Marc Richards, MD is a nephrologist at Florida Kidney Physicians, LLC and Director of the FKP Glomerulonephritis Center of Excellence in Boca Raton, Florida.

Marc Richards, MD

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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 2024;105(4S):S117-S314. doi:10.1016/j.kint.2023.10.018

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Dapagliflozin in patients with chronic kidney disease. 

 2020;383(15):1436-1446. doi:10.1056/NEJMoa2024816 

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Empagliflozin in patients with chronic kidney disease. 

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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. 

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Articles

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.

Where Are We Now? Treating Chronic Kidney Disease in 2026

centered largely on controlling blood pressure, managing diabetes, and using renin-angiotensin system blockade when appropriate. Today, that approach has expanded considerably, with a growing number of disease-modifying therapies targeting distinct pathways involved in kidney injury and progression.

CKD affects more than 1 in 7 US adults, yet many patients remain unaware they have the disease, underscoring the need for earlier recognition and more effective treatment strategies.

The emergence of sodium-glucose cotransporter 2 (SGLT2) inhibitors, nonsteroidal mineralocorticoid receptor antagonists, and other therapies has transformed the clinical approach to slowing CKD progression.

, Marc Richards, MD, a nephrologist at Florida Kidney Physicians, discusses how this expanding evidence base is changing CKD management, the role of combination therapy, and why clinicians should continue adopting new treatment strategies.

Q&A: Expanding Era of Evidence-Based CKD Care, With Marc Richards, MD

When you're thinking about managing chronic kidney disease in 2026, what do you consider the essential components of evidence-based care?

Richards: I think what's amazing is that we actually have evidence-based care now. Up until a few years ago, it was, you know, maybe take care of your blood pressure, take care of your blood sugar, maybe take an ACE inhibitor, and avoid medicines that are bad for the kidneys. And really, outside of that, there was nothing we could really tell patients.

But now our data is exploding. 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.

Also, nephrology is teeming with these new clinical trials that can help us really get more medicines to the forefront and have a really good evidence base to manage our patients.

As you’ve mentioned, there are so many new therapies that have emerged in recent years that target very different pathways. How has that shifted your thinking about combination therapy or selecting treatments for individual patients?

Richards: We like that there was the CONFIDENCE trial, which was really recent, where they looked at combining SGLT2 inhibitors with finerenone, which is the nonsteroidal mineralocorticoid receptor antagonist. They showed that you got pretty good reduction in proteinuria with either of those agents, but when you use them together, you actually had a synergistic effect and the protein in the urine got even better.

I think sometimes patients might get a little frustrated when we're adding medicine on top of medicine, but if you explain that they all work together from different angles to protect kidneys, the patients are willing to accept combination therapy.

I don't know if that answered your question totally about the individualized care, but certainly if a patient does have protein in the urine, that would make me more willing to be more aggressive with that type of therapy.

: If every nephrologist listening today could make one change in their practice tomorrow, what would you want it to be?

Richards: I really think it's being earlier adopters of this evidence. 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.

We've gone from that to now potentially three 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.

So I think we just need to wake up and realize that we have this great evidence out there. We have new classes of agents out there that are readily available to use on our patients, and we can really make a difference in the lives of our patients.

Was there anything else that I didn't ask about that you think you would want to highlight or add?

Richards: I think the only other thing would be that in addition to what we now have, we always have the potential for more. At least our practice, and a lot of academic and private practices throughout the country, are very active with clinical research.

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.

Editor’s Note: Richards reports no relevant disclosures.

National Institute of Diabetes and Digestive and Kidney Diseases. 

Kidney Disease Statistics for the United States

https://www.niddk.nih.gov/health-information/health-statistics/kidney-disease

Heerspink HJL, Stefánsson BV, Correa-Rotter R, et al. Dapagliflozin in Patients with Chronic Kidney Disease. 

. 2020;383(15):1436-1446. doi:10.1056/NEJMoa2024816.

Chronic kidney disease care has shifted from largely supportive management—blood pressure and glycemic control, ACE inhibitor/ARB use in proteinuric disease, and avoidance of nephrotoxins—to a rapidly expanding, evidence-based, disease-modifying paradigm. With CKD affecting more than 1 in 7 US adults and substantial under-recognition, earlier detection and timely initiation of kidney-protective agents are increasingly critical. SGLT2 inhibitors have become foundational, nonsteroidal mineralocorticoid receptor antagonists are gaining broader applicability beyond diabetes, and GLP‑1 agonist data are emerging alongside robust trial activity.

Marc Richards, MD, discusses how new therapies and combination treatment strategies are transforming evidence-based care for chronic kidney disease.


Expanding Era of Evidence-Based CKD Care, With Marc Richards, MD

Although inhibition of the renin-angiotensin system with angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs), followed by sodium-glucose cotransporter 2 (SGLT2) inhibitors, has transformed

management by slowing disease progression, growing attention has shifted toward additional biological pathways that contribute to ongoing kidney and cardiovascular injury.

Among these, aldosterone has emerged as an increasingly important therapeutic target through the development of steroidal and nonsteroidal mineralocorticoid receptor antagonists, as well as newer aldosterone synthase inhibitors designed to reduce hormone production upstream.

, Marc Richards, MD, a nephrologist at Florida Kidney Physicians, discusses how advances in CKD pathophysiology have reshaped treatment over the past several decades, why aldosterone has become a key focus for clinicians, and what its physiologic role means for patients with kidney and cardiovascular disease.

Q&A: Why Aldosterone Has Become a Key Target in CKD Care, With Marc Richards, MD

Over the last couple of years and decades, our understanding of CKD pathophysiology has evolved considerably. Which biological pathways do you think have most changed the way clinicians approach treatment?

Richards: I think the big ones are really with ACE inhibitors, ARBs, and SGLT2 inhibitors; it's really all about tubuloglomerular feedback, reducing stress on the kidney.

And then also 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, with older drugs like spironolactone and eplerenone, newer medicines like finerenone, and even looking into novel agents like aldosterone synthase inhibitors, which recently hit the market, to even prevent the aldosterone from being released in the first place.

Could you give a brief overview of aldosterone—what it does physiologically and why clinicians should pay attention to it?

Richards: Aldosterone is a hormone that's released by the adrenal gland, typically in response to either just being released on its own in cases of primary hyperaldosteronism, or in the setting of excess renin release, which can also increase that release because renin can stimulate that.

We know that aldosterone can lead to hypertension. It can lead to hypokalemia. It can lead to stress in patients with secondary release in patients with heart or liver dysfunction, and it probably has issues in the setting of—can possibly lead to—worsening renal dysfunction as well over time.

Fioretti F, Testani JM, Tio MC, Pitt B, et al. Aldosterone and aldosterone modulation in cardio-kidney diseases. 

. 2025;86(5):354-373. doi:10.1016/j.jacc.2025.06.012.

Chronic kidney disease therapeutics have historically centered on renin-angiotensin system blockade with ACE inhibitors and ARBs, later complemented by SGLT2 inhibitors to restore tubuloglomerular feedback and reduce intraglomerular stress. Attention is increasingly shifting toward aldosterone as an additional driver of ongoing renal and cardiovascular injury. Mineralocorticoid receptor antagonism now spans legacy steroidal agents, newer nonsteroidal options such as finerenone, and emerging aldosterone synthase inhibitors aimed at suppressing hormone production upstream, with implications for hypertension, hypokalemia, and progressive organ dysfunction.

Michael Richards, MD, discusses aldosterone's role in CKD pathophysiology and why targeting this pathway may reshape kidney disease treatment.