Background and Objectives: The comorbid association between type 2 diabetes mellitus (T2DM) and a psychological profile characterized by depression and/or anxiety has been reported to increase the risk of coronary heart disease (CAD), the most striking macrovascular complication of diabetes. The purpose of the present study was to quantify anxiety, depression and the presence of type D personality, and to correlate the scores obtained with cardiovascular risk factors and disease severity in diabetic patients. Materials and methods: The retrospective study included 169 clinically stable diabetic patients divided into two groups: group 1 without macrovascular complications (n = 107) and group 2 with CAD, stroke and/or peripheral vascular disease (n = 62). A biochemical analysis and an assessment of psychic stress by applying the Hospital Anxiety and Depression Scale (HADS)and the Type D scale (DS-14) to determine anxiety, depression and D personality scores were done in all patients. Statistical analysis was made using SPSSv17 and Microsoft Excel, non-parametric Kruskal–Wallis and Mann–Whitney tests. Results: Following application of the HAD questionnaire for the entire group (n = 169), anxiety was present in 105 patients (62.2%), and depression in 96 patients (56.8%). Group 2 showed significantly higher anxiety scores compared to group 1 (p = 0.014), while depression scores were not significantly different. Per entire group, analysis of DS-14 scores revealed social inhibition (SI) present in 56 patients (33%) and negative affectivity (NA) in 105 patients (62%). TheDS-14 SI score was significantly higher in group 2 compared to group 1 (p = 0.036). Type D personality, resulting from scores above 10 in both DS-14 parameter categories, was present in 51 patients of the study group (30%). There was a direct and significant correlation (r = 0.133, p = 0.025) between the Hospital Anxiety and Depression Scale-Anxiety (HAD-A) score and the LDL-c values. Conclusions: The results of this study demonstrated that more than a half of patients with diabetes had anxiety and/or depression and one third had Type D personality, sustaining that monitoring of emotional state and depression should be included in the therapeutic plan of these patients. New treatment strategies are needed to improve the well-being of diabetic patients with psychological comorbidities.

Background: Chronic kidney disease (CKD) progression is shaped not only by biological risk factors but also by social determinants of health. Educational attainment is a key socioeconomic indicator, yet data from Eastern Europe remain limited. Methods: We conducted a retrospective cohort study including 428 adults with cardio-renal-metabolic (CRM) syndrome having CKD stages G3a–G4 enrolled between 2022 and 2024 and followed until December 2024. Patients were stratified by educational attainment using the International Standard Classification of Education (ISCED 2011): low (ISCED 0–2) vs. high (ISCED 3–8). The primary outcome was a composite of a ≥40% decline in estimated glomerular filtration rate (eGFR) or initiation of kidney replacement therapy (KRT). Secondary outcomes were eGFR slope, doubling of urine albumin-to-creatinine ratio (uACR), and KRT initiation. Results: Of 428 patients, 245 (57.2%) had low education. These patients had lower use of renoprotective therapies. During a median follow-up of 32 months, 88 primary outcome events occurred: 66 (27%) in the low education group vs. 22 (12%) in the high education group. In adjusted analyses, low education remained independently associated with the primary outcome (HR 1.47, 95% CI 1.04–2.36, p = 0.04). The annual eGFR decline was steeper in patients with low education (−3.0 vs. −2.1 mL/min/1.73 m²/year, p < 0.001), and doubling of uACR was more frequent (24% vs. 15%, HR 1.47, 95% CI 1.02–2.19, p = 0.02). Conclusions: In a Romanian CRM-CKD cohort, lower educational attainment was an independent predictor of faster kidney function decline and adverse renal outcomes. Beyond reflecting individual disadvantage, educational status in Eastern Europe highlights systemic inequities in access to nephrology care and therapies. Incorporating education into risk stratification and implementing equity-focused interventions may improve CKD outcomes in disadvantaged populations.

Background: Acute kidney injury (AKI) is a frequent and prognostically relevant complication of COVID-19. However, reliance on static creatinine values or binary AKI definitions may overlook clinically meaningful early renal dynamics. We evaluated whether early renal function trajectories within the first 24–48 h of hospitalization provide incremental prognostic information. Methods: We conducted a retrospective, single-center cohort study of adults hospitalized with laboratory-confirmed COVID-19 between December 2020 and December 2021. Early renal function patterns were defined using KDIGO-based changes in serum creatinine between admission and 24–48 h, classifying patients as stable, early improvement, or early deterioration. The primary outcome was in-hospital mortality. Multivariable logistic regression adjusted for age, sex, chronic kidney disease, comorbidities, inflammatory burden (C-reactive protein), nutritional status (albumin), pulmonary involvement, and treatment variables. Results: Among 721 patients, 65.2% had stable renal function, 22.5% had early improvement, and 12.3% had early deterioration. In-hospital mortality differed significantly across dynamic patterns (p = 0.007). Mortality was lowest in the stable group (35.1%) and higher in both early improvement (48.1%) and early deterioration (44.9%). After multivariable adjustment, early improvement remained independently associated with higher in-hospital mortality compared with stable renal function (adjusted OR 1.53, 95% CI 1.03–2.28), while early deterioration showed a directionally similar but non-significant association. Early improvement was also associated with higher AKI burden and increased need for acute de novo hemodialysis. Conclusions: Early renal function change patterns within the first 24–48 h of hospitalization carry prognostic value beyond static creatinine measures. Apparent early creatinine improvement may reflect recovery from prior injury or systemic instability rather than true renal recovery, identifying a subgroup at heightened risk. Classification based on early renal function assessment may enhance early risk stratification in hospitalized patients with COVID-19.

Hemorrhagic shock is a leading cause of preventable death following multiple trauma, driven by a cascade of interacting cellular and molecular disturbances that extend well beyond simple volume loss. Acute blood loss initiates tissue hypoperfusion and cellular hypoxia, setting in motion the lethal triad of hypothermia, acidosis, and coagulopathy through several converging pathways: complement activation with excessive C3a and C5a production; neutrophil-mediated tissue injury; NADPH-oxidase-driven reactive oxygen species (ROS) overproduction that overwhelms superoxide dismutase defenses; mitochondrial respiratory chain impairment; dysregulation of the pro-inflammatory cytokine network; and endothelial apoptosis with degradation of the endothelial glycocalyx and disruption of interendothelial junctions, with consequent vascular hyperpermeability. These mechanisms provide the biological rationale for the resuscitation strategy. Each class of fluid acts on these pathways in a distinct way: crystalloids modulate acid–base homeostasis, chloride-mediated renal vasoconstriction, and coagulation factor activity; colloids influence oncotic pressure, endothelial integrity, and microvascular perfusion; and blood products, particularly plasma and whole blood, actively modulate mitochondrial metabolism, endothelial permeability, and pro-apoptotic signaling beyond their volume-expanding role. Translating this biology to the bedside requires a multimodal monitoring framework that converts molecular endpoints into real-time therapeutic targets, integrating lactate and base excess as markers of cellular oxygen debt, dynamic preload indices such as pulse pressure and stroke volume variation, advanced hemodynamic platforms, point-of-care ultrasonography, viscoelastic coagulation testing, and near-infrared spectroscopy of tissue oxygenation. This review synthesizes the biological basis of hemorrhagic shock and its translation into an individualized, goal-directed resuscitation strategy for the critically ill polytrauma patient.

Metallo-β-lactamase (MBL)-producing Enterobacterales represent a major antimicrobial-resistance threat because MBLs hydrolyse most clinically used β-lactams and are not inhibited by currently approved serine β-lactamase inhibitors. Aztreonam–avibactam (ATM-AVI; Emblaveo^®) addresses this therapeutic gap by combining aztreonam, a monobactam that is stable to MBL-mediated hydrolysis, with avibactam, which inhibits many co-produced class A, class C, and selected class D serine β-lactamases. This narrative review synthesizes evidence on ATM-AVI pharmacology, microbiological activity, pharmacokinetics/pharmacodynamics, clinical efficacy, safety, resistance, and regulatory positioning. Large surveillance datasets show high in vitro activity against most MBL-producing Enterobacterales, including many co-producing β-lactamases from multiple Ambler classes. Population pharmacokinetic modelling supports a renal-function-adjusted fixed 3:1 dosing ratio and more reliable joint target attainment than separately administered ceftazidime–avibactam plus aztreonam. In the phase 3 REVISIT trial, clinical cure with ATM-AVI was comparable to meropenem in the overall population; however, few participants had confirmed MBL-positive infections. Direct clinical evidence therefore remains limited, supported by convergent microbiological, pharmacokinetic, and observational data. Regulatory indications differ substantially between the European Union and the United States. ATM-AVI is an important advance for selected MBL-producing and multi-class-co-producing Gram-negative infections, but its long-term value will depend on targeted use, reliable susceptibility testing, continued surveillance, and further trials in the intended target population.