Obesity and kidney disease: Beyond the hyperfiltration

Mascali, Alberto; Franzese, Ornella; Nisticò, Salvatore; Campia, Umberto; Lauro, Davide; Cardillo, Carmine; Daniele, Nicola Di; Tesauro, Manfredi

doi:10.1177/0394632016643550

Cited by 29 publications

(33 citation statements)

References 79 publications

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“…В числе последних артериальная гипертония (АГ), метаболический синдром, сахарный диабет (СД), которые вносят дополнительный, ими обусловленный, вклад в развитие патологии почек. Дислипидемия влияет как на развитие, так и на прогрессирование О-ГП [7]. О-ГП.…”

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“…Данную гломерулопатию стали выделять в самом начале XXI века. Этот вариант поражения почек у больных ожирением клинически протекает без АГ и метаболических нарушений, морфологически проявляясь гломеруломегалией (диаметр клубочка почти в 1,5 раза больше, чем в норме) и фокально-сегментарным гломерулосклерозом (ФСГС) [7][8][9].…”

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“…При морфологическом исследовании почечной ткани больных О-ГП отмечают компенсаторную гипертрофию клубочков и канальцев почек, увеличение внутриклубочкового матрикса и числа эндотелиальных и мезангиальных клеток [7,15,9]. Выявляют ФСГС, расположенный в области ворот (hilus) клубочка, т.е.…”

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“…В клинической практике гиперлептинемия сопровождается увеличением степени гиперфильтрации и развитием альбуминурии [7,9,20,27].…”

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“…Это связывают с опосредованным действием АН через снижение активности внутрипочечной РААС. Снижение продукции ангиотензина II приводит к уменьшению окислительного стресса в области почечных канальцев, в результате чего развитие и прогрессирование патологии почек замедляется [7,30,31]. При снижении продукции АН активность РААС возрастает, что сопряжено с патологическими воздействиями как на внутрипочечную гемодинамику, так и на функцию почечных канальцев.…”

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Obesity-related glomerulopathy: Mechanisms of development, clinical course

Кутырина

2017

Ter. arkh.

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Obesity and overweight are recognized as epidemics of non-communicable diseases in the 21st century. The kidneys are a target organ for obesity, damage to which is considered to be an independent risk factor for the development of renal failure. Obesity-related glomerulopathy (OGP) is one of the types of renal injury in obesity, which is characterized by the development of proteinuria in patients with a body mass index (BMI) of >30 kg/m2 in the absence of other causes of kidney damage. The pathogenesis of OGP is multifactorial. It is associated with intrarenal hemodynamic disorders - the development of renal hyperfiltration, the damaging action of adipose tissue hormones (hyperleptinemia, activation of the renin-angiotensin-aldosterone system, decreased production of adiponectin); with ectopic lipid accumulation in the kidney. The morphological pattern of OGP is characterized by a low glomerular density (oligonephronia) that leads to glomerular and tubular hypertrophy; by the development of perihilar focal segmental glomerulosclerosis (FSGS), obvious podocyte damages, and the development of a fatty kidney. The clinical picture of OGP is characterized by the slow and gradual development of albuminuria, not exceeding Stage A3 (300-1999 mg/day). Approximately one-third of patients develop partial nephrotic syndrome with massive proteinuria, but without edema and hypoproteinemia. Complete nephrotic syndrome is observed in not more than 6% of patients with OGP. In the course of the disease, 50% of patients develop hypertension and more than 80% do dyslipidemia. Stages IV-V chronic kidney disease may develop 20-30 years after the disease occurs.

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Obesity-related glomerulopathy: Mechanisms of development, clinical course

Кутырина

2017

Ter. arkh.

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Fructooligosaccharides Ameliorate Renal Injury and Dysfunction Through the Modulation of Gut Dysbiosis, Inhibition of Renal Inflammation, Oxidative Stress, Fibrosis, and Improve Organic Anion Transporter 3 Function in an Obese Rat Model

Pengrattanachot,

Thongnak,

Promsan

et al. 2024

Molecular Nutrition Food Res

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ScopeHigh‐fat diet (HFD) consumption causes obesity and gut dysbiosis which induces kidney injury. It has been reported that prebiotics improve gut dysbiosis and insulin sensitivity and decelerate the progression of kidney disease. This study investigates the impact of fructooligosaccharides (FOS) on renoprotection and the prevention of gut dysbiosis and intestinal barrier injury in obese rats.Methods and resultsWistar rats are treated with HFD for 16 weeks. Then, the HFD fed rats (HF) are given FOS 1 g day−1 (HFFOS1), 2 g day−1 (HFFOS2), or metformin 30 mg kg−1 day−1 (HFMET), by intragastric feeding for 8 weeks. Blood, urine, feces, kidney, and intestine are collected to determine the metabolic changes, gut dysbiosis, and the expression of proteins involved in kidney and intestinal injury. FOS can attenuate insulin resistance and hypercholesterolemia concomitant with the inhibition of renal inflammation, oxidative stress, fibrosis, and apoptosis, which are related to the deceleration of the overexpression of renal Toll‐like receptor 4 (TLR4) and NADPH oxidase (NOX4). Moreover, FOS shows a greater efficacy than metformin in the reduction of the intestinal injury and loss of tight junction proteins induced by HFD.ConclusionFOS may be used as a supplement for therapeutic purposes in an obese condition to improve intestinal integrity and prevent renal complications.

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