90 percent of U.S. adults have CKM syndrome - defined in 2023

Washington Post - July 2026

  • "CKM syndrome was only recently coined, in 2023, by the American Heart Association. And roughly 9 in 10 U.S. adults — about the same number of people estimated to have it — have never heard of it."
  • "CKM syndrome is not one disease but rather “a broad disorder that recognizes the overlap between cardiovascular, kidney and metabolic conditions such as diabetes and obesity,” said Muthiah Vaduganathan, a cardiologist at Brigham and Women’s Hospital who has conducted landmark studies on CKM syndrome. Doctors have long known that people often have more than one of these conditions at once. CKM syndrome reflects a newer understanding that the very same factors — specifically, extra weight, high blood pressure, high blood sugar, abnormal cholesterol and reduced kidney function — can contribute to the onset and progression of all three types of disease, Vaduganathan said."

Overview of CKM

Claude AI July 2026CKM syndrome is well within what I can explain, but since this is a medical construct that's been actively evolving (staging systems, risk tools, and guideline updates), let me verify the current state before I lay it out for you.There's been a significant development I want to get right — the first formal guideline was just released. Let me pull the specifics on staging. Cardiovascular-Kidney-Metabolic (CKM) syndrome is a clinical framework the American Heart Association introduced in a November 2023 Presidential Advisory, defining it as a systemic disorder characterized by pathologic interactions among metabolic risk factors, chronic kidney disease, and cardiovascular disease that lead to multiorgan dysfunction and an increased rate of cardiovascular events. The core idea is that these three domains have historically been managed in separate silos (cardiology, nephrology, endocrinology) despite sharing a common pathophysiologic root — excess or dysfunctional adiposity, particularly visceral fat — and that treating them as one interconnected condition improves outcomes.

One important update since you may have last looked: on June 9, 2026, the ACC, AHA, ADA, and ASN jointly issued the first-ever formal clinical practice guideline on CKM syndrome, published in both Circulation and JACC. This moves CKM from an advisory/conceptual framework to a full guideline with graded recommendations, and it notably retires and replaces the 2013 AHA/ACC/TOS obesity management guideline.

The staging system is the heart of the framework — five stages (0–4) that can progress or regress:

  • Stage 0 — health, no CKM risk factors.
  • Stage 1 — excess/dysfunctional adiposity: BMI ≥25, waist circumference ≥88 cm (women) or ≥102 cm (men), or impaired glucose tolerance/prediabetes, without other metabolic risk factors or CKD.
  • Stage 2 — metabolic risk factors or CKD: hypertriglyceridemia (≥135 mg/dL), hypertension, metabolic syndrome, diabetes, or moderate-to-high-risk CKD.
  • Stage 3 — subclinical CVD or its risk equivalents (high predicted 10-year CVD risk or very-high-risk CKD). The new guideline pins one Stage 3 criterion at ≥20% predicted 10-year CVD risk via PREVENT.
  • Stage 4 — clinical CVD, subdivided into 4a (without kidney failure) and 4b (with kidney failure).

A key methodological point you'll appreciate: clinical staging is dynamic in the early phases — with sustained metabolic improvement, individuals can regress to earlier stages, which is a deliberate departure from the usual one-directional disease-staging model.

Risk assessment shifted with this framework. The old 2013 Pooled Cohort Equations were replaced by the PREVENT equations (Predicting Risk of Cardiovascular Disease Events), which incorporate renal and metabolic parameters and estimate both 10-year and 30-year risk of CVD, ASCVD, and heart failure in people aged 30–79. Notably, PREVENT deliberately excludes race and instead optionally incorporates UACR, HbA1c, and a zip-code-based social deprivation index. Worth flagging on the epidemiology side: the PREVENT equations may underestimate risk in South Asian adults, who face higher diabetes risk at lower BMIs — a real limitation for a tool being used to gate statin and antihypertensive decisions.

Therapeutically, the framework is built around a stage-escalating, multidrug backbone. The two drug classes doing the heavy lifting across all three domains are SGLT-2 inhibitors and GLP-1 receptor agonists, both of which offer cardiovascular and kidney protection alongside glycemic and weight effects. Layered on are ACE inhibitors/ARBs, statins, and the nonsteroidal MRA finerenone for albuminuria. A recurring theme in the trial evidence is that SGLT-2 inhibitors don't work by improving isolated disease processes but function across the whole CKM triangle, which is really the mechanistic justification for the unified framework.

Scale of the problem: nearly 90% of US adults have at least one CKM risk factor, with obesity affecting 40% of adults and 21% of children and adolescents. And the staging carries prognostic weight — a 2026 meta-analysis of over 10 million participants across 9 cohorts found mortality risk increased significantly with advancing CKM stage.

Two things I'd flag honestly given your work:

First, albuminuria is arguably the framework's most underappreciated linchpin — it reflects global vascular endothelial dysfunction and independently predicts both kidney and cardiovascular outcomes at levels as low as a UACR of 10 mg/g, well below the conventional 30 mg/g CKD threshold. That's a cheap, widely available biomarker being underused.

Second, and relevant to your domain: the CKM framework as constructed is essentially adiposity-centric and pharmacotherapy-forward. Vitamin D does not feature in the AHA staging or the core recommendations, despite the substantial observational literature linking vitamin D status to each of the three arms

  • (insulin resistance,
  • CKD progression via the FGF23/klotho axis, and
  • cardiovascular outcomes).

Critics have also noted the staging omits hepatic biomarkers even though liver fat accumulation precedes insulin resistance by 5–7 years. Whether these omissions reflect genuinely weak causal evidence or the "profitable ignorance" pattern you track — unpatentable interventions getting structurally under-weighted relative to the GLP-1/SGLT-2/finerenone drug classes that dominate the trial base — is an open and, I'd argue, worthwhile question.

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