ReviewKidney international reports2026
Beyond eGFR and Albuminuria: Biological Pathways and Multiomics in Cardiovascular-Kidney-Metabolic Disease.
Review in Kidney international reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiovascular-kidney-metabolic disease (CKM) represents a growing public health challenge driven by the convergence of obesity, diabetes, and cardiovascular risk within aging populations. Despite major therapeutic advances, risk stratification remains anchored to conventional markers such as creatinine, urine albumin-to-creatinine ratio, natriuretic peptides, troponins, lipids, and glycated hemoglobin. Although prognostically useful, these parameters largely reflect established organ dysfunction rather than the upstream biological processes responsible for disease initiation and progression. Recent advances in proteomics, metabolomics, transcriptomics, and genomics offer promise in refining CKM from an organ-based construct towards a more integrated biological network characterized by immune activation, fibrosis, endothelial dysfunction, mitochondrial impairment, and endocrine crosstalk. Lipotoxic pathways underpinning metabolic dysfunction-associated steatotic liver disease are increasingly recognized within this network but are not yet formally incorporated into CKM staging. Emerging biomarkers may quantify these processes before overt organ dysfunction becomes apparent, identifying individuals who are biologically active but clinically silent. Integrating pathway-oriented biomarkers alongside established clinical measures may enable earlier, mechanism-informed risk stratification. As therapeutic options expand, including sodium-glucose cotransporter-2 (SGLT2) inhibitors, incretin-based therapies, and nonsteroidal mineralocorticoid receptor antagonists, aligning therapy with the appropriate biological phenotype presents a further challenge. Biomarker innovation may therefore bridge disease mechanisms and targeted treatment strategies. This review synthesizes the current understanding of molecular pathways underpinning CKM and examines novel biomarkers spanning inflammatory, fibrotic, metabolic, and microvascular biology. We discuss integrated multiomics strategies and artificial intelligence in refining risk prediction, identifying molecular endotypes, and guiding personalized treatment.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.