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Reaching New Heights in CKM Care: Expert Answers to Your Commonly Asked Questions

Released: May 11, 2026

Ty J. Gluckman
Ty J. Gluckman, MD, MHA
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Key Takeaways
  • It is only through multiple personalized approaches that HCPs can effectively address polypharmacy and prioritize therapies that offer benefits across several CKM conditions.
  • Specialty care (ie, nephrology, endocrinology) is not required to confirm if an SGLT2 inhibitor or incretin-based (GLP-1 receptor agonist–based) therapy should be initiated.
  • The CKM treatment landscape continues to evolve as novel combination therapies emerge and address current challenges in patient care.

In this commentary, Ty J. Gluckman, MD, MHA, answers questions posed by healthcare professionals (HCPs) during a live symposium titled “Reaching New Heights in Cardio–Renal–Metabolic Care: Optimizing Treatment to Elevate Patient Outcomes.” Learn strategies for managing patients with cardiovascular–kidney–metabolic (CKM) syndrome, including how to address polypharmacy in those with multiple CKM conditions, how to bridge communication and treatment planning between primary and specialty care, and what to look forward to in clinical development. 

For patients with CKM syndrome who face issues with polypharmacy, how do you prioritize each therapy while minimizing adverse effects and improving adherence?
CKM syndrome represents the intersection of many different, but related, conditions that we, unfortunately, are seeing more often. Usually, it stems from overweight or obesity (with excess/dysfunctional adipose tissue) that predisposes to various harmful conditions, such as hypertension, hyperlipidemia, type 2 diabetes (T2D), atherosclerotic cardiovascular disease, chronic kidney disease (CKD), heart failure (HF), atrial fibrillation, and metabolic dysfunction–associated steatotic liver disease (MASLD). These conditions impact one another, increasing one’s cardiovascular, kidney, and metabolic risks.

Traditionally, we have initiated individual therapies for specific CKM conditions in isolation. We start antihypertensive therapy to treat hypertension and lipid-lowering therapy to treat hyperlipidemia. However, given the limitations of such an approach, how can we do better? Put a different way, how can we use therapies with broad-based benefit to maximize efficacy, minimize safety concerns, and, of more importance, deliver benefit across various CKM conditions?

SGLT2 inhibitors, incretin-based therapies (like GLP-1 receptor agonists), and mineralocorticoid receptor antagonists (MRAs) are 3 drug classes with proven efficacy across multiple CKM conditions. Most have multiple FDA-approved indications, as these therapies have been shown to improve glycemic control in T2D, reduce adiposity in obesity and overweight, decrease risk of major adverse cardiovascular events in T2D and established cardiovascular disease, address inflammation and fibrosis in MASLD, reduce risk of sustained kidney dysfunction in CKD, improve sleep outcomes in obstructive sleep apnea, and/or decrease risk of adverse outcomes in HF.

Admittedly, there are no specific therapy combinations that work for all patients. In addition, some of these therapies may be precluded in patients with specific comorbidities (eg, significantly impaired kidney function). Nonetheless, where possible, HCPs should maximize therapies that can address multiple conditions at the same time.

What common pitfalls do you see primary care HCPs struggle with when treating patients with overlapping CKM conditions? How can these be avoided?
It is challenging to be a primary care HCP for many reasons. For starters, primary care HCPs are asked to provide expertise across wide-ranging conditions. Although many primary care providers may choose to reach out to various specialties for assistance (eg, endocrinology, nephrology, cardiology, sleep, gastroenterology, and/or hepatology), with this comes the challenge of receiving feedback that is likely to be focused singularly on the condition that they were asked to evaluate, without necessarily taking into consideration other clinical issues.

How then should HCPs take into consideration suggestions or recommendations made by individual specialists and use those to create a more holistic treatment plan that is affordable and well-tolerated, without compromising adherence related to polypharmacy?

At the end of the day, primary care HCPs should feel empowered to initiate therapies like SGLT2 inhibitors, GLP-1 receptor agonists, and MRAs, but I think the future of CKM care will require us to design pathways and protocols that address multiple CKM conditions at once and, wherever possible, focus on the root cause of these conditions (ie, metabolic dysfunction).

How can primary care HCPs more effectively coordinate patient care with specialties like cardiology and nephrology without delaying essential treatment?
As previously stated, treating CKM syndrome requires bidirectional communication between primary care and specialty care. All of this comes at a time when we have ever-growing shortages of specialists and primary care HCPs across the United States. To be successful, then, we need to find ways for all HCPs to understand what effective guideline-directed medical therapy looks like in CKM syndrome, which drugs and doses are most likely to be effective, and ways they can be best implemented.

We also need to focus much more on the root cause of CKM conditions. For the overwhelming majority, this starts with the treatment of overweight or obesity. In fact, I frequently tell my patients with CKM syndrome that meaningful weight loss has the potential to reverse their metabolic dysfunction with the chance of even normalizing their blood pressure and glycemic control. Although this is likely to be consequential for many, it is much more important for patients on multiple medications to help lower their blood pressure and improve glycemic control, if for no other reason than to reduce the number of therapies that they’re on.

How can primary care HCPs identify and manage early HF, particularly HF with preserved ejection fraction, before hospitalization occurs in patients with T2D, obesity, or CKD?
HCPs are increasingly being asked to care for an aging population with a growing prevalence of HF. In fact, it is estimated that 8.5 million Americans will be diagnosed with HF by 2030.

Our treatment of HF usually starts with segmentation of patients based on their left ventricular ejection fraction (LVEF). HF with reduced ejection fraction (HFrEF) comprises those with an LVEF of 40% or lower; HF with mildly reduced ejection fraction (HFmrEF) includes those with an LVEF of 41% to 49%; and HF with preserved ejection fraction (HFpEF) encompasses those with an LVEF of 50% or higher. Of importance, multimorbidity (eg, obesity, CKD, diabetes) is much more the norm than the exception in this population, which, when present, informs one’s treatment approach.

Complicating the management of HF is the need to first diagnose it. Because HF is a clinical syndrome, there is no single test that establishes its diagnosis; rather, it requires assessment of one’s symptoms and signs, along with measurement of natriuretic peptides and/or cardiac filling pressures. If a patient’s LVEF is reduced, you likely have your answer.

However, given that roughly half of patients with HF have a normal LVEF, it is important not to dismiss HF as a diagnosis if everything else points you in that direction. Admittedly, other cardiac and noncardiac conditions can be drivers of shortness of breath, lower extremity swelling, and weight gain (eg, myocarditis, lung disease, pulmonary vascular disease), and as such, should be in the differential. At the end of the day, once HF is diagnosed, it’s really important to get patients on appropriate, evidence-based therapy in coordination with others involved in their care.

What emerging evidence or treatment approaches in CKM care should HCPs pay attention to over the next few years?
Ongoing research is focused on evaluating wide-ranging new therapies for CKM. Strong evidence supports the use of incretin-based therapy in many of these patients, and new oral formulations of these drugs are now available. In addition, multiple other therapeutic targets (eg, glucagon, amylin, PYY) are being evaluated, most often as an add-on to a GLP-1 receptor agonist. Additional data will be needed to better inform which patients benefit more from 1 formulation or therapeutic approach over another.

To help address the challenges of polypharmacy and reduced adherence, several ongoing studies are evaluating existing and novel therapies in combination with more commonly utilized therapies (eg, SGLT2 inhibitor, MRA). One such example is aldosterone synthase inhibitors, which work upstream in the renin-angiotensin-aldosterone system, rather than at the receptor level like traditional MRAs. Like MRAs, these medications offer the ability to reduce fibrosis and inflammation, which are major drivers of disease progression in CKM syndrome.

Inflammation is also receiving increased attention as a potential therapeutic target for these patients. Of importance, individuals with subclinical and overt inflammation face increased cardiovascular and cardiometabolic risk. Studies are ongoing with various anti-inflammatory therapies (eg, IL-6 inhibitors, NLRP3 inflammasome inhibitors) to better determine the role of this therapeutic approach.

The future is bright. Wide-ranging therapies are currently available for individuals with CKM syndrome, and many more are in development. Despite this, we need to find ways to do better. Acknowledging ongoing barriers to more optimal care delivery (eg, limited payer authorization, lack of affordability, limited adherence), existing therapies remain underutilized. And although investigation is certainly needed to better personalize treatment regimens, this can only happen effectively if we find ways to improve the ways in which care is delivered.

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