Aims In acute heart failure (AHF), assessment of renal function comprises estimation of glomerular filtration rate (eGFR), which does not provide any information about renal sodium/water handling. We describe the interactions between urinary sodium concentration and eGFR to better characterize AHF patients. Methods and results In 219 patients with AHF, spot urine sodium (UNa+) and eGFR were assessed on admission, day 1 and day 2 of hospitalization. We found no correlation between UNa+ and eGFR (calculated on each consecutive day, as an average of all three values, and as changes from baseline; all P > 0.05). The population was subsequently divided into four profiles based on eGFR (preserved vs. impaired; cutoff of 60 mL/min/1.73 m2) and UNa+ (sodium excreter vs. non‐excreter; cutoff of 60 mmol/L). At day 1, there were 70 (31.9%) patients classified as preserved eGFR/sodium excreter, 37 (16.8%) as impaired eGFR/sodium non‐excreter, 72 (32.9%) as impaired eGFR/sodium excreter, and 40 (18%) as preserved eGFR/sodium non‐excreter. Both sodium non‐excreter profiles were associated with an increased risk of in‐hospital heart failure worsening [odds ratio (OR) 2.8, 95% confidence interval (CI) 1.3–6.4], inotrope use (OR 2.6, 95% CI 1.1–6.7) and rehospitalization due to AHF (OR 3.2, 95% CI 1.6–6.2; all P < 0.05). The preserved eGFR/sodium non‐excreter profile was associated with highest 1‐year mortality (52.5%) and remained an independent prognosticator after adjustment for other prognosticators (hazard ratio 2.9, 95% CI 1.7–5.2; P < 0.0005). Conclusions In AHF, values of spot UNa+ and eGFR are not interrelated. Concomitant assessment of eGFR and spot UNa+ may be useful for better clinical and therapeutic profiling of patients.

BackgroundMetabolic syndrome (MetS) is a complex metabolic disease connected especially with lipid and carbohydrate disturbances. It is postulated that oxidative stress (OS) is linked to metabolic syndrome, constituting a novel component of its pathogenesis.AimWe aimed to examine the plasma level of oxidatively modified proteins––advanced oxidation protein products (AOPP) and ischemia modified albumin (IMA)––as well as thiol (SH) groups and evaluate their connection with metabolic agents in relation to MetS prevalence.Subjects and methodsThe levels of AOPP, IMA and SH groups were measured spectrophotometrically in 106 patients with MetS risk factors and in 32 control subjects.ResultsThe levels of examined parameters differed significantly between patients with MetS risk factors and the control group. AOPP significantly correlated with glucose (r = 0.30, p = 0.008), HDL-Ch (r = −0.34, p = 0.005), TG (r = 0.48, p < 0.001) and fibrinogen (r = 0.37, p < 0.001). The levels of AOPP and IMA increased progressively with the number of MetS risk factors, being the most significant for AOPP. The highest values of AOPP were associated with the presence of at least three risk factors. Only AOPP were an independent determinant for MetS occurrence in the studied population (OR = 2.72, p = 0.04). Mutual dependence between metabolic, oxidative stress and inflammatory parameters was revealed.ConclusionsOxidative modifications of proteins are increased in MetS and accumulation of MetS risk factors enhances manifestation of OS. AOPP is the most appropriate parameter for determination of OS, with potential diagnostic value in MetS patients.

Background Clinical consequences of an interplay between dysfunction/injury of different end‐organs in acute heart failure (AHF) remain unknown. Methods and results In 284 consecutive AHF patients, end‐organ dysfunction/injury was defined as cardiac [troponin I level above the upper reference limit (URL, > 0.056 ng/mL)], kidney (estimated glomerular filtration rate < 60 mL/min/1.73 m2), and liver [at least one of the following: aspartate transaminase (AST)/alanine transaminase (ALT) > 3 times the URL (> 114 IU/L and > 105 IU/L for AST and ALT, respectively), bilirubin above the URL (> 1.3 mg/mL), albumin below the lower reference limit (< 3.5 mg/dL)]. The primary endpoints were early (within first 48 h) in‐hospital worsening of heart failure and 1‐year all‐cause mortality. On admission, cardiac, kidney, liver dysfunction/injury were present in 38%, 50%, and 54% of patients, respectively. Patients were classified as having 0, 1, 2, or 3 organ injury/dysfunction (17%, 36%, 35%, and 12% of patients, respectively). Baseline clinical characteristics and co‐morbidity profile were similar across groups. Patients with three organ dysfunction/injury had the worst 1‐year survival rate [46%; hazard ratio (HR) with 95% confidence interval (CI) vs. patients without organ dysfunction: 6.75 (2.52–18.13), those with two (67%; HR 3.54, 95% CI 1.38–9.08), one (84%; HR 1.58, 95% CI 0.58–4.30), or no organ dysfunction/injury (90%); P < 0.01]. Worsening of heart failure was more frequent in patients with three and two vs. those with one or no organ dysfunction/injury (37% vs. 38% vs. 23% vs. 21%, P < 0.05). Conclusions In patients with AHF, dysfunction/injury of > 1 end‐organ dysfunction/injury identifies patients at the highest risk of poor outcomes.

Highlights Higher mortality rate in COVID-19 patients with haematologic diseases. Haematologic patients with COVID-19 have 50 % less chance of survival. Probability of death was higher in patients older than 40 yrs of age with AML/MDS.

Background: Tryptophan metabolism via the kynurenine pathway is considered the link between the immune and endocrine systems. Dysregulation of serotonergic transmission can stem from the direct influence of interferon-α on the activity of serotonergic receptors 5-HT 1A and 5-HT 2A , and from its indirect effect on tryptophan metabolism. Induction of the kynurenine pathway increases the concentration of neurotoxic kynurenine metabolites, and the activity of kynurenine derivatives is linked to the onset of depression. The aim of our study was to evaluate the relationships between depressive symptoms and kynurenine, tryptophan, anthranilic acid and kynurenic acid concentrations, indolamine 2,3-dioxygenase (IDO) activity and tryptophan availability to the brain. Methods: The study followed a prospective longitudinal cohort design. We evaluated 101 patients with chronic hepatitis C who were treated with pegylated interferon-α2a, and 40 controls who were awaiting treatment. We evaluated the relationships between total score on the Montgomery-Åsberg Depression Rating Scale and kynurenine, tryptophan, anthranilic acid and kynurenic acid concentrations, IDO activity and tryptophan availability to the brain. A logistic regression model was adapted for the diagnosis of major depressive disorder at each time point, taking into account changes in parameters of the kynurenine pathway between a given time point and the baseline measurement. Results: Of the treated patients, 44% fulfilled the criteria for major depressive disorder at least once during the 24 weeks of treatment. Anthranilic acid concentrations were significantly increased compared to baseline for all time points except week 2. Tryptophan availability showed a significant decrease (β =-0.09, p = 0.01) only in week 12 of treatment. Over time, kynurenine, tryptophan and anthranilic acid concentrations, as well as IDO activity and tryptophan availability to the brain, were significantly associated with total score on the Montgomery-Åsberg Depression Rating Scale. A logistic regression model revealed that participants with decreased tryptophan availability to the brain at 12 weeks of treatment and participants with increased anthranilic acid concentrations at week 24 of treatment were at increased risk for diagnosis of major depressive disorder (odds ratios 2.92 and 3.59, respectively). Limitations: This study had an open-label design in a population receiving naturalistic treatment. Conclusion: The present study provides the first direct evidence of the role of anthranilic acid in the pathogenesis of inflammation-induced major depressive disorder during treatment for hepatitis C with pegylated interferon-α2a.