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Integrating Timely CKM Care in Primary Care: From Risk Assessment to GDMT Initiation

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Released: September 30, 2026

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Cardiovascular–kidney–metabolic (CKM) syndrome highlights the deep, interconnected health risks of obesity, diabetes, chronic kidney disease, and cardiovascular disease. Learn why integrating comprehensive CKM risk assessment into routine care is critical for providing timely guideline-directed medical therapy and when referrals should be made to support multidisciplinary collaboration.

Biykem Bozkurt
Biykem Bozkurt, MD, PhD, FHFSA, FACC, FAHA, FACP
Primary care role in CKM syndrome

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About 2 decades ago, most healthcare professionals (HCPs) viewed conditions like hyperlipidemia and hypertension (HTN) as singular cardiovascular risk factors. Today, our understanding has evolved as the current evidence substantiates the deep, interconnected link between cardiovascular, kidney, and metabolic disease in what is known as cardiovascular–kidney–metabolic (CKM) syndrome. HCPs should now recognize a cluster of conditions across the CKM continuum as related, including dysfunctional adiposity or obesity, prediabetes and diabetes, HTN, hyperlipidemia, chronic kidney disease (CKD), liver disease such as MASLD or MASH, and subclinical or clinical cardiovascular disease.

For primary care, this means that diagnosing one CKM condition should prompt screening for others through a comprehensive risk assessment. For example, patients with diabetes should be screened for CKD, HTN, hyperlipidemia, MASLD/MASH, and cardiovascular disease, and patients with HTN and cardiovascular disease should be screened for diabetes and CKD when appropriate.

Risk assessment tools can streamline the screening process. The PREVENT risk calculator is especially helpful because it incorporates measures like urine–albumin-to-creatinine ratio (UACR) and A1C. In addition, the Kidney Disease: Improving Global Outcomes (KDIGO) heat map uses both UACR and estimated glomerular filtration rate (eGFR) to visually communicate kidney risk and potential disease trajectory. Showing patients where they are in their kidney and cardiovascular disease trajectory can make the rationale for treatment much more tangible.

The practical solution in adopting this new guidance is to build CKM workflows into clinical care pathways. That includes electronic health record–based algorithms, standardized screening, appropriate documentation and coding, and clearly defined referral pathways. All of these can help make comprehensive CKM assessment and management routine rather than dependent on individual specialty care.

Do Not Ignore UACR: A Critical Marker of Risk
To improve CKM outcomes in the primary care setting, HCPs must first recognize the importance of screening patients’ kidney function with eGFR and UACR. The latter is critical, as it is a validated biomarker for the diagnosis and prognosis of CKD as well as for monitoring response to therapy. Although eGFR testing is commonly ordered, UACR remains underused in real-world practice.

Both tests are necessary because it is not uncommon for patients to present with a normal eGFR and an abnormal UACR or vice versa. That means they can have CKD, which would otherwise go undiagnosed and likely progress, alongside increased risk for adverse kidney and cardiovascular outcomes. Persistently high UACR results reflect structural kidney abnormalities that identify patients at higher risk of cardiovascular disease and CKD progression.

My advice: if UACR is not part of the standard laboratory order set at your institution, advocate for its inclusion. And note that albuminuria should be quantified with UACR because this measurement is less affected by volume status than just albuminuria concentration.

UACR also has a valuable role in treatment monitoring. After initiation of guideline-directed medical therapy (GDMT), particularly with ACE inhibitors, ARBs, SGLT2 inhibitors, and mineralocorticoid receptor antagonists (MRAs), HCPs may observe a modest early increase in serum creatinine or a transient reduction in eGFR. Of importance, this initial change does not necessarily signify worsening kidney function or renal injury. Rather, it often reflects favorable hemodynamic effects within the kidney that accompany these therapies. Although eGFR may decline slightly in the short term, these agents have been consistently shown to reduce albuminuria, preserve kidney function, and slow the long-term rate of eGFR decline. Consequently, a modest early rise in creatinine should generally be viewed as an expected physiologic response rather than evidence of progressive kidney dysfunction, provided it remains within an acceptable range and is not accompanied by other signs of renal injury.

Prioritize Urgency and Initiate GDMT Early
With multiple GDMTs available, HCPs may wonder where to begin. In my practice, I start by identifying patients' disease burden and most urgent diagnosis. For example, established cardiovascular disease creates a particular urgency. Foundational, 4-pillar GDMT should not be viewed as something to introduce slowly and sequentially in patients with heart failure with reduced ejection fraction; rather, it is imperative that all indicated and guideline-recommended therapies are initiated and titrated early. For patients with heart failure with preserved ejection fraction, the evidence supports disease-modifying treatment approaches, including SGLT2 inhibition and nonsteroidal MRA therapy.

A similar approach should be taken for those with early CKM syndrome (ie, stages 1 and 2), considering these patients do not have subclinical or established cardiovascular disease. I look for therapies that will fulfill multiple indications. For example, those with diabetes and CKD may benefit from treatment that simultaneously addresses their metabolic and kidney risk. Then the presence of obesity, HTN, albuminuria, and other manifestations of CKM syndrome further informs how HCPs should build a comprehensive treatment regimen.

The important point is not to allow perceived stability to become therapeutic inertia. Controlled A1C, blood pressure, or low-density lipoprotein cholesterol does not mean patients' residual CKM risk is controlled.

This is particularly important in diabetes. Historically, HCPs have focused heavily on A1C, but this biomarker alone does not define one’s cardiovascular or kidney risk. How glucose is controlled matters. And today, we have therapies that can do more than improve a single laboratory value; they can modify disease trajectory and improve both cardiovascular and kidney outcomes. Therefore, when I see patients with an A1C at goal, I still ask myself, “Does this patient have CKD? Albuminuria? Obesity? Heart failure or other cardiovascular disease? Are we using the therapies that are appropriate for this risk profile?” Not being aware of residual risk does not mean that patients are at low risk.

Address Treatment Safety Concerns
Another barrier comprises patients’ concerns about polypharmacy, tolerability, and treatment-related adverse effects. These concerns deserve attention and should be addressed through education, appropriate patient selection, and monitoring, rather than by withholding indicated therapies.

With SGLT2 inhibitors, genitourinary infections are generally manageable with patient education, good hygiene practices, and appropriate treatment. Yet more complicated infections may require temporary treatment interruption. Gastrointestinal-related adverse effects with GLP-1 receptor agonists are generally manageable with clear patient education and adjustments in eating habits. Finally, hyperkalemia with MRA therapy can be addressed through potassium monitoring and, when appropriate, additional management strategies.

That said, HCPs also should not assume that older age, lower blood pressure, frailty, or a CKD diagnosis automatically makes patients unable to tolerate GDMT. These patients often have greater baseline risk and, therefore, potentially greater absolute benefit from effective disease-modifying treatment.

Share Ownership With Multidisciplinary Care
Finally, CKM care cannot belong exclusively to cardiology, nephrology, endocrinology, or primary care. We all need to work together across the continuum of the patient’s journey.

Primary care HCPs should feel empowered to diagnose and initiate treatment for CKM syndrome and its separate conditions. That means primary care HCPs should not wait for specialty consultation when GDMT is indicated. At the same time, referrals to specialties are important when patients demonstrate disease progression despite treatment, such as repeated heart failure–related hospitalizations or decompensation, worsening kidney function, difficulty tolerating GDMT, or other high-risk features.

Health systems can support this shared ownership through clearly defined referral pathways, digital consultations, multidisciplinary models, and agreements that specify responsibilities for diagnostic testing and follow-up.

The shift toward comprehensive CKM care requires us to see the whole patient rather than a collection of separate diseases and conditions. HCPs must screen broadly, include UACR in their risk assessment, and look beyond A1C, blood pressure, and lipids to identify the most urgent disease state and initiate GDMT as indicated.

Of most importance, do not wait for patients to develop advanced disease. Earlier recognition allows us to change the disease trajectory before patients present with the cardiovascular and kidney complications that we are trying to prevent.

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