Background Maintenance hemodialysis (MHD) patients are at increased risk for coronavirus disease 2019 (COVID-19). The aim of this study was to describe clinical, laboratory, and radiologic characteristics and determinants of mortality in a large group of MHD patients hospitalized for COVID-19. Methods This multicenter, retrospective, observational study collected data from 47 nephrology clinics in Turkey. Baseline clinical, laboratory and radiological characteristics, and COVID-19 treatments during hospitalization, need for intensive care and mechanical ventilation were recorded. The main study outcome was in-hospital mortality and the determinants were analyzed by Cox regression survival analysis. Results Of 567 MHD patients, 93 (16.3%) patients died, 134 (23.6%) patients admitted to intensive care unit (ICU) and 91 of the ones in ICU (67.9%) needed mechanical ventilation. Patients who died were older (median age, 66 [57–74] vs. 63 [52–71] years, p = 0.019), had more congestive heart failure (34.9% versus 20.7%, p = 0.004) and chronic obstructive pulmonary disease (23.6% versus 12.7%, p = 0.008) compared to the discharged patients. Most patients (89.6%) had radiological manifestations compatible with COVID-19 pulmonary involvement. Median platelet (166 × 103 per mm3 versus 192 × 103 per mm3, p = 0.011) and lymphocyte (800 per mm3 versus 1000 per mm3, p < 0.001) counts and albumin levels (median, 3.2 g/dl versus 3.5 g/dl, p = 0.001) on admission were lower in patients who died. Age (HR: 1.022 [95% CI, 1.003–1.041], p = 0.025), severe-critical disease clinical presentation at the time of diagnosis (HR: 6.223 [95% CI, 2.168–17.863], p < 0.001), presence of congestive heart failure (HR: 2.247 [95% CI, 1.228–4.111], p = 0.009), ferritin levels on admission (HR; 1.057 [95% CI, 1.006–1.111], p = 0.028), elevation of aspartate aminotransferase (AST) (HR; 3.909 [95% CI, 2.143–7.132], p < 0.001) and low platelet count (< 150 × 103 per mm3) during hospitalization (HR; 1.864 [95% CI, 1.025–3.390], p = 0.041) were risk factors for mortality. Conclusion Hospitalized MHD patients with COVID-19 had a high mortality rate. Older age, presence of heart failure, clinical severity of the disease at presentation, ferritin level on admission, decrease in platelet count and increase in AST level during hospitalization may be used to predict the mortality risk of these patients.

COL-induced nephrotoxicity occurred significantly more often in patients older than 60 y of age and was related to low initial GFR estimations and high CCI scores, which were basically determined by age.

Previous studies showed a link between systemic lupus erythematosus (SLE) and Epstein-Barr virus (EBV) infection. We sought to determine the features of serologic response to EBV in SLE patients and whether this response differs from those of systemic sclerosis (SSc) and primary antiphospholipid syndrome (PAPS) patients as well as healthy individuals. Sera from 198 consecutive SLE patients have been tested to detect IgG antibodies to EA/D, EBNA-1, VCA P18 and for comparison, cytomegalovirus (CMV) using commercially available ELISA kits (Trinity Biotech, USA). Forty-six SSc patients and 38 PAPS patients were enrolled as diseased control groups and sixty-five individuals as healthy controls. Significantly more SLE (54%, P = 0.001, OR 5.77, 95% CI 2.8-11.6), SSc (41.3%, P = 0.005, OR 3.4, 95% CI 1.4-8.2) and PAPS sera (36.8%, P = 0.023, OR 2.86, 95% CI 1.14-7.22) reacted against EA/D than healthy controls (16.9%). The mean age of anti-EA/D-positive SLE patients was significantly higher, and their disease duration was longer compared to anti-EA/D-negative SLE patients (41 ± 14 vs. 33.8 ± 10.8 years, P < 0.001 and 100 ± 73 vs. 71 ± 62 months, P = 0.003). In SLE patients, EA/D reactivity was associated with Raynaud's phenomenon and the presence of any anti-ENA antibodies. Although it did not reach a statistical significance, anti-EBNA-1 reactivity was slightly lower in patients with SLE. The frequency of anti-CMV Ig G positivity was found significantly higher in SLE patients (100%) when compared to patients with SSc (95.7%), PAPS (94.7%) and healthy controls (95.4%) (P = 0.035, P = 0.025 and P = 0.015 respectively). Our results support the proposed link between EBV and SLE. The finding that SSc and PAPS patients also have increased frequency of anti-EA/D response has revealed that this immune interaction may not be unique to patients with SLE, and there may be a common mechanism involving EBV in these autoimmune diseases.

OBJECTIVE: Poor recognition and monitoring of nutritional status is the most important cause of malnutrition in hospitalized patients. The aim of this study was to assess the nutritional status of a group of patients and compare the results with their serum prealbumin levels. METHODS: Ninety-seven patients admitted consecutively to the hospital were enrolled in the study. The risk of malnutrition was assessed according to anthropometric data and the Subjective Global Assessment and Nutrition Risk Screening 2002 tools. The nutritional statuses of the patients were compared with their age, gender, body mass index, medical history, weight loss and routine biochemical analyses, including prealbumin and length of hospital stay. RESULTS: According to the Nutrition Risk Screening 2002, 57% of the patients were malnourished or at risk of malnutrition, correlating well with the Subjective Global Assessment (p<0.001, r=0.700). Multivariate analysis revealed positive correlations between malnutrition and age, weight loss, malignancy and serum C-reative protein (p=0.046, p=0.001, p=0.04 and p=0.002). Nutrition Risk Screening 2002 score ³3 was associated with prolonged length of hospital stay (p=0.001). Serum prealbumin correlated with nutritional status, regardless of the number of chronic diseases and inflammation biomarkers (p=0.01). Serum prealbumin sensitivity, specificity, positive predictive value, negative predictive value and diagnostic value in the assessment of risk of malnutrition were 94%, 32%, 0.67, 0.78 and 69 respectively. After 7 days of nutritional support, the risk of malnutrition decreased by 12% (p<0.001) and serum prealbumin levels increased by 20% (p=0.003). CONCLUSION: Instead of reflecting overall nutritional status, low serum prealbumin may be regarded as a sign of increased risk of malnutrition, requiring further nutritional assessment. It can be used for monitoring patients receiving nutritional support.

Background: Immunological and inflammatory mechanisms have been shown to have role in both the development and progression of diabetic nephropathy (DNP). There is need for more specific markers for inflammation as the ones commonly used are influenced by many factors. Pentraxin-3 (PTX-3) seems to be a potential candidate. We aimed in our study to evaluate the changes of PTX-3 levels in different stages of DNP and its relationship with other inflammatory markers.Methods: This is a cross sectional study in which patients with DNP at different stages were involved. Patient were divided into three groups according to estimated glomerular filtration rate (eGFR), microalbuminuria and proteinuria levels: Group-1: eGFR >60 mL/min and microalbuminuria, Group-2: eGFR >60 mL/min and macroalbuminuria, Group-3: eGFR <60 mL/min and macroalbuminuria. Besides the routine biochemical parameters, levels of PTX-3, high sensitivity C-reactive protein (hsCRP), interleukin (IL)-1 and tumor necrosis factor (TNF)-a was measured. Groups were compared with each other regarding the study parameters and correlation of PTX-3 with other markers was evaluated. Results: The mean PTX-3 level in Group-2 (0.94 ± 0.26 ng/mL) and -3 (1.35 ± 1.55 ng/mL) were higher than in Group-1 (0.81 ± 0.25 ng/mL) (p ¼ 0.009 and p ¼ 0.012). There was a significant correlation of PTX-3 with proteinuria (r ¼ 0.266, p ¼ 0.016), microalbuminuria (r ¼ 0.304, p ¼ 0.014) and hypoalbuminemia (r ¼ 0.197, p ¼ 0.043). PTX-3 was not correlated with other markers of inflammation (IL-1, TNF-a and hsCRP) and diabetic metabolic parameters (hbA1c, C-peptide, insulin and HOMA-IR). PTX-3, IL-1 and TNF-a levels increased with the advancing stage of DNP while hsCRP level did not change. Conclusion: PTX-3 that increases similar to other markers of inflammation (IL-1, TNF-a) is a better inflammatory marker than hsCRP. Furthermore, there is a relationship between PTX-3 and proteinuria independent from eGFR.