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.