Introduction: Patients undergoing chronic hemodialysis treatment (HD patients) experience sleep quality deterioration, which is associated with lower quality of life and represents an independent predictor of mortality in HD patients. Recently, the number of research papers aimed at assessing sleep quality in HD patients has been increased, due to the fact that it is such an important factor. Thus, this study aimed to identify the main factors related with low sleep quality in HD patients by reviewing scientific literature. Materials and methods: A search based on key words was performed in the MEDLINE database and selected scientific papers were analyzed by using the matrix method. The initial search retrieved 472 scientific articles to which certain inclusion and exclusion criteria were applied, combined with a critical analysis, resulting in the selection of a total of 48 papers. Factors related with low sleep quality in HD patients were grouped in three sub-groups, while sociodemographic and clinical characteristics showed significant impact on low sleep quality in HD patients. Results: It has also been proven that low sleep quality is correlated with biochemical variables such as inflammation factors, low albumin levels and other factors, whereas knowledge concerning factors involved in hemodialysis also contributes to the efforts of medical staff aimed at improving HD patients' quality of sleep. Conclusion: Etiology of sleep quality deterioration in HD patients is manifold, and significantly affected by psychosocial, biochemical and clinical factors.

Chronic kidney disease (CKD) is an initially asymptomatic, but chronic condition characterized by a progressive loss of kidney function over the time. Etiology of CKD includes diabetes, hypertension, autoimmune diseases, polycystic kidney disease and other genetic diseases, nephrotic syndrome, etc. The development of complications such as hypertension, anemia, bone diseases, and cardiovascular complications (like heart failure, coronary artery disease, arrhythmias, valvular heart disease, cardiac arrest etc.) with an increased risk of death and hospitalization is common. Due to the significant rate of morbidity and mortality from CKD, early detection and primary prevention are extremely important. Oxidative stress affects microvascular reactivity and is considered to be one of the most important causes of endothelial dysfunction, underlying CKD. Recently, the role of miRNA, a non-coding approximately 22 nucleotides long RNA molecules which mediate post-transcriptional gene silencing, in oxidative stress has also been investigated. Individual miRNA molecules, such as miRNA-335-5p, miR-92a, miR-92a-3p relate to endothelial dysfunction. This opens new diagnostic and therapeutic possibilities and requires further research in the field of CKD. The aim of this review article is to systemize recent knowledge on the role of miRNA in the regulation of oxidative stress and microvascular reactivity in CKD.

Background and Objectives: Chronic kidney disease (CKD) is an increasingly significant global public health issue, with cardiovascular disease being the leading cause of mortality. Endothelial dysfunction plays a critical role, but diagnostic tools have certain limitations. Endocan, a soluble proteoglycan, emerged as a promising endothelial dysfunction marker and potential major adverse cardiovascular event (MACE) predictor in haemodialysis (HD) patients. Materials and Methods: In this single-centre, observational, prospective study, non-diabetic HD patients without prior MACEs were monitored. A total of 75 participants met the inclusion criteria. We measured serum endocan, standard biochemical and anthropometric parameters, and parameters of peripheral and central haemodynamics before and after HD in all participants. Results: Patients with higher endocan were older, had elevated CRP and reduced albumin concentrations, and often had a tunnelled central venous catheter (TCVC) for vascular access. Higher serum endocan levels were independently associated with an increased risk of MACEs (aHR = 4.09, 95%-CI: 1.72–9.74), MACE-related mortality (aHR = 2.64, 95%-CI: 1.23–5.66), and all-cause mortality (aHR = 1.86, 95%-CI: 1.07–3.23), both before and after adjusting for predefined confounders, with the highest endocan tercile exhibiting the shortest event-free survival. Conclusions: Endocan is a valuable marker of inflammation and endothelial dysfunction in non-diabetic HD patients. Its elevated concentration indicates an increased cardiovascular risk and more frequent MACEs. Future multicentre studies with repeated endocan assessments should validate its prognostic and diagnostic utility, particularly in long-term patient follow-up.