From visceral obesity to chronic kidney damage: A critical review of metabolic and inflammatory progression.
DOI:
https://doi.org/10.70577/asce.v5i1.591Keywords:
Visceral Obesity; Type 2 Diabetes; Arterial Hypertension; Inflammation; Chronic Kidney Disease; Self-CareAbstract
Chronic kidney disease is a global health problem in which metabolic, inflammatory, and vascular processes converge and progress in a progressive manner. It begins with unhealthy habits that favor the accumulation of abdominal fat; consequently, adipose tissue acts as an active endocrine organ and triggers a cascade of metabolic events such as the secretion of inflammatory cytokines, adipokines, and reactive oxygen species that lead to insulin resistance and endothelial dysfunction. Over time, type 2 diabetes mellitus develops due to exhaustion of pancreatic β cells and activation of the renin–angiotensin–aldosterone system. Having obesity and diabetes accelerates the onset of arterial hypertension, increased intraglomerular pressure, and capillary and mesangial damage. If these conditions persist, microalbuminuria appears, the glomerular basement membrane thickens, mesangial expansion and tubulointerstitial fibrosis occur, which gradually deteriorate glomerular filtration until chronic kidney disease develops.
The objective of this article is to carry out a critical and systematic analysis of recent scientific literature on the common pathophysiological mechanisms that interrelate type 2 diabetes mellitus, arterial hypertension, and obesity in the genesis and progression of chronic kidney disease. The methodology consists of a narrative review of recent and original articles published in indexed academic databases. The results of the analysis show that maintaining these metabolic alterations over time leads to progressive renal damage, which can be prevented through health promotion to encourage self-care and timely early medical intervention to delay or stop the development of chronic kidney disease.
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