Cardiovascular-Kidney-Metabolic Health · Educational Tool

The Kidney–Heart Connection

An interactive explorer of how the kidney shapes cardiovascular risk — built around the American Heart Association’s CKM framework and PREVENT equations, the KDIGO risk grid, and the 2026 AHA/ACC/ADA/ASN CKM guideline.

After using this tool, a learner can…

  • Explain why the kidney drives — not merely accompanies — cardiovascular disease.
  • Place a patient on the CKM staging continuum (Stage 0–4).
  • Read the KDIGO eGFR × albuminuria grid and link it to cardiovascular outcomes.
  • Recognise that eGFR and urine albumin sit inside the AHA PREVENT equations.
  • Anticipate the cardiovascular consequences of CKD — heart failure across the ejection-fraction spectrum, atherosclerotic disease, atrial fibrillation, and resistant hypertension — and match organ-protective therapy to them.

New to CKM? Start here. Cardiovascular-Kidney-Metabolic (CKM) syndrome describes how heart disease, kidney disease, and metabolic risk drive one another. The American Heart Association (AHA) defined it in 2023; in 2026 the AHA, the American College of Cardiology, the American Diabetes Association, and the American Society of Nephrology (ASN) issued the first joint guideline. The shift for practice: the kidney is an early driver of cardiovascular risk, not a late bystander.

What you get: a free, about 15-minute interactive walkthrough that lets you stage any patient on the CKM continuum, read their heart–kidney risk, and choose therapy that protects both organs at once.

1The continuum

Cardiovascular-Kidney-Metabolic (CKM) staging

In 2023 the American Heart Association defined CKM syndrome; in 2026 the first full multi-society guideline (AHA/ACC/ADA/ASN) operationalised it for practice. The pattern clinicians see daily: the heart, kidneys, and metabolism fail together — and the kidney enters the staging early and explicitly. Select a stage to explore where it fits.

2026 CKM guideline at a glance. Screen kidney risk with eGFR and UACR; a renin-angiotensin system inhibitor (especially with albuminuria) and an SGLT2 inhibitor are foundational in albuminuric CKD and in CKD with type 2 diabetes; add, where indicated, a GLP-1 receptor agonist; layer a nonsteroidal MRA (finerenone) when albuminuria persists — with benefit now reaching heart failure with mildly reduced or preserved ejection fraction (LVEF ≥40%; FINEARTS-HF). The PREVENT equations estimate 10- and 30-year risk (20% or more 10-year risk marks Stage 3), and care is coordinated through a designated interdisciplinary point person.
The kidney is not a late complication here. Moderate- or high-risk chronic kidney disease already qualifies a patient for CKM Stage 2, and very-high-risk CKD contributes to Stage 3 — before any clinical heart disease appears.
2See the risk

The kidney–heart risk grid

Two simple kidney measures — eGFR (how well the kidney filters) and albuminuria (protein leak, a marker of vascular injury) — map risk on the KDIGO grid. Moving down and to the right, the risk of kidney failure and of cardiovascular events and death rises together. Select any cell.

KDIGO risk grid — pick a kidney profile
Albuminuria category (mg/g)
A1
<30		A2
30–300		A3
>300

Colour = KDIGO risk category for adverse kidney and cardiovascular outcomes.

Low Moderately increased High Very high
Why this mattersThe AHA PREVENT equations were the first major risk tool to fold kidney and metabolic measures into cardiovascular prediction.
eGFR — base inputEstimated GFR is a core, required variable in every PREVENT model.
Urine albumin — enhancerUACR is an optional refinement that sharpens the estimate.

In short: the same grid a nephrologist uses to stage kidney disease feeds directly into the equation a cardiologist uses to predict heart attack, stroke, and heart failure. Kidney and heart risk are one conversation.

3The mechanisms

Why the kidney drives cardiovascular disease

The link is not shared risk factors alone. Failing kidneys actively injure the cardiovascular system through several pathways. Expand each to see how.

3bThe cardiovascular toll

What CKD does to the heart and vessels

Kidney damage surfaces as specific cardiovascular phenotypes — the reason CKM staging is anchored in cardiovascular outcomes, not kidney numbers alone.

Heart failure — across the ejection-fraction spectrum. Volume overload, uraemic cardiomyopathy, and left-ventricular hypertrophy drive HF with reduced and with preserved EF. Finerenone reduces heart-failure events in mildly reduced or preserved ejection fraction (LVEF ≥40%; FINEARTS-HF); SGLT2 inhibitors cut HF hospitalisation.
Atherosclerotic cardiovascular disease. CKD accelerates ASCVD through inflammation, vascular calcification, and dyslipidaemia, and acts as a risk-enhancing factor that raises predicted risk in the PREVENT equations.
Atrial fibrillation and sudden death. Electrolyte shifts, myocardial fibrosis, and autonomic dysfunction raise arrhythmia and sudden-cardiac-death risk as eGFR falls.
Hypertension and cardiorenal syndrome. Sodium retention and neurohormonal activation produce often-resistant hypertension; a failing heart and failing kidney then worsen each other in the cardiorenal syndromes.
For the clinician: staging a patient by kidney risk is, in effect, staging their cardiovascular risk — and it changes which organ-protective therapy you reach for first.
4Shared targets

One treatment, two organs protected

Interactive companion: the Organ-Protective Therapy Selector lets you build a CKM / obesity–kidney scenario and see how the RAAS inhibitor, SGLT2i, GLP-1 RA and finerenone layers are chosen, with trial evidence and safety thresholds.

Because the kidney and heart share the same disease axis, they also share therapies. Selected agents from three drug classes have shown cardiovascular and/or kidney benefit in defined populations — each proven in large randomized trials. Select a class.

These are educational summaries of trial populations, not treatment recommendations. Eligibility, drug choice, and dosing are individual clinical decisions.
5Practice

Case-based check

Short cases with immediate, referenced feedback. There is no scoring and nothing is recorded — this is for learning, not assessment.

★Self-check

Rate your confidence — before and after

A 20-second self-assessment. Rate your confidence on three core ideas, work through the explorer, then re-rate. Nothing is stored; this is a learning aid.

Are you a clinician, fellow, or student? Help improve this tool with a short, anonymous ~20-minute feedback survey — a quick knowledge check, the tool, then a few questions.
Take the feedback survey →

Go deeper — the written guides

Short, primary-source-cited companion articles to this tool.

All guides in the Learn hub →

✓Sources

References

Accessibility: designed to WCAG 2.2 AA — keyboard-navigable, screen-reader labelled (ARIA roles and live regions) and AA-contrast colours. Fully browser-based; no data is collected or transmitted. An independent WCAG 2.2 AA conformance audit is planned.

Version 1.1 · evidence current to the 2026 CKM guideline · an independent clinician-education resource (Nephrobesity is an educational platform, not a commercial or patient-marketing site).

  1. American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. 2026 AHA/ACC/ADA/ASN Guideline for the Prevention, Detection, Evaluation, and Management of Cardiovascular-Kidney-Metabolic Syndrome. J Am Coll Cardiol. 2026. doi:10.1016/j.jacc.2026.03.056
  2. Ndumele CE, Rangaswami J, Chow SL, et al. Cardiovascular-Kidney-Metabolic Health: A Presidential Advisory From the American Heart Association. Circulation. 2023;148(20):1606–1635. doi:10.1161/CIR.0000000000001184
  3. Khan SS, Coresh J, Pencina MJ, et al. Development and Validation of the American Heart Association’s PREVENT Equations. Circulation. 2024;149(6):430–449. doi:10.1161/CIRCULATIONAHA.123.067626
  4. Kidney Disease: Improving Global Outcomes (KDIGO) CKD Work Group. KDIGO 2024 Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease. Kidney Int. 2024;105(4S):S117–S314. doi:10.1016/j.kint.2023.10.018
  5. Heerspink HJL, et al. Dapagliflozin in patients with chronic kidney disease (DAPA-CKD). N Engl J Med. 2020. doi:10.1056/NEJMoa2024816
  6. The EMPA-KIDNEY Collaborative Group. Empagliflozin in patients with chronic kidney disease (EMPA-KIDNEY). N Engl J Med. 2023. doi:10.1056/NEJMoa2204233
  7. Perkovic V, et al. Effects of semaglutide on chronic kidney disease in type 2 diabetes (FLOW). N Engl J Med. 2024. doi:10.1056/NEJMoa2403347
  8. Bakris GL, et al. Effect of finerenone on chronic kidney-disease outcomes in type 2 diabetes (FIDELIO-DKD). N Engl J Med. 2020. doi:10.1056/NEJMoa2025845
  9. Pitt B, et al. Cardiovascular events with finerenone in kidney disease and type 2 diabetes (FIGARO-DKD). N Engl J Med. 2021. doi:10.1056/NEJMoa2110956
  10. Solomon SD, et al. Finerenone in heart failure with mildly reduced or preserved ejection fraction (FINEARTS-HF). N Engl J Med. 2024. doi:10.1056/NEJMoa2407107
Educational use only. This tool teaches concepts about the kidney–cardiovascular relationship for health professionals, trainees, and students. It does not calculate an individual patient’s risk, is not medical advice, and does not replace clinical judgement or formal risk calculators. The PREVENT equations are validated for adults aged 30–79 without established cardiovascular disease. Nothing entered or selected here is sent, collected, or stored — the tool runs entirely in your browser.

Written and maintained by Amir S. Naderi, MD, FASN — board-certified in Internal Medicine and Nephrology, with a clinical focus on obesity medicine. Last reviewed July 2026.

An independent educational resource. It is not affiliated with, endorsed by, sponsored by, reviewed by, or produced in cooperation with the American Heart Association or any other professional society, guideline body, or commercial entity. AHA scientific statements, guidelines, and frameworks — including the CKM construct and the PREVENT equations — are referenced and cited here as published literature; their use does not imply any endorsement by, or association with, the issuing organisations.