Visceral fat and attribute-based medicine in chronic kidney disease

Abstract

Visceral adipose tissue plays a central role in obesity and metabolic syndrome and is an independent risk factor for both cardiovascular and metabolic disorders. Increased visceral adipose tissue promotes adipokine dysregulation and insulin resistance, leading to several health issues, including systemic inflammation, oxidative stress, and activation of the renin-angiotensin-aldosterone system. Moreover, an increase in adipose tissue directly and indirectly affects the kidneys by increasing renal sodium reabsorption, causing glomerular hyperfiltration and hypertrophy, which leads to increased proteinuria and kidney fibrosis/dysfunction. Although the interest in the adverse effects of obesity on renal diseases has grown exponentially in recent years, the relationship between obesity and renal prognosis remains controversial. This may be attributed to the long clinical course of obesity, numerous obesity-related metabolic complications, and patients’ attributes. Multiple individual attributes influencing the pathophysiology of fat accumulation make it difficult to understand obesity. In such cases, it may be effective to elucidate the pathophysiology by conducting research tailored to individual attributes from the perspective of attribute-based medicine/personalized medicine. We consider the appropriate use of clinical indicators necessary, according to attributes such as chronic kidney disease stage, level of visceral adipose tissue accumulation, age, and sex. Selecting treatments and clinical indicators based on individual attributes will allow for advancements in the clinical management of patients with obesity and chronic kidney disease. In the clinical setting of obesity-related nephropathy, it is first necessary to accumulate attribute-based studies resulting from the accurate evaluation of visceral fat accumulation to establish evidence for promoting personalized medicine.

Adipose tissue is associated with kidney function parameters

“…When considering VAT, results are in line with the Framingham study observing that higher VAT was linked to reduced www.nature.com/scientificreports/ eGFR cys . Traditionally, VAT has been reported to have higher pathogenicity compared to SAT regarding metabolic, cardiovascular or kidney injury risk [24][25][26][27] . VAT accumulation seems to cause intra-renal pressure leading to compression of capillaries and Henle loop, consequently reduced intrarenal blood circulation, RAAS activation and sodium reabsorption [28][29][30] .…”

Obesity-Related Kidney Disease: Current Understanding and Future Perspectives

“…The activation of the RAAS may also lead to the increased reabsorption of sodium in the tubules [ 77 ], contributing to systemic as well as intraglomerular hypertension. In addition, because of increased mass in the abdomen, visceral adiposity causes increased intra-abdominal pressure, leading to renal compression [ 76 , 78 ]. This may impact renal blood flow and perfusion, and lead to further intraglomerular hypertension [ 76 ].…”

Fermented milk products as a component of rational nutrition (literature review and own research)

“…Результати, що представлені як середнє арифметичне та його статистична похибка ( -X ± Sx) наведені в таблицях. Значущими вважали результати при Р≤0,05 та близькими до них при 0,05<Р≤0,1 [29].…”