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An Overview of Cardiovascular-Kidney-Metabolic Syndrome
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ABSTRACT
Cardio-kidney-metabolic (CKM) syndrome is a term to describe the interconnection between cardiovascular disease, type 2 diabetes, and chronic kidney disease. The National Health and Nutrition Examination Survey from 1999 to 2020 estimated that 25% of participants had at least 1 CKM condition. It is proposed that CKM syndrome originates in excess and/or dysfunctional adipose tissue, which secretes proinflammatory and prooxidative products leading to damaged tissues in arteries, the heart, and the kidney, and reduction in insulin sensitivity. CKM syndrome is classified into 4 stages based on the presence of risk factors and clinical signs. Risk factors associated with progression of CKM syndrome include chronic inflammatory conditions, family history of diabetes or kidney disease, mental health and sleep disorders, increased levels of elevated high-sensitivity C-reactive protein, and sex-specific risk enhancers. There are substantial racial and ethnic differences, although they are likely due to social determinants of health (SDOH). The American Heart Association suggests that CKM syndrome screening should include both biological factors and SDOH. Interventions in patients with stages 0 to 3 CKM syndrome focus on preventing future cardiovascular events by management of excess adiposity, mainly through diet and exercise in the early stages, then through pharmacological treatment of metabolic syndrome components in later stages. There is a general acceptance that treatment of CKM syndrome should involve a holistic approach to prevention, screening, and management to improve outcomes and reduce long-term morbidity and mortality.
Am J Manag Care. 2024;30(suppl 10):S181-S188. https://doi.org/10.37765/ajmc.2024.89670
For author information and disclosures, see end of text.
Introduction
Type 2 diabetes (T2D), chronic kidney disease (CKD), and cardiovascular disease (CVD) represent major health challenges. An estimated 700 million1 and 523 million2 people worldwide have CKD and/or CVD. Current estimates indicate that, of the 529 million people with diabetes globally, the vast majority (96%) have T2D.3 Presence of these conditions leads to a substantial burden of morbidity and mortality, which disproportionately affects those in underrepresented racial and ethnic groups.4-7 In the US, CVD alone resulted in an age-adjusted mortality rate of 224.4 per 100,000 people in 2020.8 The US mortality rates for diabetes (diabetes refers to both type 1 and type 2 diabetes, unless otherwise specified) and CKD are estimated to be 12.9 per 100,000 people3 and 14.6 per 100,000,9 respectively. Furthermore, CVD, T2D, and CKD are now known to be more closely associated than previously thought, and this interconnection has been termed cardiovascular-renal-metabolic (CRM) syndrome. The American Heart Association (AHA) has recently redefined CRM syndrome as cardiovascular-kidney-metabolic (CKM) syndrome10; both terms are used interchangeably.
Prevalence of Cardiovascular-Kidney-Metabolic Syndrome
CKM conditions are common. A cross-sectional survey of 11,607 participants in the National Health and Nutrition Examination Survey (NHANES) from 1999 to 2020 estimated that 25% of participants had at least 1 cardiac, renal, or metabolic condition.11 The survey also showed that there is considerable overlap between CKM conditions, with 8% of participants (rising to 25% of participants aged ≥65 years) having more than 1 CKM condition.11
Comorbid CKM Conditions
The increased risk of CVD in people with T2D is well known, and in 1 study in 13 countries approximately one-third of people with T2D also had CVD.12 Increased hemoglobin A1c variability is associated with greater risk of incident CVD. Concomitant CKD is also common in patients with T2D with up to 40% of people with T2D also having CKD.13 Comorbid CKM conditions are also common in people with heart failure (HF). A meta-analysis of patients with HF across the spectrum of ejection fraction observed that 32% also had CKD.14 Similarly, a US-based study found that 64% of patients hospitalized for HF had estimated glomerular filtration rate (eGFR) <60 mL/min/1.73 m2.15 The prevalence of T2D is also common in patients with HF; an estimated 20% to 40% of people with HF have T2D16 and 16% of people with HF have both T2D and CKD.16 Approximately 35% of people with CKD also have diabetes17 and 50% of people with stage 3 to 5 CKD have CVD.18
Increasing Burden of CKM Conditions
The prevalence and burden of CKM conditions is increasing over time11 and this may be linked to increasing age,19 prevalence of T2D and obesity,20,21 physical inactivity,22 and poor control of hypertension.22,23 The prevalence of overlapping CKM conditions is also increasing.11 Ostrominski and colleagues observed a significant increase in the proportion of US adults with at least 2 CKM conditions between 1999 to 2000 and 2017 to 2020 and a doubling of the proportion of adults with all 3 CKM conditions in the same time periods.11 Multiple CKM conditions are more common with older age, male sex, self-reported non-Hispanic Black race or ethnicity, and adverse socioeconomic circumstances.11 Patients with multiple CKM conditions are at risk of increased mortality.24-27 In patients with both diabetes and CKD, the adjusted risk difference for cardiovascular (CV) mortality was 16%, compared with the risks conferred by T2D (3%) or CKD alone (6%).26 Although there has been a general decrease in CV mortality over the past 20 years,28 the decline in CVD mortality rates reversed during the COVID-19 pandemic in 2020 and mortality rates have remained high.29 Globally, overall CKD mortality is increasing despite decreasing mortality rates among patients with end-stage kidney disease.30 There remains a considerable difference in outcomes between male and female patients with components of CKM syndrome including CVD,31 CKD,32 and HF.33
Pathophysiology of Cardiovascular-Kidney- Metabolic Syndrome
The underlying pathophysiology of CKM syndrome is a result of the interrelationship among metabolic risk factors, CKD, and the CV system. Although there are a number of potential mechanisms underlying the relationships between CKM conditions (Figure 1),34 it is proposed that this syndrome primarily originates in excess and/or dysfunctional adipose tissue, which secretes proinflammatory and prooxidative products leading to damage to tissues in arteries, the heart, and the kidney,4,35-37 and reduction in insulin sensitivity.35,37
Staging of Cardiovascular-Kidney-Metabolic Syndrome
The AHA has recently proposed that CKM syndrome is classified into 4 stages (Table) based on presence of risk factors (stage 0, no CKM risk factors; stage 1, excess or dysfunctional adiposity but no evidence of subclinical or clinical CKD or CVD; stage 2, established metabolic risk factors or CKD; stage 3, subclinical CVD in CKM syndrome; stage 4, clinical CVD or Kidney Disease Improving Global Outcomes [KDIGO] stage 4 CKD).10
Risk Factors for Cardiovascular-Kidney-Metabolic Syndrome
Notably, the definition of CKM syndrome given in the AHA presidential advisory in 2023 includes patients who do not have clinical CVD but do have risk factors for CVD due to the presence of metabolic risk factors, CKD, or both; and individuals with existing CVD that is potentially related to or that may complicate metabolic risk factors or CKD.10
Further to the risk inherent in each of the CKM conditions, there are several known risk factors for progression of CKM. The AHA estimates that 1 in 3 people have risk factors that contribute to CVD, metabolic disorders, and/or kidney disease.38 In addition to the risk factors included in the staging system, these include chronic inflammatory conditions (eg, psoriasis, rheumatoid arthritis, lupus, HIV/AIDS), family history of diabetes or kidney disease, mental health and sleep disorders, increased levels of elevated high-sensitivity C-reactive protein, and sex-specific risk enhancers such as premature menopausal transition, adverse pregnancy outcomes, and polycystic ovary syndrome.10 There are substantial racial and ethnic differences in a number of these risk factors, including the metabolic risk factors.39 While some genetic factors underlie these differences (for example, people with South Asian ancestry are likely to have a higher proportion of ectopic body fat at any given body mass index [BMI]40), the primary driver of the racial and ethnic differences is the adverse effects of social determinants of health (SDOH).41,42
Social Determinants of Health
The impact of SDOH on incidence and outcomes in CVD, CKD, and diabetes has become increasingly apparent in recent years. In 1 analysis of the NHANES study, SDOH were completely responsible for the disparity in CV mortality between Black/African American and White American populations.43 In the analysis of the NHANES survey by Ostrominski et al, the burden of comorbidities in people with CKM conditions was disproportionately high among participants who were unemployed, had lower socioeconomic status, and without a high school degree.11 The AHA proposes that epigenetic factors predisposing an individual to CKM syndrome should be viewed in context of SDOH (Figure 2).44
Screening for Cardiovascular-Kidney-Metabolic Syndrome
The AHA suggests that screening should include both biological factors and SDOH.10 In adults, screening recommendations are based on CKM stage and include measurement of adiposity via annual BMI and waist circumference measurements in all patients. Adults with stage 0 CKM should be screened for components of metabolic syndrome every 3 to 5 years. In adults with stage 1 CKM, this should be done every 2 to 3 years, and in adults with stage 2 or higher CKM, annual screening should be performed. Kidney function tests (urine albumin-creatinine ratio and eGFR) are proposed for accurate KDIGO staging and should be performed annually in stage 2 or higher CKM, and more frequently in those with higher KDIGO risk.
Risk calculations are available for CVD including the Framingham Risk Score for coronary heart disease,45 the American College of Cardiology (ACC)/AHA pooled cohort equations,46 and the American Diabetes Association 2024 Standards of Care,47 although none of these adequately account for SDOH. However, recognition of the impact of SDOH on CVD risk, changes in the prevalence of risk factors, and changes in available therapies has meant that newer predictive equations are warranted to include the effects of SDOH. This was the impetus for the AHA to develop a new risk prediction equation.10 The PREVENT equation48 provides 10- and 30-year risk estimates for total CVD and includes CKM factors and SDOH. Controversially, the calculation deliberately excludes race as a factor, and instead uses the social deprivation index. The equation has shown good calibration among Black individuals but has not been extensively tested in other racial/ethnic groups. Most tools evaluate financial strain, education/literacy, personal safety, and whether the person requires assistance in addressing their social needs.49-52 Tools that incorporate assessment of behaviors affected by SDOH, such as the Oregon Community Health Information Network53 and Centers for Medicare & Medicaid Services,50 may be of particular value.
Management of Cardiovascular-Kidney-Metabolic Syndrome
Currently available treatment guidelines for CKM conditions are discussed in the other articles in this supplement.54,55 It is known that having multiple CKM conditions is associated with increased mortality11; to address the increase in CV mortality, the totality of the CKM burden should be considered.
Interventions for people with stage 0 to 3 CKM syndrome focus on preventing future CV events by management of excess adiposity. This is mainly accomplished through diet and exercise in stage 1, and through pharmacological treatment of metabolic syndrome components in stage 2 (Figure 3).10 In subclinical CVD (stage 3 CKM syndrome), patients should be treated to manage their CKM conditions. In more advanced disease (stage 4), patients should be treated according to the relevant guidelines to manage their CKM conditions (ADA, ACC/AHA/Heart Failure Society of America [HFSA], KDIGO).
Aside from specific recommendations for treatment and management, there is acceptance that treatment of CKM syndrome should include a multispecialty team. This is recognized by the AHA Life’s Essential 8 construct,56 which specifies the need to move beyond subspecialty silos to collaborative interdisciplinary care models. Studies have observed that a coordinated, multifaceted intervention increased prescription of evidence-based therapies in adults with T2D and atherosclerotic CVD.57,58 This was irrespective of sex, race, or ethnicity.59 Team-based care is crucial and time constraints should be considered for members of the multispecialty team, including physicians, physician’s assistants, nurse practitioners, nurses, pharmacists, dieticians, exercise therapists, mental health specialists, and social workers. Attention should also be paid to how the support structures around the patient can support implementation of CKD guidance, whether they be family, or community and religious groups.10 Increasing health literacy is essential for people living with, or at risk of, CKM. This is particularly important in people in different racial and ethnic populations or disadvantaged groups, who traditionally have a greater number of metabolic risk factors.
Conclusions
The complexity of CKM syndrome as a multifaceted condition requires a holistic approach to prevention, screening, and management. Because of the high burden of CKM conditions, which is magnified in patients with multiple conditions, optimal prevention, screening, and management are required to improve outcomes and reduce long-term morbidity and mortality.
Disparities in prevalence of CKM conditions and outcomes are persistent and getting worse, not only based on race and ethnicity, but also sex, geography, socioeconomic status, ability, or disability. Targeted interventions are needed to identify and eliminate these disparities, and as health care professionals, we have a moral and a practical imperative to address them.
Acknowledgments
The author meets criteria for authorship as recommended by the International Committee of Medical Journal Editors. The author did not receive payment related to the development of the manuscript. Writing support was provided by Jonathon Gibbs of Elevate Scientific Solutions LLC, contracted and funded by Boehringer Ingelheim Pharmaceuticals, Inc (BIPI) and Lilly USA, LLC. BIPI and Lilly were given the opportunity to review the manuscript for medical and scientific accuracy as well as intellectual property considerations.
Author Affiliation: Section of Cardiology, Tulane University School of Medicine, New Orleans, LA.
Funding Source: This supplement was supported by Boehringer Ingelheim Pharmaceuticals, Inc and Lilly USA, LLC.
Author Disclosures: Dr Ferdinand reports serving as a consultant for Boehringer Ingelheim, Janssen, Lilly, Medtronic, and Novartis.
Authorship Information: Concept and design; drafting of the manuscript; and critical revision of the manuscript for important intellectual content.
Address Correspondence to: Keith C. Ferdinand, MD, Tulane University School of Medicine, 1430 Tulane Ave #8540, New Orleans, LA 70112. Email: kferdina@tulane.edu
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