Nefrología · Nov 2026
Early Vascular Aging in Diabetic Kidney Disease: Mechanisms, Clinical Assessment, and Emerging Therapeutic Strategies
By Piko N, Morales E, Jose MV et al.
Diabetic chronic kidney disease (CKD) is associated with a markedly increased risk of cardiovascular disease, largely driven by accelerated early vascular aging (EVA). EVA results from the interplay between traditional cardiovascular risk factors and CKD-specific mechanisms that promote premature structural and functional arterial damage. Emerging pathophysiological processes, including chronic inflammation, oxidative stress, mitochondrial dysfunction, cellular senescence, accumulation of advanced glycation end-products and uremic toxins, gut dysbiosis, vitamin K deficiency, and vascular calcification, contribute to arterial stiffness, endothelial dysfunction, and cardiovascular complications. Clinical assessment of vascular aging extends beyond conventional kidney function measures and includes biomarkers such as albuminuria, inflammatory mediators, coronary artery calcium score, and carotid–femoral pulse wave velocity, the current gold standard for assessing arterial stiffness. Current management relies on aggressive control of cardiovascular risk factors and implementation of evidence-based therapies, including renin–angiotensin system inhibitors, sodium–glucose cotransporter-2 inhibitors, finerenone, and glucagon-like peptide-1 receptor agonists. However, substantial residual cardiovascular risk remains. Novel therapeutic strategies targeting inflammation, oxidative stress, cellular senescence, vascular calcification, and the gut–kidney axis may further attenuate vascular aging. A deeper understanding of these mechanisms may facilitate precision medicine approaches and improve cardiovascular and renal outcomes in patients with diabetic CKD.