Cardio-Renal-Metabolic connection – Do we have possibilities for solving this problem?

Within the continuum of cardiometabolic diseases, a cardiovascular-kidney-metabolic (CKM) syndrome has been conceptualised. The CKM syndrome is a systemic disorder characterised by pathophysiological interactions between metabolic risk factors, chronic kidney disease (CKD), and the cardiovascular system. CKM syndrome is characterised by multiorgan dysfunction and confers a high risk of adverse cardiovascular outcomes. Relevant haemodynamic and neurohormonal pathologies of the include the metabolic syndrome (central adiposity, insulin resistance, hypertension, hyperglycaemia, atherogenic dyslipidaemia), overactivity of the renin-angiotensin-aldosterone system (RAAS), oxidative stress, and systemic inflammation. The American Heart Association subdivides CKM syndrome into five stages according to risk factors and manifestations of the syndrome. Stage 0 is defined as having no risk factors for CKM and offers opportunities for primordial prevention. By stage 4, cardiovascular disease (CVD) is clinically evident in concert with metabolic risk factors. Stage 4 is partitioned by (a) the absence or (b) presence of chronic kidney disease (CKD). An interdisciplinary approach to clinical care is recommended. For each CKM stage, personalised management options are recommended to manage the syndrome and/or to prevent disease progression. Phenotypic heterogeneity is recognised which further complicates optimal prevention and management. Unhealthy lifestyles and relevant social determinants of disease should be identified and addressed where possible. The recently developed American Heart Association PREVENT equations offer risk estimates for total CVD that include atherosclerotic CVD and heart failure. Individual therapies are available that simultaneously improve multiple disease states within CKM. Pharmacotherapeutics with proven benefits in CKM syndrome include angiotensin-converting-enzyme inhibitors and angiotensin II receptor blockers, sodium-glucose cotransporter-2 inhibitors, the nonsteroidal mineralocorticoid receptor antagonist finerenone, and glucagon-like peptide 1 receptor agonists.