Aim. To assess the relationship between hypertriglyceridemia (THG) and left ventricular remodeling types in patients with chronic kidney disease(CKD). Materials and methods. A total of 152 patients with CKD from stages 1 to 3 were examined, 98 of them with CKD without THG (subgroup 1) and 54 with CKD and THG. All patients were assessed for the parameters of anthropometry, hemodynamics, lipid spectrum, uric acid, calcium, C-reactive protein (CRP), and serum cystatin C measurement with calculation of glomerular filtration rate. The parameters of vascular stiffness (augmentation index and stiffness) and echocardiography are analyzed. Results and discussion. In the 2nd subgroup (CKD + THG), the number of patients suffering from type 2 diabetes, a stable form of coronary heart disease, gout, and their combination with hypertension, as well as cerebrovacular disorders and hyperuricemia was significantly higher compared with patients with CKD without GTG (p
Steady increase in the prevalence of chronic kidney disease (CKD) is a serious public health problem, since CKD potentially leads to the development of end-stage renal disease (ESRD) that requires high-cost replacement therapy and is closely associated with increased risk of developing cardiovascular diseases (CVD), which are the cause of death in most patients. Progression of renal dysfunction and development of CVD are significantly affected by hyper- and dyslipidemia. This review contains results of studies evaluating the effect of hypolipidemic therapy on reduction of cardiovascular risk and slowdown of renal dysfunction in patients with CKD at pre-dialysis and dialysis stages of renal failure, as well as in patients with kidney transplant. In addition, recommendations on nutrition and new therapeutic approaches to lipid-lowering therapy in patients with CKD, as well as prospects for the usage of new hypolipidemic drugs are also presented.
Infectious disease COVID-19 caused by the SARS-CoV-2 coronavirus is characterized by high contagiousness, complexity of pathogenesis and unpredictability of the clinical course. In severe cases, which are especially susceptible to men, the elderly and people with underlying medical conditions such as obesity, diabetes, hypertension, cardiovascular and chronic respiratory diseases, the infection leads to respiratory failure and death due to the development of an extensive inflammatory reaction. As a result of many studies, it has been established that one of the leading causes of the severe course and death of patients with COVID-19 is the development of coagulopathy, that is, increased thrombus formation in small vessels due to excessive activity of neutrophils, which form the so-called neutrophil extracellular traps (NETs). Although NETs play a useful role in protecting their host from pathogens, their overgrowth can trigger a cascade of adverse reactions including: the production of antibodies against the host’s DNA (autoimmunization); damage to surrounding tissue; or the occurrence of thromboembolic complications. Therefore, extracellular neutrophil traps and their markers have been identified as targets for new therapeutic strategies aimed at reducing the severity of COVID-19 disease and/or mortality. This article describes the structure of NETs, as well as analyzes the molecular mechanisms that contribute to their overgeneration. In addition, the prospects for COVID-19 therapy aimed at regulating the formation of extracellular traps by creating drugs both limiting the production of NET structures and dissolving their excess amounts in the body of patients are discussed.
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