Atherosclerosis is a closely related complication of diabetes mellitus (DM), driven by endothelial dysfunction, inflammation, and oxidative stress. The progression of atherosclerosis is accelerated by hyperglycemia, insulin resistance, and hyperlipidemia. Novel antidiabetic agents, SGLT2 inhibitors, and GLP-1 agonists improve glycemic control and offer cardiovascular protection, reducing the risk of major adverse cardiovascular events (MACEs) and heart failure hospitalization. These agents, along with nonsteroidal mineralocorticoid receptor antagonists (nsMRAs), promise to mitigate metabolic disorders and their impact on endothelial function, oxidative stress, and inflammation. This review explores the potential molecular mechanisms through which these drugs may prevent the development of atherosclerosis and cardiovascular disease (CVD), supported by a summary of preclinical and clinical evidence.

Acute kidney injury (AKI) is a frequent and severe complication in trauma patients, affecting up to 28% of intensive care unit (ICU) admissions and contributing significantly to morbidity, mortality, and long-term renal impairment. Trauma-related AKI (TRAKI) arises from diverse mechanisms, including hemorrhagic shock, ischemia–reperfusion injury, systemic inflammation, rhabdomyolysis, nephrotoxicity, and complex organ crosstalk involving the brain, lungs, and abdomen. Pathophysiologically, TRAKI involves early disruption of the glomerular filtration barrier, tubular epithelial injury, and renal microvascular dysfunction. Inflammatory cascades, oxidative stress, immune thrombosis, and maladaptive repair mechanisms mediate these injuries. Trauma-related rhabdomyolysis and exposure to contrast agents or nephrotoxic drugs further exacerbate renal stress, particularly in patients with pre-existing comorbidities. Traditional markers such as serum creatinine (sCr) are late indicators of kidney damage and lack specificity. Emerging structural and stress response biomarkers—such as neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule 1 (KIM-1), liver-type fatty acid-binding protein (L-FABP), interleukin-18 (IL-18), C-C motif chemokine ligand 14 (CCL14), Dickkopf-3 (DKK3), and the U.S. Food and Drug Administration (FDA)-approved tissue inhibitor of metalloproteinases-2 × insulin-like growth factor-binding protein 7 (TIMP-2 × IGFBP-7)—allow earlier detection of subclinical AKI and better predict progression and the need for renal replacement therapy. Together, functional indices like urinary sodium and fractional potassium excretion reflect early microcirculatory stress and add clinical value. In parallel, risk stratification tools, including the Renal Angina Index (RAI), the McMahon score, and the Haines model, enable the early identification of high-risk patients and help tailor nephroprotective strategies. Together, these biomarkers and risk models shift from passive AKI recognition to proactive, personalized management. A new paradigm that integrates biomarker-guided diagnostics and dynamic clinical scoring into trauma care promises to reduce AKI burden and improve renal outcomes in this critically ill population.

Thyroid hormone (TH) imbalances, particularly subclinical hypothyroidism (SCHT), are associated with chronic kidney disease (CKD) and end-stage kidney disease (ESKD). SCHT is more prevalent in CKD and ESKD patients than in the general population, and this condition increases the risk of cardiovascular disease (CVD) morbidity and mortality. The risk of CVD is higher in CKD and ESKD patients compared with the general population. Traditional and nontraditional risk factors, including TH abnormalities, contribute to the high CVD burden in CKD and ESKD patients. The review discusses the link between CKD and hypothyroidism, with a focus on SCHT, and the mechanisms that lead to CVD burden.

Even though nephrology has made much progress, reducing the progression of the chronic kidney disease remains, in fact, one of the biggest challenges. Long before the renal replacement therapy (RRT), it was known that limiting the protein could help almost all uremia symptoms. Although it was proposed as early as the 1960s, it only became widely used in the 1980s. By lowering the urea and other nitrogen wastes and lowering the metabolic acidosis, oxidative stress, and insulin resistance, limiting the amount of protein in your diet can help improve uremic symptoms. Also, limiting the protein in the diet positively controls the cardiovascular complications, including the arterial blood pressure and proteinuria reduction, which are risk factors for CKD progression. This mini-review examines the impact of protein restriction on the possibility of slowing CKD progression in depth.