Abstract
Characterized by persistent hyperglycemia, diabetes mellitus triggers metabolic and inflammatory pathways that underlie microvascular (retinopathy, nephropathy, neuropathy) and macrovascular (coronary artery disease, stroke, peripheral arterial disease) complications. This article presents a critical synthesis of these outcomes, articulating pathophysiology, clinical implications, and therapeutic horizons. An integrative review (2015–2025) was conducted in PubMed/MEDLINE, SciELO, LILACS, Web of Science, and Scopus, including original studies, reviews, meta-analyses, guidelines, and reference chapters. The findings indicate that oxidative stress, glycation end products, endothelial dysfunction, and low-grade inflammation explain the progression of lesions, with clinical translation into preventable visual loss, renal function decline, pain, and dysautonomia, as well as diabetic foot, increased susceptibility to infections, slow wound healing, sexual dysfunction, and cognitive impairment. The discussion argues that glycemic control alone is insufficient: reducing events depends on multifactorial management, risk stratification, and timely screening. The conclusion is that therapies with cardiorenal benefits, the use of biomarkers, continuous glucose monitoring, and integrated care models represent promising avenues for reducing morbidity and mortality and preserving quality of life.