Key result
This letter discusses the transition from mechanistic biomarker signals to clinically actionable evidence in the management of cardiovascular-kidney-metabolic disease.
This letter emphasizes the need for cardiovascular-kidney-metabolic biomarkers to demonstrate clinical utility and trigger actionable management changes beyond biological plausibility.
We read with interest the review by Marshall et al.,1 which reframes cardiovascular-kidney-metabolic disease as an interconnected biological network and highlights the limits of conventional markers, such as estimated glomerular filtration rate, albuminuria, natriuretic peptides, lipids, and glycated hemoglobin. Its discussion of biomarker “silence,” metabolic dysfunction-associated steatotic liver disease (MASLD), and multiomics-enabled endotyping is timely. Our aim is not to diminish this contribution, but to clarify where mechanistic signal should end and clinically actionable evidence should begin.
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Wu et al. (2026) conducted a letter in Cardiovascular-kidney-metabolic disease. This letter discusses the transition from mechanistic biomarker signals to clinically actionable evidence in the management of cardiovascular-kidney-metabolic disease.
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