Congestion is a key clinical feature of heart failure (HF), contributing to hospitalizations, disease progression, and poor outcomes. While traditionally considered a hemodynamic issue, congestion is now recognized as a systemic process affecting multiple organs. Renal dysfunction arises from impaired perfusion and sodium retention, leading to maladaptive left ventricular remodeling. Hepatic congestion contributes to cholestatic liver injury, while metabolic disturbances drive anemia, muscle wasting, and systemic inflammation. Additionally, congestion disrupts the intestinal barrier and immune function, exacerbating HF progression. Given its widespread impact, effective congestion management requires a shift from a cardiovascular-centered approach to a comprehensive, multidisciplinary strategy. Targeted decongestive therapy, metabolic and nutritional optimization, and immune modulation are crucial in mitigating congestion-related organ dysfunction. Early recognition and intervention are essential to slow disease progression, preserve functional capacity, and improve survival. Addressing HF congestion through personalized, evidence-based strategies is vital for optimizing long-term care and advancing treatment paradigms.

Congestion not only represents a cardinal sign of heart failure (HF) but is also now recognized as the primary cause of hospital admissions, rehospitalization, and mortality among patients with acute heart failure (AHF). Congestion can manifest through various HF phenotypes in acute settings: volume overload, volume redistribution, or both. Recognizing the congestion phenotype is paramount, as it implies different therapeutic strategies for decongestion. Among patients with AHF, achieving complete decongestion is challenging, as more than half still experience residual congestion at discharge. Residual congestion is one of the strongest predictors of future cardiovascular events and poor outcomes. Through this review, we try to provide a better understanding of the congestion phenomenon among patients with AHF by highlighting insights into the pathophysiological mechanisms behind congestion and new diagnostic and management tools to achieve and maintain efficient decongestion.

This paper demonstrates the ability of a functional food based on probiotics and selenium nanoparticles (SeNPs) to annihilate the toxic effect of cadmium on the kidneys. SeNPs were obtained by eco-friendly method used Lactobacillus casei. The morphological features and size of SeNPS were characterized by Atomic Force Microscopy (AFM) and Dynamic Light Scattering (DLS). Two kind of SeNPs were used, purified and Lacto-SeNPs (LSeNPs), administered by gavage at three concentrations (0.1, 0.2, and 0.4 mg/Kg b.w.) for 30 days in a mouse model of cadmium renal toxicity. The blood marker of renal injury (creatinine) significantly decreased in groups where the mice were treated with both form of SeNPs. The antioxidant capacity of plasma was evaluated by Trolox Equivalent Antioxidant Capacity (TEAC) assay and revealed that SeNPs in co-treatment with Cd, promotes maintaining antioxidant activity at the control level. Histopathological analysis of kidneys demonstrated morphological alteration in the group that received only cadmium and restored after administration of SeNPs or LSeNPs. In addition, immunohistochemical analysis revealed anti-apoptotic effects through reduction of pro-apoptotic bax and increasing of anti-apoptotic Bcl-2 protein expressions. Moreover, co-administration of Cd with SeNPs significantly decreased gene expression of kidneys inflammatory markers (TNF-α, IL-6, NF-ĸB) in a dose dependent manner, with the best results for LSeNPs at highest dose (0.4 mg/kg). Therefore, the L. casei strain is a potential SeNPs-enriched probiotic for application as functional food in the future to annihilate cadmium-induced kidneys toxicity.

Little information exists on YKL-40—a key protein in tissue remodeling—and complete blood count (CBC) parameters during acute exacerbations of advanced chronic obstructive pulmonary disease (COPD). This pilot exploratory study (August 2020–January 2021) investigated the connection between serum YKL-40 levels and CBC profile in sex- and age-matched individuals with severe COPD (GOLD stage III, n = 23, median age = 66 years, 65.21% males) and very severe COPD (GOLD stage IV, n = 24, median age = 66.5 years, 74.81% males). The measured parameters were serum YKL-40, absolute leukocyte count (ALLC), absolute neutrophil count (ANC), neutrophil percentage, absolute lymphocyte count (ALC), lymphocyte percentage, neutrophil-to-lymphocyte ratio (NLR), absolute eosinophil count (AEC), eosinophil percentage, absolute monocyte count (AMC), monocyte percentage, absolute basophil count (ABC), basophil percentage, hemoglobin levels, and hematocrit concentrations. No significant inter-group differences were observed. However, high YKL-40 subjects (n = 23)—as stratified via median YKL-40 (3934.5 pg/mL)—showed significantly increased neutrophil percentage and NLR but significantly lower lymphocyte-, eosinophil-, and basophil-related parameters compared to low YKL-40 patients (n = 24). These results reveal multidimensional, YKL-40-associated changes in leukocyte profile of patients with advanced COPD during acute exacerbations, with potential implications for personalized treatment.

Background and Objectives: episodes of acute decompensation in chronic heart failure (ADHF), a common health problem for the growing elderly population, pose a significant socio-economic burden on the public health systems. Limited knowledge is available on both the endothelial function in and the cardio-metabolic health profile of old adults hospitalized due to ADHF. This study aimed to investigate the connection between asymmetric dimethylarginine (ADMA)—a potent inhibitor of nitric oxide—and key health biomarkers in this category of high-risk patients. Materials and Methods: this pilot study included 83 individuals with a known ADHF history who were admitted to the ICU due to acute cardiac decompensation. Selected cardiovascular, metabolic, haemogram, renal, and liver parameters were measured at admission to the ICU. Key renal function indicators (serum creatinine, sodium, and potassium) were determined again at discharge. These parameters were compared between patients stratified by median ADMA (114 ng/mL). Results: high ADMA patients showed a significantly higher incidence of ischemic cardiomyopathy and longer length of hospital stay compared to those with low ADMA subjects. These individuals exhibited significantly higher urea at admission and creatinine at discharge, indicating poorer renal function. Moreover, their lipid profile was less favorable, with significantly elevated levels of total cholesterol and HDL. However, no significant inter-group differences were observed for the other parameters measured. Conclusions: the present findings disclose multidimensional, adverse ADMA-related changes in the health risk profile of patients with chronic heart failure hospitalized due to recurrent decompensation episodes.

HIV disease continues to be a serious health issue all over the world. By the end of 2016, 36.7 million people were living with HIV, 1.8 million people became newly infected and 1 million died of HIV-related causes/diseases. In order to develop effective treatment strategies, is important to assess the risk factors that affect negatively the HIV-positive patients. HIV-infected patients are at high risk of developing psychiatric disorders in every stage of the illness. Psychiatric disorders can negatively influence the treatment adherence, induce risk behavior and influence the quality of life. The purpose of this study is to determine if the severity of HIV disease is associated with increased frequency of psychiatric disorders. We evaluated 101 HIV-positive patients receiving antiretroviral therapy in Western Romania via Psychiatric Diagnostic Screening Questionnaire (PDSQ). We conducted a risk analysis in order to see if the patients have a higher risk of developing psychiatric disorders depending on HIV serostatus factor (HIV asymptomatic, symptomatic, AIDS converted). Our study shows that, the patients having AIDS and symptomatic HIV have a higher prevalence for the most common psychiatric disorders: major depressive disorder (OR = 5.81;p < 0.001), panic disorder (OR = 3.11; p = 0.016), agoraphobia (OR = 4.31; p = 0.024), social phobia (OR = 2.81; p = 0.038), generalized anxiety disorder (OR = 4.79; p = 0.006), somatization (OR = 8.72; p < 0.0010) and hypochondria (OR = 4.66; p = 0.0013). Symptomatic HIV and AIDS converted serostatus is also a risk factor for post-traumatic stress disorder, obsessive-compulsive disorder and psychosis. The main conclusion of this study is that the more severe HIV clinical disease was associated with increased frequency of psychiatric disorders. As a consequence, we conclude that psychiatric disorders and HIV/AIDS treatment should be addressed simultaneously, depending on the risk specific factors such as the HIV infection stage and, due to psychiatric repercussions of HIV is expected to become more relevant in the coming years.