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- W2396680965 abstract "The effect of reactive oxygen species (ROS) on pathophysiology of many diseases is widely documented in numerous scientific publications. Nephropathies belong to pathologies in which ROS undoubtedly play a role. Imbalance between ROS and antioxidants results in destructive effect on mesangial cells by altering lipid metabolism. This phenomenon is frequently observed in patients with glomerulonephritis and nephritic syndrome. Accumulation of hypoxanthine and oxygen in the mechanism of reperfusion damages renal cells by the produced ROS in patients with acute renal failure. Inactivation of nitric oxide by superoxide anion radical increases vascular resistance in renal arteries and contributes to the development of hypertensive nephropathy. Diabetic nephropathy, in which a significant role is ascribed to glycation end products, oxidative stress and decrease of antioxidant mechanisms, is another nephropathy associated with oxidant/antioxidant imbalance. Pro-inflammatory processes with activation of nonspecific system cells and destruction of kidney structure by free radical processes play an important role in urinary system infections. Similar phenomena are observed in patients with urinary system neoplastic diseases. Each of the above pathological conditions may in consequence lead to chronic renal failure (CRF) requiring nephro-substitute therapy. The therapy substituting for normal kidney function but not devoid of disadvantages. Despite of the application of numerous techniques of detoxification in patients with CRF, none of them has become the gold standard yet, because according to the so far carried out research they all induce free radical reactions in the course of dialysis and decrease total antioxidant potential of plasma. It is a very crucial problem of nephro-substitute therapy which will be developed in our next review paper." @default.
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- W2396680965 date "2010-01-01" @default.
- W2396680965 modified "2023-09-29" @default.
- W2396680965 title "[Oxidative stress in nephrology]." @default.
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