Background: COVID-19 pandemic caused by SARS-CoV2 has seriously impacted the global economy. Medical facilities around the world were not prepared for the enormous challenges posed by the growing number of patients each day, the shortage of personal protective equipment, and insufficient numbers of medical staff. Governments have tried to counteract the impact of the pandemic, but the measures taken have not always been sufficient to maintain access to and quality of health services at the same level as before the pandemic. The disruption of health services has resulted in more and more research reports from different parts of the world on the accessibility of health services during the COVID-19 pandemic.Methodology: This review article presents 21 selected scientific studies on access to health services in different regions of the world. Articles were found in PubMed, GoogleScholar, Medline, and ScienceDirect databases, then grouped, and significant data were extracted from each article. The results were summarized in a table.Results: The range of limited health services included a variety of specialties, including primary care, psychiatry, orthopedics, cardiology, neurosurgery, and more. Methods used in the studies were based on retrospective analysis or on the subjective assessment of patients in the form of a questionnaire or interview. Most authors claimed a decrease in accessibility to health services during the COVID-19 pandemic compared to the pre-pandemic period, including a decrease in planned surgeries, doctor appointments, patient admission to hospital or ER, and access to medicines. Additionally, some authors observed an increase in the mortality rate. One of the few medical services that have expanded rapidly during the pandemic was online appointments.Conclusions: The COVID-19 pandemic has most certainly affected the accessibility of health services worldwide. Lessons should be learned to prevent inaccessibility to medical services, especially as experts predict another wave of COVID-19 cases.

This study aimed to assess cardiac troponin T (cTnT) and hydration state as cardiovascular (CV) risk markers in hemodialysis (HD) patients. Two hundred and forty one patients were divided according to HD vintage into two groups: SV (HD ≤24 months) and LV. Water balance was assessed with overhydration (OH%; bioimpedance analysis) and daily diuresis (DD); CV dysfunction with cTnT and heart ultrasound; nutrition with subjective global assessment (SGA), cholesterol (TC) and albumin. SV had lower OH% (2.8 vs. 3.5, p < 0.05) and higher DD (1,161 vs. 637 ml, p < 0.001), while LV had higher cTnT (0.1 ± 0.04 vs. 0.1 ± 0.07 ng/ml, p < 0.05) and lower interventricular septum thickness (IVS; 13.4 vs. 14.5 mm, p < 0.05). Nutritional state as reflected by lower TC was worse in LV (184.7 vs. 169.5 mg/dl, p < 0.05). Mortality was higher in patients in the LV group (15 vs. 27 deaths, p < 0.05). OH% correlated inversely with albumin (r = -0.36, p < 0.001), TC (r = -0.31, p < 0.001) and cTnT (r = -0.4, p < 0.001). cTnT correlated positively with IVS (r = 0.39, p < 0.001), SGA (r = 0.23, p = 0.001) and mortality rate (r = 0.21, p < 0.01), and negatively with DD (r = -0.34, p < 0.001) and albumin (r = -0.25, p < 0.001). Longer dialysis vintage associates with CV dysfunction, overhydration and increased mortality, which may be predicted with OH% and cTnT. Video Journal Club ‘Cappuccino with Claudio Ronco' at http://www.karger.com/?doi=376603.

Background/Aims: Dysfunction of the arterial endothelial cells promotes the progression of atherosclerosis. We studied how exposure of human arterial endothelial cells to atherosclerotic serum from patients with peripheral artery disease changes the secretory activity of these cells, and whether that reaction is modified by sulodexide. Methods: Endothelial cells in in vitro culture were exposed to standard culture medium ± 100pg/mL Interleukin-1(IL-1) or to medium supplemented with 20% atherosclerotic serum. Afterwards, the expression of genes responsible for the synthesis of Interleukin-6 (IL-6), Vascular Cell Adhesion Protein-1 (VCAM-1) and Von Willebrand Factor (VWF) was evaluated, together with the secretion of these compounds. Additionally, the effect of sulodexide on these processes was studied. Results: Atherosclerotic serum stimulated the expression of IL6, VCAM-1 and VWF genes in endothelial cells, which was followed by increased secretion of these compounds by 179%, 121% and 116%, respectively. Sulodexide (0.5 LRU/mL) reduced atherosclerotic serum-induced increased expression of genes for IL-6 (-32%), VCAM-1 (-20%) and VWF (-42%), and lowered secretion of these molecules: IL-6 (-27%), VCAM-1(-27%), VWF (-25%). Sulodexide also reduced, in a dose- dependent manner, secretion of IL6 from unstimulated and stimulated with IL-1 endothelial cells. Conclusions: Atherosclerotic serum induces proinflammatory and prothrombotic phenotype in arterial endothelium, which is partially reduced by sulodexide, via inhibition of genes expression, and in consequence lower secretory activity.

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Experimental animal models improve our understanding of technical problems in peritoneal dialysis PD, and such studies contribute to solving crucial clinical problems. We established an acute and chronic PD model in nonuremic and uremic rats. We observed that kinetics of PD in rats change as the animals are aging, and this effect is due not only to an increasing peritoneal surface area, but also to changes in the permeability of the peritoneum. Changes of the peritoneal permeability seen during chronic PD in rats are comparable to results obtained in humans treated with PD. Effluent dialysate can be drained repeatedly to measure concentration of various bioactive molecules and to correlate the results with the peritoneal permeability. Additionally we can study in in vitro conditions properties of the effluent dialysate on cultured peritoneal mesothelial cells or fibroblasts. We can evaluate acute and chronic effect of various additives to the dialysis fluid on function and permeability of the peritoneum. Results from such study are even more relevant to the clinical scenario when experiments are performed in uremic rats. Our experimental animal PD model not only helps to understand the pathophysiology of PD but also can be used for testing biocompatibility of new PD fluids.

Hemodialysis induces oxidative stress causing intravascular inflammation, which may cause endothelial dysfunction. We evaluated how hemodialysis-induced changes in blood affect the function of endothelial cells in in vitro culture. Serum samples were collected from 42 uremic patients treated with hemodialysis, one before the start of dialysis and the other one at the end of session. All patients were dialysed with polysulfone dialyzer. Concentrations of the inflammatory molecules carbonyl protein and metabolites of NO synthesis were measured in blood. Additionally, the effect of the serum obtained before and after dialysis on the function of endothelial cells in in vitro culture was studied. Hemodialysis caused increase of monocyte chemoattractant protein (MCP)-1 (+17%), hepatocyte growth factor (+91%), and pentraxin-3 (+30%) concentration in serum. Concentration of carbonyl protein was decreased by 30%. Decrease of blood level of asymmetric dimethylarginine (-25%) and nitrate/nitrites (-62%) was observed. Serum obtained after hemodialysis stimulated proliferation of endothelial cells (+10%) and synthesis of MCP-1(+11%) in these cells. Hemodialysis-induced intravascular inflammation changes the function of endothelial cells, which may lead to acceleration of atherosclerosis.

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IntroductionBody mass decomposition and hydration state imbalances affect patients on maintenance dialysis. We compared body composition, hydration and nutritional state of patients on peritoneal dialysis (PD) and hemodialysis (HD) based on dialysis vintage (DV).Material and methodsThree hundred and fifty-nine prevalent patients on HD (n = 301) and PD (n = 58) were divided into 3 subgroups depending on DV: < 2 years HD (n = 41) and PD (n = 28), 2–4 years HD (n = 111) and PD (n = 17), > 4 years HD (n = 149) and PD (n = 13). Bioimpedance analysis delivered data including overhydration (OH), Lean (LTM) and adipose lipids mass (FAT). Other measurements included daily diuresis (DD), subjective global assessment (SGA) and serum albumin (alb), C-reactive protein (CRP) and total cholesterol (TChol), and hemoglobin (Hb).ResultsDialysis vintage < 2 years. Hemodialysis patients were older (65.5 ±18.5 vs. 50.9 ±17.1; p < 0.01) with a higher mortality (28 vs. 1; p < 0.01) and OH (8.0 ±4.3 vs. 1.6 ±3.1; p < 0.001). Hemoglobin (10.6 ±1.5 vs. 11.8 ±1.7; p < 0.05), TChol (180.2 ±47.0 vs. 211.7 ±46.3; p < 0.05), DD (871 ±729 vs. 1695 ±960; p < 0.001) and LTM (46.5 ±12.9 vs. 53.8 ±14.4; p < 0.05) were lower on HD. Dialysis vintage 2–4 years: when compared to PD, HD patients had higher OH (11.7 ±5.9 vs. 2.1 ±3.2; p < 0.001) and lower Hb (10.8 ±1.5 vs. 11.9 ±1.4; p < 0.01). Dialysis vintage > 4 years: compared to PD, HD patients had higher LTM (44.3 ±11.7 vs. 38.6 ±7.9; p < 0.05) and lower FAT (34.4 ±11.1 vs. 42.8 ±6.4; p < 0.01).ConclusionsDialysis patients’ body composition depends on dialysis modality and DV. Dialysis vintage < 2 years is associated with better hydration, nutritional state, and survival in PD patients, but longer DV reduces these benefits. Dialysis vintage > 4 years associated with similar hydration and mortality in both PD and HD while body composition was better on HD.