otsuka and the PKD Foundation.

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The EMPA-KIDNEY Collaborative Group.
Empagliflozin in patients with chronic kidney disease. 

 2023;388(2):117-127. doi:10.1056/NEJMoa2204233 

Bakris GL, Agarwal R, Anker SD, et al.
Effect of finerenone on chronic kidney disease outcomes in type 2 diabetes. 

 2020;383(23):2219-2229. doi:10.1056/NEJMoa2025845 

Perkovic V, Tuttle KR, Rossing P, et al.
Effects of semaglutide on chronic kidney disease in patients with type 2 diabetes. 

 2024;391:109-121. doi:10.1056/NEJMoa2403347 

Agarwal R, Green JB, Heerspink HJL, et al.
Finerenone with empagliflozin in chronic kidney disease and type 2 diabetes. 

 2025;393:533-543. doi:10.1056/NEJMoa2410659

Chronic kidney disease management has shifted from supportive measures toward multi-pathway, disease-modifying therapy. RAS blockade remains foundational for proteinuric disease, with SGLT2 inhibitors now broadly nephroprotective and cardioprotective across CKD populations. Nonsteroidal MRAs such as finerenone add incremental benefit, particularly in proteinuria, while GLP-1 receptor agonists are increasingly positioned within cardio-kidney-metabolic risk reduction as complementary agents. Optimal care emphasizes individualized phenotyping beyond single eGFR values, attention to AKI as a progression driver, and faster implementation of evidence into routine practice.

Nephrology experts discuss how CKD care has evolved in 2026, including SGLT2 inhibitors, finerenone, GLP-1 receptor agonists, and personalized treatment.

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