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Review
. 2025 Sep;41(6):e70083.
doi: 10.1002/dmrr.70083.

Metabolic Cardiovascular Renal Disease (Met-CVRD): A New Nomenclature

Affiliations
Review

Metabolic Cardiovascular Renal Disease (Met-CVRD): A New Nomenclature

Paolo Pozzilli et al. Diabetes Metab Res Rev. 2025 Sep.

Abstract

Cardiovascular Renal Disease (CVRD) has been introduced as a syndrome describing the coexistence of certain common diseases. However, this terminology misses the role of metabolic abnormalities not only as relevant comorbidities, but even more as key causal factors. Thus, the word 'metabolic' should come first to define this syndrome as its joint underlying pathogenesis. Although, CVRD and type 2 diabetes (T2D) have historically been treated as coexisting but separate conditions, growing evidence underscores a bidirectional and metabolically driven relationship between the heart and kidneys, mediated by upstream processes. These comprise insulin resistance, ectopic lipid deposition, mitochondrial abnormalities, dyslipidaemia and chronic low-grade inflammation, typical of T2D and the metabolic syndrome. These metabolic disturbances begin silently in early adulthood, well before traditional clinical markers can signal CVRD onset. Here, we introduce the new terminology of Metabolic Cardiovascular Renal Disease (Met-CVRD), to indicate that the word 'Metabolic' represents its major pathogenic factor. We then discuss then the necessity of prioritising early at-risk individual identification and prompt intervention with cardiorenal-protective therapies like glucagon-like peptide-1 (GLP-1) receptor agonists and sodium-glucose cotransporter-2 (SGLT2) inhibitors. Met-CVRD provides a cohesive and proactive strategy to halt the advancement of cardiorenal disease across several systems by transcending organ-specific frameworks.

Keywords: cardiovascular renal disease; metabolic syndrome; type 2 diabetes.

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Conflict of interest statement

The authors declare no conflicts of interest.

Figures

FIGURE 1
FIGURE 1
The central role of metabolic dysfunction in the pathogenesis of CVKD. This diagram illustrates the progressive development of Met‐CVRD in different stages, starting from early metabolic dysfunction to advanced clinical outcomes. Stage 1: Characterized by excess or dysfunctional adipose tissue, leading to metabolic disturbances such as overweight/obesity, impaired glucose tolerance, and fatty liver (ectopic fat). Stage 2: Involves key metabolic risk factors including elevated fasting blood glucose, hypertension, hypertriglyceridaemia, low HDL cholesterol, and abdominal obesity, all contributing to the development of cardiorenal damage. Stage 3: Represents the subclinical stage of atherosclerotic cardiovascular disease (ASCVD), heart failure (HF), and CKD, marked by early atherosclerosis, declining kidney function, and early signs of HF. Stage 4: Reflects overt Met‐CVRD associated with advanced CKD, Coronary Heart Disease (CHD), myocardial infarction, HF, Stroke, Peripheral Artery Disease (PAD), T2D, and Atrial Fibrillation (Afib).

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