Sandra García Fuentes

Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD) has emerged as one of the most prevalent chronic liver diseases worldwide and represents a growing challenge for healthcare systems due to its close relationship with obesity, insulin resistance, type 2 diabetes mellitus, dyslipidemia, and metabolic syndrome. This review aimed to integrate current scientific evidence regarding the epidemiology, pathophysiology, clinical progression, diagnosis, treatment, and emerging role of precision medicine in MASLD. International scientific literature was reviewed through recognized biomedical databases, incorporating original studies, systematic reviews, meta-analyses, clinical practice guidelines, and international consensus statements relevant to the disease. The evidence demonstrates a substantial global burden of MASLD, with particularly high prevalence estimates reported in Latin America and other regions experiencing rapid growth in cardiometabolic disorders. Disease progression is heterogeneous, ranging from hepatic steatosis to metabolic dysfunction-associated steatohepatitis, advanced fibrosis, cirrhosis, and hepatocellular carcinoma, with fibrosis representing one of the most important predictors of adverse clinical outcomes. Advances in non-invasive biomarkers, serum-based fibrosis scores, transient elastography, and magnetic resonance-based techniques have improved risk stratification and reduced dependence on liver biopsy. Lifestyle modification remains fundamental to treatment, while emerging pharmacological therapies provide additional opportunities for patients with specific metabolic and hepatic profiles. The integration of clinical characteristics, metabolic phenotype, fibrosis stage, imaging findings, and biological markers supports the transition toward precision medicine. MASLD should therefore be approached as a multisystem metabolic disease requiring early identification, multidisciplinary management, comprehensive cardiometabolic control, and individualized therapeutic strategies to reduce progression and long-term complications.

Chronic kidney disease (CKD) without diabetes mellitus has become an increasingly recognized clinical entity whose progression cannot be explained exclusively by traditional hemodynamic mechanisms. Growing evidence indicates that endocrine dysregulation, metabolic remodeling, mitochondrial dysfunction, chronic inflammation, oxidative stress, and altered communication between the kidney and other organ systems play fundamental roles throughout disease development and progression. The present review critically analyzes current scientific evidence regarding the endocrine and metabolic mechanisms involved in non-diabetic CKD, integrating findings from nephrology, endocrinology, and internal medicine while incorporating information relevant to Latin American populations. A narrative review based on the Scientific Method was conducted using high-quality publications retrieved from internationally recognized databases and clinical practice guidelines. The available evidence demonstrates that persistent activation of the renin–angiotensin–aldosterone system, disruption of the fibroblast growth factor 23–Klotho axis, impaired vitamin D metabolism, insulin resistance, obesity-related endocrine alterations, mitochondrial dysfunction, and gut–kidney interactions contribute substantially to renal fibrosis, progressive loss of kidney function, and cardiovascular complications. Contemporary therapeutic approaches, particularly sodium–glucose cotransporter-2 inhibitors, have significantly modified disease management by providing nephroprotective effects beyond glycemic control. Emerging biomarkers and precision medicine strategies also show considerable potential for improving early diagnosis, individualized risk assessment, and targeted therapeutic interventions. Nevertheless, additional multicenter studies, particularly involving underrepresented regions such as Latin America, remain necessary to strengthen the current evidence base. Overall, non-diabetic CKD should be regarded as a complex multisystem disorder requiring an integrated clinical approach that combines endocrine, metabolic, cardiovascular, and nephrological perspectives to optimize patient outcomes.

Metabolic frailty has traditionally been associated with older populations; however, accumulating evidence suggests that frailty-related metabolic alterations may emerge much earlier in the life course. This narrative review examines metabolic frailty in young adults as an early vulnerability state characterized by metabolic dysregulation, adverse body composition, chronic low-grade inflammation, and reduced physiological reserve, even in the absence of overt chronic disease. Drawing on international literature and integrating evidence relevant to Latin American contexts, particularly Mexico, Colombia, and Ecuador, this study synthesizes current knowledge on the biological and clinical pathways linking central adiposity, insulin resistance, sarcopenia-related changes, and cardiometabolic risk clustering to early frailty-related processes. The findings support the interpretation of metabolic frailty as a continuous, multidimensional construct that extends classical frailty frameworks beyond geriatric populations. Early identification of metabolic frailty using combined anthropometric, metabolic, and muscle-related indicators may provide a valuable opportunity to prevent or delay the onset of chronic noncommunicable diseases and preserve long-term functional capacity.