Obesity-Related Chronic Kidney Disease: From Diagnosis to Treatment

Abstract

Obesity has emerged as a global epidemic with far-reaching health complications, including its role as an independent risk factor for chronic kidney disease (CKD). Increasing evidence suggests that obesity contributes to CKD through multiple mechanisms, including chronic inflammation, hemodynamic alterations, insulin resistance, and lipid accumulation. These processes can culminate in histopathological changes collectively referred to as obesity-related glomerulopathy (ORG). This review aims to provide a comprehensive overview of the current knowledge regarding the prevalence, clinical manifestations, and pathophysiology of ORG. Furthermore, we emphasize the importance of identifying key biomarkers that facilitate the early detection of ORG. Finally, we explore emerging therapeutic strategies that offer promise in mitigating this growing global health crisis.

Keywords: RAAS blockade; biomarkers; chronic kidney disease; ectopic lipid accumulation; obesity; obesity-related glomerulopathy.

Figure 1

The development of obesity-related glomerulopathy (ORG) involves key mechanisms such as glomerular hyperfiltration, overactivation of the RAAS, and podocyte injury leading to fibrosis and proteinuria. Inflammatory mediators and ectopic lipid deposition further exacerbate glomerular damage through lipotoxicity and mechanical stress. Pro-inflammatory and vasoconstrictive effects of adipokines, along with hyperinsulinemia and insulin resistance, contribute to podocyte dysfunction and glomerulosclerosis. Emerging research highlights the role of microbiota alterations and genetic factors in ORG pathogenesis. Abbreviations—RAAS: Renin–Angiotensin–Aldosterone System. Created with www.BioRender.com (accessed on 12 October 2024) [20].