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Chronic Kidney Disease and Diabetes / Liver Disease Diagnosis and Treatment / Diabetes, Cardiovascular Risks, and Lipoproteins · Review
Medicina · September 10, 2026
A consensus or society position rather than new primary data.
This narrative review synthesizes current evidence and expert opinion on the overlapping cardiovascular-kidney-metabolic syndrome and its hepatic dimension, proposing a broader cardio-reno-hepato-metabolic axis. It covers definitions, pathophysiology, diagnostic strategies, and emerging pharmacotherapies including resmetirom, semaglutide, SGLT2 inhibitors, GLP-1 receptor agonists, and non-steroidal mineralocorticoid receptor antagonists, but does not present new comparative effectiveness data or hard clinical outcomes.
Narrative review. Individuals with or at risk for metabolic syndrome, prediabetes, metabolic dysfunction-associated steatotic liver disease, and cardiovascular-kidney-metabolic comorbidities..
Metabolic syndrome defined by coexistence of hypertension, central obesity, dyslipidemia, and impaired glucose metabolism with underlying insulin resistance, chronic inflammation, and oxidative stress Prediabetes defined by American Diabetes Association as HbA1c 5.7–6.4%, fasting plasma glucose 100–125 mg/dL, or two-hour plasma glucose 140–199 mg/dL Growing evidence indicates metabolic dysfunction-associated steatotic liver disease (MASLD) interacts bidirectionally with cardiovascular, renal, and metabolic dysfunction
Does not report comparative effectiveness or clinical outcomes (mortality, cardiovascular events, disease progression rates) for any therapeutic strategy.
Clinicians should recognize the bidirectional interaction between hepatic, cardiovascular, renal, and metabolic dysfunction and consider integrated diagnostic and therapeutic approaches. Recent approvals of resmetirom and semaglutide for metabolic dysfunction-associated steatohepatitis, alongside SGLT2 inhibitors and GLP-1 receptor agonists, expand pharmacological options, though this review does not quantify their comparative benefit.
This is a narrative review synthesizing current understanding of cardiovascular-kidney-metabolic syndrome and hepatic involvement, offering diagnostic and therapeutic recommendations rather than reporting original research evidence.
As stated by the source record.
Quoted from the source exactly as published.
Clinicians should recognize the bidirectional interaction between hepatic, cardiovascular, renal, and metabolic dysfunction and consider integrated diagnostic and therapeutic approaches. Recent approvals of resmetirom and semaglutide for metabolic dysfunction-associated steatohepatitis, alongside SGLT2 inhibitors and GLP-1 receptor agonists, expand pharmacological options, though this review does not quantify their comparative benefit.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
Metabolic syndrome came to the attention of the scientific community several decades ago, and its definition has undergone multiple changes over time. It is currently defined by the coexistence of hypertension, central obesity, dyslipidemia, and impaired glucose metabolism, with insulin resistance, chronic inflammation, and oxidative stress representing important underlying pathophysiological mechanisms. The latter two processes are major promoters of the onset and progression of atherosclerosis. In parallel, many individuals develop metabolic dysfunction-associated steatotic liver disease (MASLD), formerly called non-alcoholic fatty liver disease (NAFLD). Growing evidence indicates that MASLD may interact bidirectionally with cardiovascular, renal, and metabolic dysfunction and may contribute to cardiometabolic risk. These observations have prompted proposals for a broader cardio–reno–hepato–metabolic axis. However, MASLD is not currently included in the established cardiovascular-kidney-metabolic (CKM) definition or staging system, and its incorporation remains an evolving conceptual extension. Prediabetes is a reversible condition characterized by abnormal glucose levels that do not meet the diagnostic criteria for diabetes. The American Diabetes Association defines prediabetes as glycated hemoglobin (HbA1c) = 5.7–6.4%, fasting plasma glucose = 100–125 mg/dL, or two-hour plasma glucose during an oral glucose tolerance test = 140–199 mg/dL. This comprehensive review examines traditional and genetic risk determinants, shared pathophysiological mechanisms, diagnostic strategies, clinical manifestations, emerging phenotypes, circulating microRNAs as non-invasive biomarkers, complications, and the principal therapeutic strategies, including diet, exercise, and pharmacotherapy. Particular attention is given to the recent approvals of resmetirom and semaglutide for metabolic dysfunction-associated steatohepatitis and to the expanding roles of sodium-glucose cotransporter 2 (SGLT2) inhibitors, glucagon-like peptide-1 (GLP-1) receptor agonists and non-steroidal mineralocorticoid receptor antagonists. Cardiovascular, renal, metabolic, and hepatic disorders are frequently present in the same patient. Other individuals may develop this high-risk cluster over time. The aim of this article is to define the interplay between different metabolic conditions and to outline the best approach to diagnosis, monitoring, and effective integrated therapy.
Taken from the source record, never inferred. Follow any of these and new work involving them reaches your briefing.