Tubulointerstitsial'nyy fibroz pri diabeticheskoy nefropatii: mekhanizmy razvitiya i podkhody k lecheniyu

Бондарь, Ирина Аркадьевна; Аркадьевна, Бондарь Ирина; Климонтов, Вадим Валерьевич; Валерьевич, Климонтов Вадим

doi:10.14341/2072-0351-5752

Cited by 4 publications

(2 citation statements)

References 85 publications

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“…Альбуминурия, являясь одним из главных рутинных маркеров почечной дисфункции, в настоящее время рассматривается, в основном, в качестве показателя степени клубочковых нарушений [4]. Длительное время в качестве пускового механизма развития альбуминурии под воздействии описанных при СД 2 типа метаболических и гемодинамических факторов рассматривалось повреждение структур гломерулярного фильтрационного барьера в условиях формирования внутриклубочковой гипертензии [17].…”

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The role of metformin in the prevention of diabetic nephropathy in experimental type 2 diabetes

Bayrasheva

Babenko

Dmitriev

et al. 2016

Regional blood circulation and microcirculation

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Introduction and purpose. A number of landmark trials have demonstrated clear benefits of metformin therapy in the prevention of macrovascular outcomes. Nevertheless, there is a lack of robust evidence to suggest whether metformin therapy will have similar beneficial outcomes in one of the most serious type 2 diabetes-related renal microvascular complications known as diabetic nephropathy. The study aimed to evaluate the effects of ten-week metformin treatment on renal morphofunctional changes in rats with non-genetic type 2 diabetic nephropathy. Materials and methods. Starting at 3 weeks after unilateral nephrectomy, adult male Wistar rats were fed the high-fat diet for 5 weeks, and then successively received nicotinamide (230 mg/kg) and streptozotocin (65 mg/kg) intraperitoneally in 15-min interval. Results. Starting at 11 weeks after confirmation of diabetes, metformin treatment did not attenuate routine renal dysfunction markers such as creatinine, creatinine clearance and albuminuria compared to placebo-treated diabetic group, and glomerulosclerosis index and glomerular expression of type IV collagen didn't significantly change either. Nevertheless, level of urinary kidney injury molecule-1, considered to be the marker of tubular damage in diabetes, was significantly lower in metformin-treated animals. Moreover, reduction of tubulointerstitial lesion tended to be significant. Conclusions. Under conditions of diabetic nephropathy modeling, metformin has shown direct protective effects against diabetic tubular disturbance. To assess long-term renal outcomes of these findings, more pre-clinical studies and clinical trials are required.

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Section: Introductionunclassified

The role of metformin in the prevention of diabetic nephropathy in experimental type 2 diabetes

Bayrasheva

Babenko

Dmitriev

et al. 2016

Regional blood circulation and microcirculation

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show abstract

“…На сегодняшний день многие аспекты патогенеза ДН остаются открытыми. Ранее рассматривали ДН как невоспалительное поражение почек, но исследования последних лет показывали, что развитие ДН протекает на фоне воспалительной реакции почечной системы [3][4].…”

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Participation of Interleukins in Diabetes Mellitus and Diabetic Nephropathy in Children and Adolescents in Kyrgyzstan

Terekhova

2019

BSP

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The data presented in interleukins plasma concentrations of diabetic nephropathy in children. It studied 130 children and adolescents with type 1 diabetes without diabetic nephropathy with type 1 diabetes mellitus complicated by diabetic nephropathy. It is shown that nephropathy complicated by diabetes is accompanied by activation of cytokine (interleukin) in the blood system reflecting the severity of kidney damage and the whole organism.

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Disorders of Proteoglycan and Collagen Metabolism in the Kidneys in Diabetes Mellitus: Clinical and Pathogenetic Mechanisms and Laboratory Markers

Морозенко¹,

Yeromenko²,

Gliebova³

et al. 2020

Ukr. ž. med. bìol. sportu

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The article considers the issue of disorders of connective tissue metabolism in diabetes mellitus. Glycosylation of structural components of connective tissue and glucose toxicity have been found to determine the pathogenesis of late complications of diabetes mellitus. The most common concept of the pathogenesis of diabetes is metabolic, according to which all variants of diabetes mellitus, including blood vessels, their basement membrane, are associated with primary disorders of lipid, glycoprotein, protein and carbohydrate metabolism due to complete or partial insufficiency. It has been found that the formation of interstitial fibrosis in the kidneys of patients with diabetes begins in the preclinical stages of diabetic nephropathy. The leading cause of interstitial fibrogenesis is hyperglycemia; exacerbate proteinuria fibrosis, activation of the renin-angiotensin system, chronic inflammation and the formation of myofibroblasts in the interstitium. According to the results of the study of aspects of early diagnosis of kidney damage in type 1 diabetes mellitus, it was found that the development of diabetic nephrosclerosis is characterized by qualitative and quantitative changes in collagen composition in the glomeruli and interstitium, rebalance between collagen synthesis and breakdown, glycosaminoglycans, increased synthesis of fibrogenic growth factors and oxidative modification of proteins. The formation of diabetic nephropathy in patients with diabetes is also characterized by the accumulation of collagen types IV and VI, the appearance of interstitial collagen types III and I in the glomeruli, as well as the accumulation of collagen of all types in tubulointerstitium. Quantitative and qualitative characteristics of sulfated glycosaminoglycans of urine in human diabetes indicated different degrees of development of diabetic nephropathy. Glycosaminoglycans hyperexcretion was observed in patients with diabetes mellitus without proteinuria. In patients with microalbuminuria, glycosaminoglycans hyperexcretion was even more pronounced. It was also found that in diabetes, the total excretion of sulfated glycosaminoglycans in the urine doubles. Conclusion. Thus, in diabetes mellitus, an important pathogenetic link in the violation of the morpho-functional state of the kidneys is the degradation of collagen and proteoglycans of the basement membranes of the glomeruli, as well as interstitial fibrosis. This is reflected in changes in urinary glycosaminoglycans excretion, in particular heparansulfate and chondroitin sulfate, which may serve as a marker of proteoglycan metabolism disorders in the kidneys. Patients with diabetes also have an increase in the urine of hydroxyproline, which indicates an increase in the intensity of collagen metabolism in patients

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Tubulointerstitsial'nyy fibroz pri diabeticheskoy nefropatii: mekhanizmy razvitiya i podkhody k lecheniyu

Cited by 4 publications

References 85 publications

The role of metformin in the prevention of diabetic nephropathy in experimental type 2 diabetes

The role of metformin in the prevention of diabetic nephropathy in experimental type 2 diabetes

Participation of Interleukins in Diabetes Mellitus and Diabetic Nephropathy in Children and Adolescents in Kyrgyzstan

Disorders of Proteoglycan and Collagen Metabolism in the Kidneys in Diabetes Mellitus: Clinical and Pathogenetic Mechanisms and Laboratory Markers

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