Comorbidity in Internal Medicine: Shared Mechanisms of Cardiovascular, Metabolic and Kidney Diseases

Cardiovascular, metabolic and kidney diseases frequently coexist and can accelerate one another through hemodynamic, inflammatory and metabolic pathways. The evidence base was assessed across the biological mechanisms and clinical implications of cardiovascular-metabolic-kidney overlap. Adipose dysfunction and insulin resistance affect vascular and renal physiology, while kidney impairment alters fluid balance, toxin clearance and endothelial function. Experimental work implicates oxidative stress and inflammasome signaling, but clinical outcomes cannot be inferred from pathway changes alone. Trials of sodium–glucose cotransporter-2 inhibitors, finerenone and semaglutide demonstrate that selected interventions can benefit more than one organ system in defined populations. Their effects nevertheless depend on the indication, baseline disease and endpoint; neutral results in other settings limit class-wide extrapolation. Risk assessment should integrate kidney function, albuminuria and conventional cardiovascular and metabolic factors rather than treat each diagnosis independently. Integrated care is supported by convergent biology and clinical trials, but treatment combinations and monitoring must remain grounded in the populations and outcomes actually studied.