Obesity-Related Kidney Disease: A Growing Threat to Renal Health

Abstract

Obesity represents a serious and growing disease worldwide. The pathophysiological changes secondary to chronic inflammation lead to the development of diseases that increase the morbidity and mortality of individuals. Chronic kidney disease (CKD) is a condition with deleterious effects that acts bidirectionally with obesity. From approximately 20% to 30% of individuals share phenotypes of CKD and obesity, increasing their cardiovascular risk and the risk of other complications. Obesity and CKD form a vicious cycle in which inflammation is the central axis of multiorgan damage. Despite increasing the risk of cardiac and renal mortality, CKD progresses in relation to body mass index and albuminuria. Nowadays, the implementation of the new medications aimed at mitigating the peak of inflammation is becoming a cornerstone of treatments for obesity, diabetes, cardiovascular diseases, and renal disease.

Keywords: cardiovascular disease; kidney disease; obesity.

Figure 1

Pathophysiology of obesity. The mechanisms of renal disease in obesity. Three pathways have been described: hemodynamic, adipose tissue, and insulin resistance. These three pathways interact with each other, secreting adipokines and cytokines, activating the sympathetic nervous system, and promoting the pathological activation of the RAAS. All three pathways lead to renal damage, as the pro-inflammatory state and profibrotic factors favor glomerular hyperfiltration and, consequently, promote endothelial, podocyte, and tubular damage, increasing albuminuria excretion. RAAS: renin-angiotensin-aldosterone system. SNS: sympathetic nervous system. CKD: chronic kidney disease. TNF- α: tumor necrosis factor-α. IL: interleukin. PAI-1: plasminogen activator inhibitor 1.

Figure 2

The cardiovascular–kidney–metabolic syndrome. The cardiovascular–kidney–metabolic (CKM) syndrome is the result of diseases affecting the organs and systems previously discussed, following exposure to environmental and/or genetic factors. These factors promote a pro-inflammatory state, triggering chronic pathologies based on inflammation and fibrosis. In addition to increasing cardiovascular and renal risk, obesity interferes with sleep physiology and increases the risk of developing neoplasms. All these clinical manifestations are part of a vicious cycle where inflammation is the cornerstone of the pathological process.