Preventing Type 2 Diabetes in At-Risk Cardiorenal Populations

The convergence of cardiovascular disease, chronic kidney disease, and type 2 diabetes, collectively known as cardiovascular-kidney-metabolic syndrome, affects the majority of US adults. That construct spans a broader population than kidney disease alone, and this review is concerned with a narrower one: patients with chronic kidney disease who are prediabetic or otherwise at risk for incident type 2 diabetes. In these patients, prediabetes represents both a warning and an opportunity. Dysglycemia is common, its progression is detectable early, and preventing it is expected to benefit both the heart and the kidney, a benefit inferred from the mechanisms the two organs share rather than demonstrated directly in outcome trials in this population. Prediabetes is not uniform, and rates of progression and regression vary. Prevention here is not a metabolic problem applied to sicker patients. It is a cardiorenal strategy, because dysglycemia contributes to several of the mechanisms coupling the heart and kidney. This review examines the evidence for diabetes prevention in patients with chronic kidney disease, the identification of patients at highest risk, and the operational structure required to translate evidence into practice. Lifestyle modification remains the foundation and is supported by decades of durable evidence, adapted to the dietary and functional constraints of kidney disease, though real-world adherence falls short of what trial conditions achieved. Metformin is a reasonable pharmacologic addition in selected patients. The agents that have most powerfully transformed cardiorenal medicine, sodium-glucose cotransporter-2 inhibitors and glucagon-like peptide-1 receptor agonists, are not diabetes prevention agents on current evidence, but the prediabetic patient often already qualifies for them on renal and cardiac grounds alone. This fact is frequently missed in clinical practice. Prevention succeeds when the modifiable drivers of disease are addressed early and without deferral, when organ-protective therapy is initiated on the indications that exist rather than withheld pending a diagnosis not yet made, and when responsibility is shared explicitly between nephrology and cardiology rather than defaulted at the interface between them. The principal barriers to prevention are organizational rather than clinical.