Katherine Tuttle, MD, is Executive Director for Research at Providence Inland Northwest Health and Professor of Medicine at the University of Washington.

Katherine Tuttle, MD

 in Denver, Colorado, cohosts Brendon Neuen, MBBS, PhD, and Shikha Wadhwani, MD, MS, welcomed back Katherine Tuttle, MD, of Providence Inland Northwest Health and the University of Washington School of Medicine. 

The group broke down new analyses from the FIND-CKD trial of finerenone in non-diabetic chronic kidney disease (CKD), presented during a dedicated finerenone session. Topics included combination therapy with SGLT2 inhibitors, hyperkalemia, IgA nephropathy, and outcomes across CKD severity.

Kidney Compass: New FIND-CKD Finerenone Data From ASN Kidney Week 2026

Does Finerenone Benefit Patients With CKD Already Taking an SGLT2 Inhibitor?

FIND-CKD randomized 1584 patients with non-diabetic CKD, an eGFR of 25 to below 90 mL/min/1.73 m², and albuminuria on optimized renin-angiotensin system blockade to finerenone or placebo.¹ Finerenone slowed total eGFR decline by 0.7 mL/min/1.73 m² per year versus placebo over 32 months, and the effect was similar in the 17% of patients receiving an SGLT2 inhibitor at baseline (

 for interaction = .71). The composite kidney-cardiovascular outcome was also reduced (hazard ratio, 0.77) regardless of SGLT2 inhibitor use.

00:05 - Welcome and episode overview
01:54 - Finerenone with and without SGLT2 inhibitors in FIND-CKD
03:38 - Hyperkalemia risk and management
07:01 - Finerenone in IgA nephropathy
13:31 - Cardiovascular risk and holistic care in IgAN
15:34 - Sequencing therapies for residual albuminuria
17:58 - Kidney injury biomarkers and innate immunity
22:07 - Finerenone effects across CKD severity

Tuttle called the consistency reassuring, noting the 2 drug classes act on different pathways. Neuen added time-updated analyses, accounting for SGLT2 inhibitor use increasing during the trial, showed the same pattern.

On hyperkalemia, Neuen noted potassium above 6.0 mmol/L occurred in about 4% of patients receiving finerenone compared with 2% with placebo, with few events leading to hospitalization or discontinuation. Across CKD severity, hyperkalemia rates ranged from 5.7% with finerenone vs 5.8% with placebo in the least severe group to 29.4% vs 20.6% in the most severe group.²

“So pay attention and manage it,” Tuttle said. “And most of the time, people can tolerate these therapies, and it’s worth it because these really are kidney, heart, and life-saving therapies.”

What Did FIND-CKD Show for Finerenone in IgA Nephropathy?

Of 1584 FIND-CKD participants, 416 (26%) had IgA nephropathy, and 93% had biopsy confirmation.³ Finerenone reduced urine protein-to-creatinine ratio (UPCR) by 51% versus placebo at month 12 and increased the likelihood of reaching UPCR below 500 mg/g (odds ratio, 6.8; 95% CI, 3.7–13.1).

The effect on total eGFR slope was similar in participants with and without IgA nephropathy (0.6 vs 0.7 mL/min/1.73 m² per year; 

 for interaction = .755).³ Finerenone did not reduce galactose-deficient IgA1 or other immunoglobulins but did lower kidney injury biomarkers, particularly KIM-1 and urinary MMP7.

Wadhwani said the ability to reach proteinuria targets without adding immunosuppression is meaningful, given many patients are diagnosed with advanced CKD. Tuttle pointed to cardiovascular disease, particularly heart failure, as the leading cause of death in this population.

Asked how to prioritize therapies, Tuttle advised letting residual albuminuria guide add-on treatment. She urged clinicians to “aspire to extinguish albuminuria even in people with IgA nephropathy, and not just to protect their kidneys, but protect the rest of them.” For patients at risk of heart failure, she said she would favor finerenone, while noting the opinion is not based on a head-to-head trial.

On the biomarker data, Tuttle said reductions in KIM-1 and MMP7 support a complementary mechanism targeting tubulointerstitial inflammation and fibrosis driven by innate immunity, which immunologic therapies leave unaddressed.

Does Finerenone Work Across All Stages of CKD Severity?

In an analysis presented by Tuttle, finerenone reduced the rate of eGFR decline and the composite kidney-cardiovascular outcome vs placebo irrespective of baseline eGFR and urine albumin-to-creatinine ratio.² Tuttle also described a pooled individual participant–level analysis of FIDELIO-DKD, FIGARO-DKD, and FIND-CKD showing consistent benefits, with greater kidney benefit in high-risk groups and greater cardiovascular benefit in lower-risk groups. She said the findings also carry a message for cardiologists, who often manage lower-risk patients, as finerenone can markedly reduce cardiovascular complications regardless of diabetes status.

“So no therapeutic inertia,” Tuttle said. “Initiate finerenone because it preserves kidney function in people with advanced CKD, where kidney failure is their most imminent risk.”

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

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

 include Eli Lilly and Company, Boehringer Ingelheim, Astra Zeneca, Gilead, Goldfinch Bio, Novo Nordisk, Travere Therapeutics, and Bayer.

Cherney D, Heerspink HJL, Agarwal R, et al. Finerenone in patients with CKD by SGLT2 inhibitor treatment: a FIND-CKD analysis. Presented at: ASN Kidney Week 2026; October 21-25, 2026; Denver, CO. doi:10.1681/ASN.2026a8de76t0

Tuttle KR, Heerspink HJL, Agarwal R, et al. Effects of finerenone on clinical outcomes by CKD severity: a FIND-CKD analysis. Presented at: ASN Kidney Week 2026; October 21-25, 2026; Denver, CO. doi:10.1681/ASN.2026aepxagfn

Neuen BL, Barratt J, Floege J, et al. Finerenone in patients with IgA nephropathy: a FIND-CKD analysis. Presented at: ASN Kidney Week 2026; October 21-25, 2026; Denver, CO. doi:10.1681/ASN.2026q6qqpem2

Podcasts

Katherine Tuttle, MD, joins Brendon Neuen, MBBS, PhD, and Shikha Wadhwani, MD, MS, to unpack new FIND-CKD finerenone analyses from ASN 2026.

Katherine Tuttle, MD
Credit: University of Washington

 affects an estimated 850 million people worldwide, yet awareness remains critically low among both patients and clinicians. 

Survey data indicate that only approximately 20% of patients and healthcare professionals recognize CKD in an individual patient, and most diagnoses surface only after stage 4 disease prompts a referral to nephrology. This detection gap means that many patients never access the therapies now available to slow or stop nephron loss.

Over the past several years, a pillared approach to CKD management has taken hold across the field, drawing on strategies already proven in cardio-metabolic conditions such as heart failure. The framework encompasses renin-angiotensin-aldosterone system inhibition, SGLT-2 inhibitors, GLP-1 receptor agonists, and mineralocorticoid receptor antagonists, each targeting distinct but overlapping mechanisms including hemodynamic dysregulation, metabolic dysfunction, inflammation, and fibrosis.

Together, these therapies have redefined what preservation of kidney function can look like. The language of "watchful waiting" and inevitable progression is giving way to a clinical posture centered on kidney health preservation and, in some disease subtypes, remission.

Yet questions remain about sequencing, how to address the upstream etiology that the pillared approach does not directly treat, which patient populations carry the highest residual risk, and how emerging disease-modifying therapies for conditions such as 

 should be integrated alongside established CKD regimens.

Katherine Tuttle, MD, professor of medicine and executive director for research at Providence Healthcare, spoke with HCPLive at the 10th Annual Heart in Diabetes meeting to share her perspective on optimizing CKD management through the pillared approach and beyond.

Q&A: The Pillared Approach and Reframing Goals of CKD Care, With Katherine Tuttle, MD

HCPLive: As we move beyond implementation and try to cascade that down toward optimized management, what's the next frontier in optimizing management of chronic kidney disease for the field?

 We now have delivered highly efficacious and safe therapies that save kidneys, hearts, and lives. The big lift now is increasing CKD awareness and detection to get to intervention, because we don't treat what we don't see or measure. 

I think that is a huge effort that needs to happen globally — there may be different approaches depending on the region and how that may be accomplished — but the awareness is so low. We know from surveys of both patients and healthcare professionals that only about 20% of patients and healthcare professionals are aware of CKD in a person, and that's mostly in people with stage 4 disease by the time they're referred to nephrology. 

So, I think our obligation now is really to get the message out.

HCPLive: With recent advances, have we shifted the goals of chronic kidney disease management to completely stoppingprogression of chronic kidney disease or are we still focused on slowing function loss?

 I have eliminated "CKD progression" from my lexicon. We now have such efficacious therapies that we should really be focusing on preservation of function and kidney health, and aspirationally, remission — especially for some forms of kidney disease. 

For example, in the glomerular diseases, we have highly effective therapies that treat the inciting factors, like in IgA nephropathy, preventing production of abnormal IgA and the immune response to it, plus the CKD therapies that stop the vicious feedback cycle that historically led to CKD progression. 

I say "led" because in the future it won't, because if we get it right and treat both the upstream inciting factor and the downstream progression factors, people should be able to maintain kidney function and kidney health for a lifetime. We need to completely reframe the conversation about what the goals of care are.

HCPLive: Where do you think the current approach to CKD management is falling short the most and what patient population still has the highest unmet need?

 One of the things we have neglected is cause — etiology — and it matters for the reasons I just described. We have highly effective therapies that deal with what we used to call progression, or nephron loss from final common pathways. 

Those pathways are mostly metabolic, hemodynamic, fibrosis, and inflammation. Our pillared approach deals with progressive nephron loss: ACE inhibitors and ARBs are largely hemodynamic therapies; SGLT-2 inhibitors are largely hemodynamic with some metabolic benefits; and GLP-1 receptor agonists and finerenone are anti-inflammatory and anti-fibrotic. 

That's all great — but if we haven't addressed the inciting factors, we can still drive progression through upstream mediators. That's why identifying cause is important. We know from biopsy studies, like the Kidney Precision Medicine Project, that even in people we have clinically diagnosed with diabetic kidney disease only, about half have good old-fashioned diabetic nephropathy. And these are protocol biopsies — not people who have some unusual form of kidney disease in the setting of diabetes where we're looking for something else. 

About a quarter have diabetic nephropathy mixed with another disease, and these are largely glomerular diseases — IgA nephropathy was the most common. And then others have no diabetes-related kidney disease at all; they have something else entirely. So if we just treat them for diabetes, we've missed the boat. We need to pursue diagnosis, and in many cases that will include a kidney biopsy.

HCPLive: How would you encourage nephrologists to approach treatment sequencing as we move forward into an era that includes targeted therapies, such as with IgA nephropathy? 

 With IgA nephropathy, there is a four-hit hypothesis: abnormal IgA production, antibody formation, formation of immune complexes, and complement activation. Understanding the biology was critical to targeting therapies. 

Those therapies have been studied as individual treatments, so what we don't know yet is sequencing, timing, which one first, and combinations — that's a topic for future inquiry. But in the meantime, we should not have therapeutic inertia. Not all of these therapies are available everywhere, so use what you have. And this is where the practice and art of medicine comes in: look at the person in front of you and assess their totality of risks, because some of these drugs have side effects. Are they going to be able to tolerate this medicine? What might work best for them, considering their own priorities and preferences?

It wasn't very many years ago that we were talking about fish oil and aspirin for IgA nephropathy — it seems so primitive now. Yes, there are new challenges, but they're a delight, because we have tools to work with. And it's not just IgA nephropathy. We're seeing amazing progress with lupus nephritis, membranous nephropathy, and focal segmental glomerulosclerosis — the most common forms of primary kidney disease outside of diabetes and hypertension. 

We've got our common CKDs from diabetes and hypertension pretty well managed now with the four pillars, and there's more work to do. There's residual risk. But if we just got it right on awareness and detection and applied what we know now, we would see a significant improvement in survival, a reduction in major cardiovascular risks — which are the competing risks to kidney failure — and take so many people off the road to kidney failure. 

People with diabetes who get CKD: 9 out of 10 will die on the road to kidney failure. They'll never make it to kidney failure. And of that surviving 10% who used to make it to kidney failure, that should be preventable too. 

So, our goal should really be to prevent premature mortality and give treatments that save heart and kidney function. That's why our tagline now is "Save Kidneys, Hearts, and Lives." We have several highly effective therapies that can accomplish these goals, but we have to do the heavy lifting now — which is getting these treatments to the patients who can benefit.

Editor’s Note: This transcript was edited for grammar and clarity using artificial intelligence tools. 

Francis A, Harhay MN, Ong ACM, et al. Chronic kidney disease and the global public health agenda: an international consensus. 

Chu CD, Chen MH, McCulloch CE, et al. Patient Awareness of CKD: A Systematic Review and Meta-analysis of Patient-Oriented Questions and Study Setting. 

. 2021;3(4):576-585.e1. Published 2021 Jun 1. doi:

Articles

Chronic kidney disease affects ~850 million globally, yet recognition by patients and clinicians remains near 20%, leading to late-stage referrals and missed opportunities for nephroprotection. A four-pillar regimen—RAAS blockade, SGLT2 inhibitors, GLP-1 receptor agonists, and mineralocorticoid receptor antagonists—targets hemodynamic, metabolic, inflammatory, and fibrotic pathways and reframes goals toward kidney function preservation and, in selected etiologies, remission. Persistent gaps include etiologic misclassification, sequencing of emerging targeted agents (e.g., IgA nephropathy), and implementation at scale to reduce cardiovascular death and kidney failure.

Katherine Tuttle, MD, discusses shifting the goals of chronic kidney disease management from slowing progression to preserving kidney function.

A 20-minute podcast discussuion around the nsMRA finerenone, FIND-CKD, and its role in the broader CKM landscape.

Don't Miss a Beat: Finerenone, FIND-CKD, and the Evolution of CKM, with Katherine Tuttle, MD

Finerenone's expansion into non-diabetic kidney disease is prompting a broader rethink of how 

 is measured, mechanistically understood, and treated across its many causes.

On an episode of Don't Miss a Beat recorded at the 

, hosts Stephen Greene, MD, meeting co-chair and heart failure specialist at Duke University School of Medicine, and Muthiah Vaduganathan, MD, MPH, codirector of the Center for Cardiometabolic Implementation and cardiologist at Brigham and Women's Hospital, spoke with Katherine Tuttle, MD, professor of medicine at the University of Washington, about the phase 3 FIND-CKD trial and how it informs on the overall role of finerenone (Kerendia) in management of cardiovascular-kidney-metabolic syndrome.

FIND-CKD showed finerenone slowed total estimated glomerular filtration rate (eGFR) slope by 0.7 mL/min/1.73 m² per year versus placebo, irrespective of diagnosis. Much of the discussion focused less on the number and more on why it counts as clinically meaningful.

Drawing on CKD Prognosis Consortium data from hundreds of thousands of patients, Tuttle explained why eGFR slope reliably predicts kidney failure when a trial runs at least 2 years. CKD progresses rather than striking as a discrete event, so the field has moved toward endpoints measurable without waiting for organ failure or death.

On safety, hyperkalemia occurred more often with finerenone than placebo, about 12% versus 3%, though fewer than 1% of patients discontinued. The framing was practical, with background SGLT2 inhibition expected to lower the risk.

Mechanism anchors much of the conversation between Tuttle, Greene, and Vaduganathan. 

Tuttle highlighted how glomerular diseases, like 

, are immunologic disorders needing disease-specific therapy, yet all CKD converges on shared final common pathways of inflammation and fibrosis. Broad agents like finerenone target those pathways, making combination therapy the emerging model, pairing treatment of the inciting disease with control of progression.

The group also discussed the field’s trend toward precision nephrology. Protocol biopsies from the Kidney Precision Medicine Project showed only about half of patients labeled as diabetic CKD had classic diabetic nephropathy. A parallel to oncology followed, where deep phenotyping replaced uniform regimens, suggesting not every patient will need every drug.

Tuttle positioned finerenone alongside renin-angiotensin system inhibitors and SGLT2 inhibitors as an emerging pillar for non-diabetic CKD, with GLP-1 receptor agonists and endothelin antagonists possibly to come. A pooled analysis of FIDELIO-DKD, FIGARO-DKD, and FIND-CKD showed roughly 30% reductions in kidney and cardiovascular outcomes and an 11% drop in all-cause mortality. The closing point held the cardiorenal patient often arrives through either specialty's door, making preservation of organ function and quality of life the shared aim.

Relevant disclosures for Tuttle include Alnylam, AstraZeneca, Bayer, Boehringer Ingelheim, Eli Lilly, GSK, Novo Nordisk, Roche, and Travere Therapeutics. Relevant disclosures for Vaduganathan include Amgen, AstraZeneca, Bayer AG, Boehringer Ingelheim Pharmaceuticals, Cytokinetics, Lexicon, and others. Relevant disclosures for Greene include Amgen, AstraZeneca, Bayer Healthcare Pharmaceuticals, Boehringer Ingelheim Pharmaceuticals, Cytokinetics, and others.

Heerspink HJL, Neuen BL, Agarwal R, et al. Finerenone in Persons with Chronic Kidney Disease without Diabetes. 

Bayer. Bayer to Present First Full FIND-CKD Results Investigating KERENDIA® (finerenone) in Non-Diabetic Chronic Kidney Disease at ERA 2026. Bayer.com. Published June 2, 2026. Accessed June 21, 2026. 

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

Phase 3 FIND-CKD data show finerenone slows kidney function decline in non-diabetic chronic kidney disease, extending the agent's role beyond diabetic CKD.

From FLOW to REMODEL: Understanding Semaglutide in CKD, With Katherine Tuttle, MD

Chronic kidney disease (CKD) in the setting of type 2 diabetes represents one of the most high-risk clinical scenarios in medicine, driven not only by progression to kidney failure but by a substantial burden of cardiovascular morbidity and premature death.

While recent therapeutic advances have improved outcomes, understanding how these treatments exert their benefits has remained a critical gap. The REMODEL trial was designed to address this question, offering a detailed mechanistic complement to landmark outcome data on semaglutide’s benefit in this patient population.

 at the World Congress of Nephrology (WCN) in Yokohama, Japan, Katherine Tuttle, MD, explained that REMODEL builds on the success of the FLOW trial, which demonstrated significant reductions in kidney events, cardiovascular outcomes, and all-cause mortality with semaglutide, ultimately leading to the agent’s US Food and Drug Administration approval for this indication. While those findings established clinical efficacy, they did not fully explain the underlying biology. REMODEL, she explains, was specifically designed as a mechanistic “deep dive,” integrating advanced imaging, kidney biopsy, and transcriptomic analyses to uncover how these benefits are achieved.

The study confirmed key clinical findings, including a 40% reduction in albuminuria and stabilization of kidney function. Of note, functional MRI revealed significant reductions in kidney fat far exceeding overall weight loss as well as improved vascular health, reflected by decreased renal arterial resistance. Markers of fibrosis progression were halted in the treatment group, suggesting a protective structural effect.

Biopsy data provided further depth. Tuttle highlights a marked reduction in peri-glomerular immune cells, particularly natural killer T cells, alongside broad downregulation of fibroinflammatory pathways, pointing to a direct anti-inflammatory effect within the kidney microenvironment. Transcriptomic analyses additionally identified glomerular endothelial cells as a key site of regulation, supporting the concept of improved integrity of the glomerular filtration barrier and even evidence of repair, not just stabilization, over time.

She emphasizes that these results align closely with preclinical models, strengthening confidence in translational research approaches. Beyond individual findings, the study design itself represents a major advance, demonstrating that rigorous mechanistic trials can be successfully conducted in humans.

Looking ahead, Tuttle underscores the implications for precision medicine. While current therapies are broadly applied, variability in response remains a major challenge. By linking mechanistic signatures to treatment outcomes, REMODEL provides a framework for identifying responders and tailoring therapy. Ultimately, she suggests, this approach could shift care toward selecting the right treatment for the right patient at the right time, marking a significant step forward in the management of diabetic kidney disease.

Editors’ note: relevant disclosures for Tuttle include Eli Lilly and Company, Boehringer Ingelheim, Astra Zeneca, Gilead, Goldfinch Bio, Novo Nordisk, Travere Therapeutics, and Bayer.

Campbell P. Semaglutide 1.0 mg (Ozempic) Reduced Kidney Events 24% in FLOW Trial. HCPLive. March 5, 2024. Accessed March 31, 2026. 

https://www.hcplive.com/view/semaglutide-1-0-mg-ozempic-reduced-kidney-events-24-in-flow-trial

Brooks A. FDA Approves Semaglutide (Ozempic) for Type 2 Diabetes, Chronic Kidney Disease. HCPLive. January 28, 2025. Accessed March 31, 2026. 

https://www.hcplive.com/view/fda-approves-semaglutide-ozempic-type-2-diabetes-chronic-kidney-disease

Pruijm M, Belmar N, Bjornstad P, et al. REMODELing mechanistic trials for kidney disease: a multimodal, tissue-centered approach to understand the renal mechanism of action of semaglutide. 

Videos

REMODEL reveals how semaglutide protects kidneys, showing reduced inflammation, improved vascular health, and evidence of structural repair in diabetic CKD.